Alterations of lung microbiota in a mouse model of LPS-induced lung injury
Valeriy Poroyko , Fanyong Meng , Angelo Meliton , Taras Afonyushkin , Alexander Ulanov , Ekaterina Semenyuk , Omar Latif , Vera Tesic , Anna A. Birukova , Konstantin G. Birukov
American Journal of Physiology - Lung Cellular and Molecular Physiology Published 8 May 2015 Vol. no. , DOI: 10.1152/ajplung.00061.2014
The origin of microorganisms that
colonize the lung in the background of acute inflammation, and indeed, the
acute respiratory distress syndrome (ARDS), is currently unclear. Much early
work proposed that the origin of these colonizing bacteria was the introduction
into the lung of external infectious agents that gave rise to the initiating
conditions (such as bacterial pneumonia or aspiration-induced ARDS). In a
recent issue of the Journal, Poroyko and colleagues hypothesized that the
pathomechanisms that drive ARDS, including increased vascular permeability and
the expression of cell-surface adhesion molecules, created an environment that
was permissive for the growth of selected bacterial pathogens. Using a model of
sterile acute lung injury in mice, where the administration of LPS drove lung
injury and edema formation, the investigators demonstrated that this mode of
lung injury created an ecological niche that promoted a “bloom” of previously
dormant (but resident) microbial species. This phenomenon was attributed – at
least in in part – to the influence of hypoxia on glucose metabolism, which led
to abnormal lactate production and accumulation. This, together with other
metabolic and permeability disturbances, created a niche that was optimal for
bacterial growth. The most noteworthy conclusion of the investigators is that
the morbid transformation of the lung microbiota could be attributed to the
pre-existing innate pulmonary microbiota that were able to flourish in the
environment of the acutely-inflamed lungs, rather than external infectious
agents. Clearly, this study has its limitations, having been conducted in the
setting of sterile lung inflammation. No doubt, future work will follow, which
might address the development of septic lung injury in other contexts, such as
(sterile) acid aspiration or saline lavage; or more directly clinically
relevant approaches, such as caecal ligation and puncture. We look forward to
seeing the results of these investigations in the pages of the Journal in the
future, which will contribute much to our understanding of the basis of
bacterial colonization of the lung in the background of an acute insult.
Commentary by Dr. Rory Morty, Deputy Editor AJP-Lung
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