The historical hypothesis of sterility of the lungs was invalidated over a decade ago when studies demonstrated the existence of sparse but very diverse bacterial populations in the normal lung and the association between pulmonary dysbiosis and chronic respiratory diseases. Under mechanical ventilation, dysbiosis occurs rapidly with a gradual decline in diversity over time and the progressive predominance of a bacterial pathogen (mainly Proteobacteria) when lung infection occurs. During acute respiratory distress syndrome, an enrichment in bacteria of intestinal origin, mainly Enterobacteriaceae, is observed. However, the role of this dysbiosis in the pathogenesis of ventilator-associated pneumonia and acute respiratory distress syndrome is not yet fully understood. The lack of exploration of other microbial populations, viruses (eukaryotes and prokaryotes) and fungi is a key issue. Further analysis of the interaction between these microbial kingdoms and a better understanding of the host-microbiome interaction are necessary to fully elucidate the role of the microbiome in the pathogenicity of acute diseases. The validation of a consensual and robust methodology in order to make the comparison of the different studies relevant is also required. Filling these different gaps should help develop preventive and therapeutic strategies for both acute respiratory distress syndrome and ventilator-associated pneumonia.
Keywords: 16S rRNA gene; acute respiratory distress syndrome; dysbiosis; high-throughput sequencing; lung microbiome; lung mycobiota; lung virome; mechanical ventilation; metagenomics; ventilator-associated pneumonia.