PMC:4801059 / 26608-29202
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4801059","sourcedb":"PMC","sourceid":"4801059","source_url":"https://www.ncbi.nlm.nih.gov/pmc/4801059","text":"CONCLUSIONS\nIn this review, we discussed how the respiratory tract is an ecosystem with two niches, the URT and the LRT; each with ecological and microbial pressures that determine bacterial selection. We hypothesized that viruses influence bacterial selection in the URT leading to colonization of the LRT and sometimes pneumonia. There appears to be a complex network of interactions among viruses and bacteria in the URT that responds to viral introduction by altering what bacteria are present or modifying their relative abundance. For a least one species, S. pneumoniae, viruses can increase nasopharyngeal carriage density and increase risk of pneumococcal pneumonia. Whether this is true for other URT bacteria that cause pneumonia is uncertain. We also proposed that bacterial selection in the LRT could be altered by viral infection. The LRT is normally inhabited by low density of microbes, a state maintained by local host defenses and bacterial mechanisms of evasion. In vitro and in vivo studies suggest viruses can promote entry and colonization of the LRT for select bacterial species via a range of biological mechanisms including URT biofilm dispersion, increased bacterial adhesion to host epithelial cell by upregulation of cell receptors, reduced pulmonary clearance, impairment of multiple components of the innate immune response and changes in inflammatory response. Although there are limitations in interpreting the results of experiments, evidence of numerous mechanisms observed under various conditions strongly suggest that viruses also play an important role in the selection of bacteria in the LRT and pneumonia etiology.\nThe greatest difficulty in addressing our hypotheses was our inability to determine the relative contributions of URT bacterial community structure and local host defenses on bacterial selection into the LRT. In the simplest case, how much is the risk of pneumonia following viral infection attributable to the presence of a known bacterial pneumonia pathogen (such as S. pneumoniae) in the URT? To determine this, studies must examine time-dependent carriage of bacteria, species-specific pneumonia outcomes and the effects of viral co-infection among other known risk factors—which, to the best of our knowledge, do not currently exist. Nonetheless, the literature strongly supports the presence of an interaction between viral infection and secondary bacterial pneumonia; the failure to fully understand the mechanisms should act as a spur for future studies while continuing current efforts to reduce the worldwide burden of pneumonia.\n","divisions":[{"label":"Title","span":{"begin":0,"end":11}}],"tracks":[]}