Skip to main content
Download PDF

The impact of environmental factors on respiratory tract microbiome and respiratory system diseases

European Journal of Medical Research volume 30, Article number: 236 (2025) Cite this article

Abstract

The respiratory tract microbiome, a complex ecosystem of microorganisms colonizing the respiratory mucous layers and epithelial surfaces along with their associated microenvironment, plays a vital role in maintaining respiratory function and promoting the maturation of the respiratory immune system. Current research suggests that environmental changes can disrupt the respiratory microbiota, potentially leading to disease. This review summarizes existing research on the impact of environmental factors on the respiratory microbiome and associated diseases, aiming to offer new insights into the prevention and treatment of respiratory disease.

Introduction

The respiratory microbiome is a multi-kingdom microbial ecosystem inhabiting the respiratory tract mucosal layer and epithelial surfaces, from the nasal cavity to the alveoli, along with the microenvironment on which these microorganisms depend [1]. The normal respiratory microbiota serves as a barrier against pathogenic microorganisms entering the lungs, and is essential for maintaining the health of the respiratory system [2, 3]. When the respiratory microbiome becomes imbalanced and microbial diversity decreases, it can trigger or exacerbate respiratory diseases [4]. Due to the direct connection of the respiratory tract to the external environment, the respiratory microbiota is exposed to various environmental factors. Although some environmental factors have been found to potentially affect the stability and diversity of the respiratory microbiota, comprehensive systematic research remains limited. This review aims to summarize current research on the impact of environmental factors on the respiratory microbiome and related diseases, with the goal of providing new insights for the prevention and treatment of respiratory diseases.

The literature search for this study was conducted in the following databases: PubMed, Web of Science, and Google Scholar. The search period spanned from January 2010 to February 2025, with the search terms including:

Respiratory tract

(lung[MeSH Terms]) OR (lungs[Title/Abstract]) OR (airway[Title/Abstract]) OR (pulmonary[Title/Abstract]) OR (alveolar[Title/Abstract]) OR (nasopharynx[Title/Abstract]) OR (nasopharyngeal[Title/Abstract])

Microbiome

(Microbio* [Title/Abstract])

Temperature

(temperature[MeSH Terms]) OR (thermal exposure[Title/Abstract]) OR (ambient temperature[Title/Abstract]) OR (body temperature[Title/Abstract])

Heat

(heat[Title/Abstract]) OR (hyperthermia[Title/Abstract]) OR (high temperature[Title/Abstract]) OR (thermal stress[Title/Abstract]) OR (heat exposure[Title/Abstract]) OR (heat wave[Title/Abstract]) OR (extreme heat[Title/Abstract]) OR (environmental hyperthermia[Title/Abstract]) OR (exertional heat[Title/Abstract]) OR (heatstroke[Title/Abstract]) OR (heat stroke[Title/Abstract]) OR (heat shock[Title/Abstract]) OR (heat exhaustion[Title/Abstract]) OR (heat-related illness[Title/Abstract]) OR (heat syncope[Title/Abstract]) OR (heat cramps[Title/Abstract])

Humidity

(humidity[Title/Abstract]) OR (moisture[Title/Abstract]) OR (humid climate[Title/Abstract])

Environment

(environment[Title/Abstract]) OR (environmental[Title/Abstract]) OR (climate[Title/Abstract]) OR (season[Title/Abstract]) OR (seasonality[Title/Abstract])

Air pollution

(air pollution[Title/Abstract]) OR (PM2.5[Title/Abstract]) OR (PM10[Title/Abstract]) OR (ozone[Title/Abstract])

Altitude

altitude*[Title/Abstract]

Lung injury

("Lung Injury"[Mesh]) OR (Lung Injuries[Title/Abstract]) OR (Pulmonary Injury[Title/Abstract])

COPD

Chronic Obstructive Pulmonary Disease[Title/Abstract]

Asthma

Asthma [Title/Abstract]

Lung Cancer

Lung Cancer [Title/Abstract]

Interstitial lung disease

Interstitial lung disease [Title/Abstract]

The criteria for literature screening were: (i) the research was original (such as clinical trials, cohort studies, and case–control studies); (ii) it addressed the influence of the microbiota on lung health or diseases; (iii) the articles appeared in peer-reviewed journals. We excluded case reports and studies of lower quality (such as those with insufficient sample sizes or inadequate methodologies). All the literature was screened and quality-assessed by two independent researchers, with a total of 94 studies ultimately included. We qualitatively analyzed these studies, focusing on discussing their similarities and differences, and proposed the potential role of the microbiome in pulmonary health.

The composition of the respiratory microbiome

The respiratory system is crucial for gas exchange between the human body and the external environment. Historically, the lower respiratory tract was considered sterile. However, advances in genetic technologies and the widespread use of high-throughput sequencing have gradually revealed the presence of microbial communities in the lower respiratory tract and lungs. Colonization of the respiratory microbiota begins shortly after birth, with bacterial DNA detectable in tracheal aspirates from newborns within 24 h [5].

The respiratory tract is divided into the upper and lower sections, with the cricoid cartilage serving as the boundary. The upper respiratory tract includes the nasal cavity, paranasal sinuses, pharynx, and the supraglottic portion of the larynx, while the lower respiratory tract comprises the trachea, bronchi, bronchioles, respiratory bronchioles, alveolar ducts, and alveoli. The upper respiratory tract is continuously exposed to the external environment, lacking physical barriers, and its microbial composition directly impacts respiratory health. The microbiota of the oropharynx and nasopharynx share similarities, particularly at birth, when both are predominantly colonized by Streptococcus [6]. By one week postpartum, the nasopharynx is predominantly colonized by Moraxella and Haemophilus. By one month, the nasopharyngeal microbiome exhibits a high abundance of Moraxella, Staphylococcus, Streptococcus, Corynebacterium, and Haemophilus [7, 8]. However, the oropharyngeal microbiota tends to remain relatively stable over time, predominantly consisting of Streptococcus [6]. Additionally, the oropharyngeal microbiome also comprises Neisseria, Prevotella, Veillonella, and Haemophilus [7,8,9].

Current research indicates that the microbiota of the upper and lower respiratory tracts exhibits a high degree of homology. The microbiota of the lower respiratory tract primarily originates from the oropharynx, migrating to the lower respiratory tract via aspiration. However, the lower respiratory tract microbiota possesses distinct characteristics [10, 11]. The lung microbiome is predominantly composed of Proteus, Prevotella, Streptococcus, and Veillonella [12,13,14].

Relationship between respiratory microbiome alterations and respiratory diseases

The stability of the respiratory microbiome is crucial for maintaining normal respiratory function and facilitating the maturation of the neonatal immune system [5]. Normal respiratory microbiota aids in pathogen clearance, regulates host immune cell functions [15], and prevents pathogen colonization through competitive exclusion or the production of inhibitory substances [13]. An imbalance in the normal composition of the respiratory microbiota can lead to immune dysfunction, potentially triggering or exacerbating respiratory diseases [16,17,18,19,20]. Recent research has confirmed substantial differences in the lung microbiome between individuals with prevalent respiratory diseases and healthy controls, aberrant microbial populations (dysbiosis) have been confirmed in many prevalent lung diseases that are traditionally not considered to be of microbial origin [2, 21].

Chronic obstructive pulmonary disease (COPD)

Compared with the healthy control group, stable COPD patients showed a decrease in pulmonary microbiota diversity, characterized by an increased presence of Moraxella, Streptococcus, Veillonella and Prevotella [22,23,24], while those experiencing acute exacerbations of COPD exhibited elevated levels of Pseudomonas aeruginosa and Klebsiella pneumoniae in their lung microbiome [25, 26].

A prospective study of 101 patients with the exacerbation of COPD revealed that there was an increased abundance of Haemophilus, whereas the abundances of Prevotella and Veillonella decreased [27]. A cross-sectional study of 72 COPD patients revealed that airflow obstruction correlated with an elevated relative abundance of Pseudomonas in the sputum [28].

A study investigating the association between COPD severity and changes in the microbiome revealed that as the disease advanced and ventilatory function progressively worsened, the microbial diversity in the sputum of advanced COPD patients diminished, with the main microbial phyla comprising Proteobacteria, Firmicutes, Actinobacteria, and Bacteroidota [29].

A multivariate modeling analysis of sputum microbiome, host transcriptome, and proteome data demonstrated that in the host-microbiome interplay within the airways of COPD patients, Moraxella and Haemophilus were predominantly involved in linking host interferon and pro-inflammatory signaling pathways with neutrophil inflammation [23].

Distinct respiratory tract microbiota have also been confirmed among various inflammatory endotypes of COPD. A study that analyzed sputum samples from 510 subjects revealed that the respiratory tract microbiome in neutrophilic COPD was heterogeneous. One subgroup is characterized by a predominance of Haemophilus. Another subgroup represents a neutrophilic subgroup characterized by a balanced microbial composition [30]. A cohort study involving 87 COPD patients demonstrated an association between neutrophilic inflammation and elevated Moraxella levels in sputum samples [31]. Analysis of a 43-subject cohort identified positive correlations between neutrophilic predominance and increased sputum abundances of Haemophilus and Neisseria [23]. Neutrophilic inflammation exhibited lower microbial diversity compared to other COPD inflammatory endotypes [32]. Conversely, eosinophilic inflammation in COPD correlated with reduced bacterial infections and enhanced lung microbiota diversity [28, 30,31,32,33,34]. Therefore, inflammation-specific alterations in respiratory microbiota composition may serve as viable biomarkers to track and anticipate inflammatory phenotypes in COPD patients.

Nonetheless, a study examining whether the lower respiratory tract microbiome composition could forecast the risk of future exacerbations in COPD patients found that the relative abundance of various microbial communities displayed considerable variability among samples and individuals, and that the individual differences in the lower respiratory tract microbiome were far greater than the differences between frequent and infrequent exacerbators [35]. Consequently, substantial experimental validation is required to determine if the respiratory tract microbiome can be utilized as a biomarker for predicting disease severity and inflammatory states in COPD.

Asthma

Asthma patients demonstrate elevated abundances of Proteus, Haemophilus, Moraxella, and Neisseria in their pulmonary microbiome compared to healthy controls [21, 36,37,38,39]. Sputum samples from asthma patients show a higher relative abundance of Neisseria and Proteus and increased microbial diversity, whereas Firmicutes and Actinobacteria dominate in healthy individuals [40]. Actinobacteria abundance is significantly higher in severe asthma patients relative to healthy controls or individuals with mild-to-moderate asthma [41].

Asthmatic children exhibit elevated nasal abundances of Moraxella and Haemophilus compared to healthy controls [42, 43]. A cohort study involving 234 Australian children (2- to 12-month-old) with asthma revealed that their nasopharyngeal microbiome was dominated by Haemophilus, Streptococcus, Moraxella, Alloiococcus, Corynebacterium, and Staphylococcus [44].

Asthma and COPD demonstrate overlapping inflammatory phenotypes (neutrophilic and eosinophilic infiltration) with analogous microbiome profiles. Patients presenting with neutrophilic asthma show reduced microbial diversity in the respiratory microbiome relative to other inflammatory endotypes [31, 38, 45, 46].

In contrast to adults, childhood asthma risk correlates with the composition of the respiratory microbiome during early developmental stages. A prospective cohort study demonstrated that elevated relative abundances of Veillonella and Prevotella in the neonatal respiratory microbiome at 1 month of age are linked to an increased risk of asthma by 6 years [42], increased nasal colonization by Haemophilus and sustained low Moraxella abundance in infancy (0–12 months) are correlated with asthma diagnosis by 7 years of age [47], oropharyngeal Neisseria abundance during the second year of life shows a positive correlation with asthma incidence [48]. Elevated airway bacterial loads in asthmatic children are characterized by suppressed TNF-α/IL-1β production and upregulated CCL2/CCL17 expression [42]. Given that CCL2 and CCL17 serve as independent asthma biomarkers [49], these findings imply microbial-driven immune dysregulation may contribute significantly to asthmatic mechanisms.

Lung cancer

Emerging research highlights the association between lung cancer and chronic inflammatory respiratory conditions, with mounting evidence underscoring the pathological interplay between lung cancer and COPD [50]. Prospective cohort analysis revealed a significant association between pulmonary Veillonella enrichment and adverse clinical outcomes in lung cancer patients [51], highlighting the potential involvement of lung microbiome dysbiosis in tumorigenesis and disease progression.

Patients with lung cancer exhibit elevated abundances of Streptococcus and Prevotella in the lower respiratory tract relative to healthy individuals [52, 53]. Compared to healthy subjects, salivary microbiome profiling of NSCLC patients revealed increased Veillonella colonization and decreased Neisseria abundance [54]. Research indicates that elevated abundances of Streptococcus and Veillonella in cancer patient bronchoalveolar lavage fluid (BALF) correlate with enhanced infiltration of inflammatory cells and activation of the PI3K/ERK signaling axis in bronchial epithelial cells [55]. Another study found that Bacteroidota enrichment in the lower respiratory tract exerts protective effects against lung carcinogenesis [56], compositional shifts in Prevotella, Streptococcus, and Clostridium within the lower airways show significant correlations with the magnitude of localized pulmonary inflammation [57].

Interstitial lung disease

Compared with the healthy control group, patients with interstitial pneumonia exhibited a decreased abundance of Streptococcus in BALF, while the abundance of Prevotella and Veillonella increased [58]. Research has shown that the bacterial burden in BALF from patients with idiopathic pulmonary fibrosis (IPF) exceeds that of healthy controls, with microbial communities like Streptococcus and Staphylococcus linked to accelerated disease progression [59,60,61,62]. Consequently, factors affecting the respiratory microbial ecosystem could exert an indirect influence on the development and clinical outcomes of these diseases.

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS)

By constructing a standard ALI murine model through intratracheal LPS administration, researchers observed that Firmicutes, Proteobacteria, and Bacteroidetes in ALI mouse BALF exhibited positive correlations with total cell counts, while Actinobacteria was inversely associated [63]. Accumulating clinical evidence demonstrates marked dysbiosis in the lung microbiota of ALI/ARDS patients [64, 65], which may be mechanistically linked to injury-driven upregulation of inflammation-promoting factors that enhance bacterial proliferation and destabilize the pulmonary microenvironment.

Experimental studies revealed that hyperoxic exposure (FiO2 95%) induced lung microbiota alterations in mice as early as 24 h, preceding the development of hyperoxia-mediated lung injury observed at 72 h post-exposure [66]. This temporal pattern implies potential involvement of airway microbiota in the initiation of ALI/ARDS pathology.

Consequently, factors affecting the respiratory microbial ecosystem could exert an indirect influence on the development and clinical outcomes of these diseases.

The impact of environmental factors on the respiratory microbiome

Environmental temperature and humidity

Variations in ambient temperature can influence the composition of the respiratory microbiome. Wang et al. observed that periodic exposure to elevated environmental temperatures significantly altered the diversity of the respiratory microbiota in 11-week-old healthy Isa brown layer-type pullets. Specifically, the group exposed to 30 °C exhibited a marked increase in Proteobacteria and a concurrent decrease in Firmicutes in BALF compared to the control group maintained at 24 °C [67]. In female mice, concurrent exposure to 1 ppm ozone and a 36 °C thermal environment resulted in a reduction of Firmicutes in BALF, alongside an increase in total protein, tumor necrosis factor-alpha (TNF-α), and 8-hydroxydeoxyguanosine (8-OHdG) levels [68]. High-temperature environments can enhance the proliferation of pathogenic bacteria, including Staphylococcus aureus and Streptococcus pneumoniae, thereby diminishing the diversity of the normal respiratory microbiota. Conversely, low-temperature environments also impact the respiratory microbiota [69]. Clinical studies have indicated that prolonged inhalation of cold air at 26 °C can decrease the abundance of Moraxella species in the pharynx of healthy individuals [70]. Furthermore, rabbits exposed to 4 °C and 20 °C environments demonstrated significant differences in their lung microbiome composition, with a higher prevalence of Proteus at 4 °C compared to 20 °C [69].

The detrimental health implications of prolonged exposure to high temperatures are widely recognized. Additionally, unsuitable environmental humidity levels can adversely impact health, especially when compounded by high temperatures [71]. Studies have demonstrated that under hot and humid conditions, characterized by 31–33 °C with 91–95% relative humidity, the diversity of the gut microbiota in mice is observed to be distinct from that under standard conditions [72]. Within these environments, there is a notable reduction in Firmicutes and a corresponding increase in Bacteroidota in mouse feces [73]. Research investigating changes in oropharyngeal microbiota and their association with environmental conditions among school-aged children in Ivorian demonstrated an inverse relationship between Neisseria abundance and humidity levels [74].

Air pollutants

Environmental pollution is emerging as a critical social issue in contemporary society. Sources such as industrial emissions, vehicular exhaust, combustion of fossil fuels, construction dust, and natural phenomena (e.g., sandstorms) contribute to the production of various air pollutants, including particulate matter (PM2.5, PM10), sulfur dioxide, carbon monoxide, nitrogen oxides, volatile organic compounds (VOCs), and ozone [75]. Research indicates that exposure to elevated concentrations of PM2.5 significantly impacts the lung microbiota in mice, leading to an increased abundance of Bacteroidota and Firmicutes [76]. Prolonged exposure to air pollutants can facilitate the colonization of pathogenic bacteria in the respiratory tract, such as Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella [77]. A study examining the correlation between air pollutants during winter heating periods in northeastern China and respiratory microbiota imbalance revealed that individuals in highly polluted areas exhibited higher relative abundances of Firmicutes and Proteobacteria in their throat swabs compared to those in less polluted regions. Furthermore, as air pollution levels rise, the relative abundance of Fusobacterium and Prevotella species declines [78].

Compound factors

Relative to environmental temperature, seasonal variation represents a more intricate factor, encompassing variations in temperature, precipitation, daylight duration, biodiversity, and human activities. The upper respiratory tract microbiota composition fluctuates across different seasons [79]. Research has indicated that during the fall and winter seasons, the nasopharyngeal abundance of Proteobacteria is elevated in children, whereas Bacteroidota becomes predominant in the spring [80].

The impact of altitude on the human body is also multifaceted. Regions at high altitude are defined by reduced atmospheric pressure, diminished oxygen partial pressure, intense ultraviolet radiation, low temperatures, arid conditions, and powerful winds [81]. The respiratory microbiota under normal circumstances encompasses both aerobic and anaerobic bacteria, which exhibit distinct adaptive mechanisms in response to fluctuating oxygen levels. In hypoxic conditions prevalent at high altitudes, there may be a reduction in the diversity of aerobic bacteria within the respiratory tract [82]. Nonetheless, scientific inquiry into this domain is exceedingly constrained.

Mechanisms of environmental factors affect the respiratory microbiome

Direct effects

Changes in environmental factors can directly influence the proliferation and reproduction of respiratory microorganisms, consequently impacting their prevalence in the respiratory tract. In vitro research has demonstrated that modifications to the culture environment can alter the quantity and vitality of respiratory microorganisms. One study explored the effects of environmental oxygen concentration (anaerobic environment, or aerobic environment provided by catalase) and temperature (30–39 °C) on the growth of multiple Streptococcus pneumoniae strains in vitro. Under aerobic conditions provided by catalase and at temperatures of 30–35 °C (normal nasal cavity temperature), the strains reached maximum density after 24 h of incubation. As the incubation temperature rose, the density of the strains diminished, with the minimum density recorded at temperatures between 37 °C and 39 °C. The majority of strains displayed optimal growth rates at temperatures of 35 °C to 37 °C and exhibited more rapid growth under aerobic conditions compared to anaerobic ones [83]. An additional study determined that the storage temperature of sputum samples significantly influenced the viability of Streptococcus pneumoniae, with a marked decrease in viability observed at 4 °C relative to room temperature [84].

Changes in environmental factors can also affect the virulence of respiratory microorganisms elicit inflammatory responses within the respiratory tract, thereby disrupting the respiratory microenvironment and affecting its stability. Under environmental conditions of 26 °C, the expression of the outer membrane protein UspA1 in Moraxella catarrhalis escalates, which facilitates bacterial adhesion to upper respiratory tract cells, augmenting its virulence and perturbing the normal respiratory microenvironment [85]. At 26 °C, Moraxella also enhances the bacteria-induced release of IL-8, exacerbating the inflammatory response [70].

The gut-lung axis

The gut–lung axis has emerged as a prevalent area of investigation, delineating the intricate interactions between the gut microbiota and pulmonary health, and its pivotal role in modulating immune and inflammatory responses [86]. The BALF of ARDS patients exhibits a high prevalence and abundance of the gut-specific genus Bacteroides, which is linked to the severity of systemic inflammation [65]. Notably, Bacteroides fragilis has been demonstrated to contribute to the prevention of respiratory infections [87, 88]. Evidence has established an association between intestinal microbial changes and the development of asthma [89]. Emerging research has uncovered that the intestinal protozoan Tritrichomonas musculis regulates the lung immune environment, thereby mediating immune reactions associated with allergic airway inflammation and pulmonary infections [90].

Current researches indicate that short-chain fatty acids, produced by the gut microbiota, along with their extracellular vesicles, can permeate the pulmonary system via the circulatory or lymphatic pathways, thereby influencing the pulmonary microenvironment [91, 92]. Moreover, when the intestinal mucosal barrier is disrupted, gut microbiota have the potential to infiltrate the bloodstream or lymphatic system, subsequently reaching the lungs and modulating the composition of the pulmonary microbiota [92]. Persistent exposure to elevated temperatures or intense physical exertion under such conditions can amplify heat stress, intensify oxidative stress within the intestines, impair intestinal epithelial cells and tight junction proteins, and erode the intestinal physical barrier. Consequently, this enables gut bacteria to invade the bloodstream and migrate to the lungs, subsequently impacting the lung microbiome [93]. Nonetheless, comprehensive research focusing on the precise alterations within the gut–lung axis under various environmental conditions and their association with the respiratory microbiome and pulmonary diseases remains sparse.

Conclusion and outlook

As global warming intensifies and air pollution worsens, the impact of environmental factors on health is gaining increasing attention. The respiratory tract is directly exposed to atmospheric physical and chemical parameters, making it a keyway through which environmental factors affect human health. Existing evidence has indicated that environmental temperature, humidity, and air pollutants potentially alter the incidence of respiratory diseases by affecting the respiratory microbiome. However, there is a dearth of comprehensive and systematic research in this area. Additionally, investigations into microorganisms aid in preventing both the initiation and advancement of diseases. Existing evidence confirms that probiotic intake reduces susceptibility to respiratory infections [94]. Future studies should aim to investigate the variations in the respiratory microbiome under diverse environmental conditions, to enhance our understanding of its role in perpetuating homeostasis and to clarify its regulatory mechanisms. Such investigations could yield novel insights and therapeutic strategies for disease prevention and management.

Availability of data and materials

No datasets were generated or analysed during the current study.

References

  1. Pérez-Cobas AE, Rodríguez-Beltrán J, Baquero F, et al. Ecology of the respiratory tract microbiome. Trends Microbiol. 2023;31(9):972–84.

    Article  PubMed  Google Scholar 

  2. Budden KF, Shukla SD, Rehman SF, et al. Functional effects of the microbiota in chronic respiratory disease. Lancet Respir Med. 2019;7(10):907–20.

    Article  PubMed  Google Scholar 

  3. Perdijk O, Azzoni R, Marsland BJ. The microbiome: an integral player in immune homeostasis and inflammation in the respiratory tract. Physiol Rev. 2024;104(2):835–79.

    Article  PubMed  CAS  Google Scholar 

  4. Li R, Li J, Zhou X. Lung microbiome: new insights into the pathogenesis of respiratory diseases. Signal Transduct Target Ther. 2024;9(1):19.

    Article  PubMed  PubMed Central  Google Scholar 

  5. Pattaroni C, Watzenboeck ML, Schneidegger S, et al. Early-life formation of the microbial and immunological environment of the human airways. Cell Host Microbe. 2018;24(6):857-865.e4.

    Article  PubMed  CAS  Google Scholar 

  6. Man WH, Clerc M, De Steenhuijsen PWAA, et al. Loss of microbial topography between oral and nasopharyngeal microbiota and development of respiratory infections early in life. Am J Respir Crit Care Med. 2019;200(6):760–70.

    Article  PubMed  CAS  Google Scholar 

  7. Natalini JG, Singh S, Segal LN. The dynamic lung microbiome in health and disease. Nat Rev Microbiol. 2023;21(4):222–35.

    Article  PubMed  CAS  Google Scholar 

  8. De Steenhuijsen PWAA, Binkowska J, Bogaert D. Early life microbiota and respiratory tract infections. Cell Host Microbe. 2020;28(2):223–32.

    Article  Google Scholar 

  9. Charlson ES, Bittinger K, Haas AR, et al. Topographical continuity of bacterial populations in the healthy human respiratory tract. Am J Respir Crit Care Med. 2011;184(8):957–63.

    Article  PubMed  PubMed Central  Google Scholar 

  10. Human Microbiome Project Consortium. Structure, function and diversity of the healthy human microbiome. Nature. 2012;486(7402):207–14.

    Article  Google Scholar 

  11. Di Simone SK, Rudloff I, Nold-Petry CA, et al. Understanding respiratory microbiome-immune system interactions in health and disease. Sci Trans Med. 2023;15(678):5126.

    Article  Google Scholar 

  12. Barcik W, Boutin RCT, Sokolowska M, et al. The role of lung and gut microbiota in the pathology of asthma. Immunity. 2020;52(2):241–55.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  13. Drigot ZG, Clark SE. Insights into the role of the respiratory tract microbiome in defense against bacterial pneumonia. Curr Opin Microbiol. 2024;77: 102428.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  14. Wypych TP, Wickramasinghe LC, Marsland BJ. The influence of the microbiome on respiratory health. Nat Immunol. 2019;20(10):1279–90.

    Article  PubMed  CAS  Google Scholar 

  15. Park YC, Choi SY, Cha Y, et al. Microbiome-mucosal immunity nexus: driving forces in respiratory disease progression. J Microbiol. 2024;62(9):709.

    Article  PubMed  Google Scholar 

  16. Molyneaux PL, Mallia P, Cox MJ, et al. Outgrowth of the bacterial airway microbiome after rhinovirus exacerbation of chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2013;188(10):1224–31.

    Article  PubMed  PubMed Central  Google Scholar 

  17. Dickson RP, Martinez FJ, Huffnagle GB. The role of the microbiome in exacerbations of chronic lung diseases. Lancet. 2014;384(9944):691–702.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  18. Opron K, Begley LA, Erb-Downward JR, et al. Lung microbiota associations with clinical features of COPD in the SPIROMICS cohort. npj Biofilms Microbio. 2021;7(1):14.

    Article  Google Scholar 

  19. Rogers GB, van der Gast CJ, Cuthbertson L, et al. Clinical measures of disease in adult non-CF bronchiectasis correlate with airway microbiota composition. Thorax. 2013;68(8):731–7.

    Article  PubMed  Google Scholar 

  20. Zhao J, Schloss PD, Kalikin LM, et al. Decade-long bacterial community dynamics in cystic fibrosis airways. Proc Natl Acad Sci USA. 2012;109(15):5809–14.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  21. Whiteside SA, McGinniss JE, Collman RG. The lung microbiome: progress and promise. J Clin Investig. 2021;131(15): e150473.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  22. Bowerman KL, Rehman SF, Vaughan A, et al. Disease-associated gut microbiome and metabolome changes in patients with chronic obstructive pulmonary disease. Nat Commun. 2020;11(1):5886.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  23. Wang Z, Maschera B, Lea S, et al. Airway host-microbiome interactions in chronic obstructive pulmonary disease. Respir Res. 2019;20(1):113.

    Article  PubMed  PubMed Central  Google Scholar 

  24. Erb-Downward JR, Thompson DL, Han MK, et al. Analysis of the lung microbiome in the “healthy” smoker and in COPD. PLoS ONE. 2011;6(2): e16384.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  25. Einarsson GG, Comer DM, McIlreavey L, et al. Community dynamics and the lower airway microbiota in stable chronic obstructive pulmonary disease, smokers and healthy non-smokers. Thorax. 2016;71(9):795–803.

    Article  PubMed  CAS  Google Scholar 

  26. Xue Q, Xie Y, He Y, et al. Lung microbiome and cytokine profiles in different disease states of COPD: a cohort study. Sci Rep. 2023;13(1):5715.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  27. Mayhew D, Devos N, Lambert C, et al. Longitudinal profiling of the lung microbiome in the AERIS study demonstrates repeatability of bacterial and eosinophilic COPD exacerbations. Thorax. 2018;73(5):422–30.

    Article  PubMed  Google Scholar 

  28. Millares L, Pascual S, Montón C, et al. Relationship between the respiratory microbiome and the severity of airflow limitation, history of exacerbations and circulating eosinophils in COPD patients. BMC Pulm Med. 2019;19(1):112.

    Article  PubMed  PubMed Central  Google Scholar 

  29. Garcia-Nuñez M, Millares L, Pomares X, et al. Severity-related changes of bronchial microbiome in chronic obstructive pulmonary disease. J Clin Microbiol. 2014;52(12):4217–23.

    Article  PubMed  PubMed Central  Google Scholar 

  30. Wang Z, Locantore N, Haldar K, et al. Inflammatory endotype-associated airway microbiome in chronic obstructive pulmonary disease clinical stability and exacerbations: a multicohort longitudinal analysis. Am J Respir Crit Care Med. 2021;203(12):1488–502.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  31. Wang Z, Bafadhel M, Haldar K, et al. Lung microbiome dynamics in COPD exacerbations. Eur Respir J. 2016;47(4):1082–92.

    Article  PubMed  Google Scholar 

  32. Wang Z, Singh R, Miller BE. Sputum microbiome temporal variability and dysbiosis in chronic obstructive pulmonary disease exacerbations: an analysis of the COPDMAP study. Thorax. 2018;73(4):331–8.

    Article  PubMed  Google Scholar 

  33. Ghebre MA, Pang PH, Diver S. Biological exacerbation clusters demonstrate asthma and chronic obstructive pulmonary disease overlap with distinct mediator and microbiome profiles. J Allergy Clin Immunol. 2018;141(6):2027–36.

    Article  PubMed  PubMed Central  Google Scholar 

  34. Dicker AJ, Huang JTJ, Lonergan M, et al. The sputum microbiome, airway inflammation, and mortality in chronic obstructive pulmonary disease. J Allergy Clin Immunol. 2021;147(1):158–67.

    Article  PubMed  CAS  Google Scholar 

  35. Leiten EO, Nielsen R, Wiker HG, et al. The airway microbiota and exacerbations of COPD. ERJ Open Res. 2020;6(3):168–2020.

    Article  Google Scholar 

  36. Durack J, Lynch SV, Nariya S. Features of the bronchial bacterial microbiome associated with atopy, asthma, and responsiveness to inhaled corticosteroid treatment. J Allergy Clin Immunol. 2017;140(1):63–75.

    Article  PubMed  CAS  Google Scholar 

  37. Yagi K, Huffnagle GB, Lukacs NW, et al. The lung microbiome during health and disease. Int J Mol Sci. 2021;22(19):10872.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  38. Simpson JL, Daly J, Baines KJ, et al. Airway dysbiosis: haemophilus influenzae and tropheryma in poorly controlled asthma. Eur Respir J. 2016;47(3):792–800.

    Article  PubMed  Google Scholar 

  39. Diver S, Richardson M, Haldar K, et al. Sputum microbiomic clustering in asthma and chronic obstructive pulmonary disease reveals a haemophilus-predominant subgroup. Allergy. 2020;75(4):808–17.

    Article  PubMed  CAS  Google Scholar 

  40. Marri PR, Stern DA, Wright AL, et al. Asthma-associated differences in microbial composition of induced sputum. J Allergy Clin Immunol. 2013;131(2):346–52.

    Article  PubMed  CAS  Google Scholar 

  41. Huang YJ, Nariya S, Harris JM, et al. The airway microbiome in patients with severe asthma: associations with disease features and severity. J Allergy Clin Immunol. 2015;136(4):874–84.

    Article  PubMed  PubMed Central  Google Scholar 

  42. Thorsen J, Rasmussen MA, Waage J, et al. Infant airway microbiota and topical immune perturbations in the origins of childhood asthma. Nat Commun. 2019;10(1):5001.

    Article  PubMed  PubMed Central  Google Scholar 

  43. van Beveren GJ, Said H, van Houten MA, et al. The respiratory microbiome in childhood asthma. J Allergy Clin Immunol. 2023;152(6):1352–67.

    Article  PubMed  Google Scholar 

  44. Teo SM, Mok D, Pham K, et al. The infant nasopharyngeal microbiome impacts severity of lower respiratory infection and risk of asthma development. Cell Host Microbe. 2015;17(5):704–15.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  45. Taylor SL, Leong LEX, Choo JM, et al. Inflammatory phenotypes in patients with severe asthma are associated with distinct airway microbiology. J Allergy Clin Immunol. 2018;141(1):94-103.e15.

    Article  PubMed  Google Scholar 

  46. Durack J, Christian LS, Nariya S, et al. Distinct associations of sputum and oral microbiota with atopic, immunologic, and clinical features in mild asthma. J Allergy Clin Immunol. 2020;146(5):1016–26.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  47. Toivonen L, Karppinen S, Schuez-Havupalo L, et al. Longitudinal changes in early nasal microbiota and the risk of childhood asthma. Pediatrics. 2020;146(4): e20200421.

    Article  PubMed  Google Scholar 

  48. Raita Y, Pérez-Losada M, Freishtat RJ, et al. Integrated omics endotyping of infants with respiratory syncytial virus bronchiolitis and risk of childhood asthma. Nat Commun. 2021;12(1):3601.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  49. Leung TF, Wong CK, Chan IHS, et al. Plasma concentration of thymus and activation-regulated chemokine is elevated in childhood asthma. J Allergy Clin Immunol. 2002;110(3):404–9.

    Article  PubMed  CAS  Google Scholar 

  50. Mouronte-Roibás C, Leiro-Fernández V, Fernández-Villar A, et al. COPD, emphysema and the onset of lung cancer a systematic review. Cancer Lett. 2016;382(2):240–4.

    Article  PubMed  Google Scholar 

  51. Tsay JCJ, Wu BG, Sulaiman I, et al. Lower airway dysbiosis affects lung cancer progression. Cancer Discov. 2021;11(2):293–307.

    Article  PubMed  CAS  Google Scholar 

  52. He JQ, Chen Q, Wu SJ, et al. Potential implications of the lung microbiota in patients with chronic obstruction pulmonary disease and non-small cell lung cancer. Front Cell Infect Microbiol. 2022;12: 937864.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  53. Goto T. Microbiota and lung cancer. Semin Cancer Biol. 2022;86:1–10.

    Article  PubMed  Google Scholar 

  54. Yan X, Yang M, Liu J, et al. Discovery and validation of potential bacterial biomarkers for lung cancer. Am J Cancer Res. 2015;5(10):3111.

    PubMed  PubMed Central  CAS  Google Scholar 

  55. Tsay JCJ, Wu BG, Badri MH, et al. Airway microbiota is associated with upregulation of the PI3K pathway in lung cancer. Am J Respir Crit Care Med. 2018;198(9):1188–98.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  56. Pindling S, Klugman M, Lan Q, et al. Narrative review: respiratory tract microbiome and never smoking lung cancer. J Thorac Dis. 2023;15(8):4522–9.

    Article  PubMed  PubMed Central  Google Scholar 

  57. Segal LN, Clemente JC, Tsay JCJ, et al. Enrichment of the lung microbiome with oral taxa is associated with lung inflammation of a Th17 phenotype. Nat Microbiol. 2016;1(5):16031.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  58. Vázquez-Pérez JA, Carrillo CO, Iñiguez-García MA, et al. Alveolar microbiota profile in patients with human pulmonary tuberculosis and interstitial pneumonia. Microb Pathog. 2020;139: 103851.

    Article  PubMed  Google Scholar 

  59. Molyneaux PL, Cox MJ, Willis-Owen SAG, et al. The role of bacteria in the pathogenesis and progression of idiopathic pulmonary fibrosis. Am J Respir Crit Care Med. 2014;190(8):906–13.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  60. Invernizzi R, Barnett J, Rawal B, et al. Bacterial burden in the lower airways predicts disease progression in idiopathic pulmonary fibrosis and is independent of radiological disease extent. Eur Respir J. 2020;55(4):1901519.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  61. O’Dwyer DN, Ashley SL, Gurczynski SJ, et al. Lung microbiota contribute to pulmonary inflammation and disease progression in pulmonary fibrosis. Am J Respir Crit Care Med. 2019;199(9):1127–38.

    Article  PubMed  PubMed Central  Google Scholar 

  62. Han MK, Zhou Y, Murray S, et al. Lung microbiome and disease progression in idiopathic pulmonary fibrosis: an analysis of the COMET study. Lancet Respir Med. 2014;2(7):548–56.

    Article  PubMed  PubMed Central  Google Scholar 

  63. Zheng L, Liu C, Wang H, et al. Intact lung tissue and bronchoalveolar lavage fluid are both suitable for the evaluation of murine lung microbiome in acute lung injury. Microbiome. 2024;12(1):56.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  64. Panzer AR, Lynch SV, Langelier C, et al. Lung microbiota is related to smoking status and to development of acute respiratory distress syndrome in critically ill trauma patients. Am J Respir Crit Care Med. 2018;197(5):621–31.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  65. Dickson RP, Singer BH, Newstead MW, et al. Enrichment of the lung microbiome with gut bacteria in sepsis and the acute respiratory distress syndrome. Nat Microbiol. 2016;1(10):16113.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  66. Ashley SL, Sjoding MW, Popova AP, et al. Lung and gut microbiota are altered by hyperoxia and contribute to oxygen-induced lung injury in mice. Sci Trans Med. 2020;12(556):9959.

    Article  Google Scholar 

  67. Wang M, Lin X, Jiao H, et al. Mild heat stress changes the microbiota diversity in the respiratory tract and the cecum of layer-type pullets. Poult Sci. 2020;99(12):7015–26.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  68. Xu F, Wu Q, Yang Y, et al. High temperature exacerbates ozone-induced airway inflammation: implication of airway microbiota and metabolites. Sci Total Environ. 2023;903: 166795.

    Article  PubMed  CAS  Google Scholar 

  69. Lawrence KE, Lam KC, Morgun A, et al. Effect of temperature and time on the thanatomicrobiome of the cecum, ileum, kidney, and lung of domestic rabbits. J Vet Diagn Invest. 2019;31(2):155–63.

    Article  PubMed  PubMed Central  Google Scholar 

  70. Spaniol V, Troller R, Aebi C. Physiologic cold shock increases adherence of moraxella catarrhalis to and secretion of interleukin 8 in human upper respiratory tract epithelial cells. J Infect Dis. 2009;200(10):1593–601.

    Article  PubMed  CAS  Google Scholar 

  71. Fang W, Li Z, Gao J, et al. The joint and interaction effect of high temperature and humidity on mortality in China. Environ Int. 2023;171: 107669.

    Article  PubMed  Google Scholar 

  72. Wu Y, Feng X, Li M, et al. Gut microbiota associated with appetite suppression in high-temperature and high-humidity environments. EBioMedicine. 2024;99:104918.

    Article  PubMed  CAS  Google Scholar 

  73. Weng H, Deng L, Wang T, et al. Humid heat environment causes anxiety-like disorder via impairing gut microbiota and bile acid metabolism in mice. Nat Commun. 2024;15(1):5697.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  74. Diallo K, Missa KF, Tuo KJ, et al. Spatiotemporal dynamics of the oropharyngeal microbiome in a cohort of Ivorian school children. Sci Rep. 2024;14(1):30895.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  75. Klimkaite L, Liveikis T, Kaspute G, et al. Air pollution-associated shifts in the human airway microbiome and exposure-associated molecular events. Future Microbiol. 2023;18(9):607–23.

    Article  PubMed  CAS  Google Scholar 

  76. Li J, Hu Y, Liu L, et al. PM2.5 exposure perturbs lung microbiome and its metabolic profile in mice. Sci Total Environ. 2020;721:137432.

    Article  PubMed  CAS  Google Scholar 

  77. Qin T, Zhang F, Zhou H, et al. High-level PM2.5/PM10 exposure is associated with alterations in the human pharyngeal microbiota composition. Front Microbiol. 2019;10:54.

    Article  PubMed  PubMed Central  Google Scholar 

  78. Li X, Sun Y, An Y, et al. Air pollution during the winter period and respiratory tract microbial imbalance in a healthy young population in northeastern China. Environ Pollut. 2019;246:972–9.

    Article  PubMed  CAS  Google Scholar 

  79. McCauley KE, Flynn K, Calatroni A, et al. Seasonal airway microbiome and transcriptome interactions promote childhood asthma exacerbations. J Allergy Clin Immunol. 2022;150(1):204–13.

    Article  PubMed  CAS  Google Scholar 

  80. Bogaert D, Keijser B, Huse S, et al. Variability and diversity of nasopharyngeal microbiota in children: a Metagenomic analysis. PLoS ONE. 2011;6(2): e17035.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  81. Chen P, Liu Y, Liu W, et al. Impact of high-altitude hypoxia on bone defect repair: a review of molecular mechanisms and therapeutic implications. Front Med. 2022;9: 842800.

    Article  Google Scholar 

  82. Geng X, Qu C, Zhao L, et al. Effects of high-/low-temperature and high-altitude hypoxic environments on gut microbiota of sports people: a retrospective analysis. Sports Med Health Sci. 2023;5(2):83–90.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  83. Tóthpál A, Desobry K, Joshi SS, et al. Variation of growth characteristics of pneumococcus with environmental conditions. BMC Microbiol. 2019;19(1):304.

    Article  PubMed  PubMed Central  Google Scholar 

  84. Allicock OM, York A, Waghela P, et al. Impact of temporary storage conditions on the viability of streptococcus pneumoniae in saliva. mSphere. 2022;7(6):e00331-e422.

    Article  PubMed  PubMed Central  Google Scholar 

  85. Jones MM, Murphy TF. Expression of the oligopeptide permease operon of moraxella catarrhalis is regulated by temperature and nutrient availability. Infect Immun. 2015;83(9):3497–505.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  86. Kloepfer KM, Kennedy JL. Childhood respiratory viral infections and the microbiome. J Allergy Clin Immunol. 2023;152(4):827–34.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  87. Johnson JL, Jones MB, Cobb BA. Polysaccharide-experienced effector T cells induce IL-10 in FoxP3+ regulatory T cells to prevent pulmonary inflammation. Glycobiology. 2018;28(1):50–8.

    Article  PubMed  CAS  Google Scholar 

  88. Zhu W, Wu Y, Liu H, et al. Gut-lung axis: microbial crosstalk in pediatric respiratory tract infections. Front Immunol. 2021;12: 741233.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  89. Arrieta MC, Stiemsma LT, Dimitriu PA, et al. Early infancy microbial and metabolic alterations affect risk of childhood asthma. Sci Trans Med. 2015;7(307):307152.

    Article  Google Scholar 

  90. Burrows K, Ngai L, Chiaranunt P, et al. A gut commensal protozoan determines respiratory disease outcomes by shaping pulmonary immunity. Cell. 2025;188(2):316-330.e12.

    Article  PubMed  CAS  Google Scholar 

  91. Galeana-Cadena D, Gómez-García IA, Lopez-Salinas KG, et al. Winds of change a tale of: asthma and microbiome. Front Microbiol. 2023;14:1295215.

    Article  PubMed  PubMed Central  Google Scholar 

  92. Özçam M, Lynch SV. The gut-airway microbiome axis in health and respiratory diseases. Nat Rev Microbiol. 2024;22(8):492.

    Article  PubMed  Google Scholar 

  93. Jakobsson HE, Abrahamsson TR, Jenmalm MC, et al. Decreased gut microbiota diversity, delayed bacteroidetes colonisation and reduced Th1 responses in infants delivered by caesarean section. Gut. 2014;63(4):559–66.

    Article  PubMed  CAS  Google Scholar 

  94. Takeshita K, Hishiki H, Takei H, et al. The effectiveness of heat-killed pediococcus acidilactici K15 in preventing respiratory tract infections in preterm infants: a pilot double-blind, randomized, placebo-controlled study. Nutrients. 2024;16(21):3635.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

Download references

Funding

This work was supported by National Key R&D Program of Ministry of Science and Technology (2022YFC2403603,2021YFC2501899).

Author information

Authors and Affiliations

  1. Emergency Department of West China Hospital, Sichuan University, No. 37 Guoxue Alley, Chengdu, 610041, Sichuan, China

    Yutao Ge, Guo Tang, Yawen Fu, Peng Deng & Rong Yao

Authors
  1. Yutao Ge
    View author publications

    You can also search for this author inPubMed Google Scholar

  2. Guo Tang
    View author publications

    You can also search for this author inPubMed Google Scholar

  3. Yawen Fu
    View author publications

    You can also search for this author inPubMed Google Scholar

  4. Peng Deng
    View author publications

    You can also search for this author inPubMed Google Scholar

  5. Rong Yao
    View author publications

    You can also search for this author inPubMed Google Scholar

Contributions

Each author is expected to have made substantial contributions to the conception OR design of the work,Y.G. wrote the main manuscript text, R.Y. and G.T. had substantively revised the manuscript text, P.D. and Y.F. had put forward an innovative perspective. All authors reviewed the manuscript. AND to have approved the submitted version (and any substantially modified version that involves the author's contribution to the study);AND to have agreed both to be personally accountable for the author's own contributions and to ensure that questions related to the accuracy or integrity of any part of the work, even ones in which the author was not personally involved, are appropriately investigated, resolved, and the resolution documented in the literature.

Corresponding author

Correspondence to Rong Yao.

Ethics declarations

Ethical approval and consent to participate

Not applicable.

Competing interests

The authors declare no competing interests.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Ge, Y., Tang, G., Fu, Y. et al. The impact of environmental factors on respiratory tract microbiome and respiratory system diseases. Eur J Med Res 30, 236 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s40001-025-02517-3

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s40001-025-02517-3

Keywords

European Journal of Medical Research

ISSN: 2047-783X

Contact us