The pulmonary microbiota was unknown for a long time, since it was commonly accepted that healthy lungs are sterile. This paradigm was cast into doubt with the discovery of the various human microbiota.
Past the upper respiratory tract (nasal and oral cavities), the lower respiratory tract plays host to a specific bacterial ecosystem. Although quantitatively very modest, it is qualitatively very diverse1-2 . This is explained in particular by the presence of specific protective systems downstream of the trachea: the mucociliary system, the glottic closure reflex and cough form physical barriers against the entrance of pathogenic organisms.
The composition of the pulmonary microbiota, far from being uniform, varies widely between the upper respiratory tract (nose, mouth) and the lower respiratory tract (lungs, bronchi, etc.)1-4. In healthy individuals, the predominant phyla are Bacteroidetes, Firmicutes, and Proteobacteria (Streptococcus, Prevotella, Fusobacterium, Veillonella and Pseudomonas)5 ahead of Haemophilus and Neisseria6. Because of the possible presence of viruses and fungi in the lungs, potential in situ interactions between these microorganisms and bacteria could be involved in the onset of diseases6 .
Presumed role and dysbiosis
Bacterial colonization in the lungs may be due, in part, to the contamination of the lower respiratory tract by the upper tract when bronchial exams are conducted1 , but biopsies conducted on explanted lungs suggest that this ecosystem truly is specific to the lungs2,7 . The complication in studying this microbiota therefore lies in the need to avoid any exterior contamination.
The exact role of the respiratory microbiota has not been well defined: it is very probably involved in defending the host against certain diseases, particularly respiratory allergy8. The balance of this microbiota can be modified by exogenous factors (tracheal tubes, tobacco, viruses, or medications) or endogenous factors (change in mucociliary clearance, glottic closure reflex, or local immunity). The resulting dysbiosis could potentially explain the onset of certain pulmonary diseases.
1 - Charlson ES et al. Topographical continuity of bacterial populations in the healthy human respiratory tract. Am J Resp Crit Care Med 2011 : 184 : 957-63. https://www.ncbi.nlm.nih.gov/pubmed/21680950
2 – Erb-Downward JR et al. Analysis of the lung microbiome in the « healthy » smokers and in COPD. PLOs ONE 2011 ;6 :e16384. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0016384
3 - Hilty M et al. Disordered microbial communities in asthmatic airways. PLoS ONE 2010 ; 5(1):e8578. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0008578
4 - Charlson ES et al. Lung-enriched organisms and aberrant bacterial and fungal respiratory microbiota after lung transplant. Am J Respir Crit Care Med 2012 ; 186(6) : 536-45. https://www.ncbi.nlm.nih.gov/pubmed/22798321
5 - Huang YJ, Lynch SV. The emerging relationship between the airway microbiota and chronic respiratory disease : clinical implications. Expert Rev Respir Med 2011 ; 5(6) : 809-21. https://www.ncbi.nlm.nih.gov/pubmed/22082166
6 - Beck JM, Young VB, Huffnagle GB. The microbiome of the lung. Transl Res 2012 ; 160(4) : 258-66. https://www.ncbi.nlm.nih.gov/pubmed/22683412
7 – Sze MA et al. The lung tissue microbiome in chronic obstructive pulmonary disease. Am J Resp Crit Care Med 2012 ; 185(10) : 1073-80. https://www.ncbi.nlm.nih.gov/pubmed/22427533
8 – Nembrini C et al. Bacterial-induced protection against allergic inflammation through a multi-component immunoregulatory mechanism. Thorax 2011 ; 66(9) : 755-63. https://www.ncbi.nlm.nih.gov/labs/articles/21422039/