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