The pulmonary microbiome: challenges of a new paradigm

Abstract

The study of the human microbiome-and, more recently, that of the respiratory system-by means of sophisticated molecular biology techniques, has revealed the immense diversity of microbial colonization in humans, in human health, and in various diseases. Apparently, contrary to what has been believed, there can be nonpathogenic colonization of the lungs by microorganisms such as bacteria, fungi, and viruses. Although this physiological lung microbiome presents low colony density, it presents high diversity. However, some pathological conditions lead to a loss of that diversity, with increasing concentrations of some bacterial genera, to the detriment of others. Although we possess qualitative knowledge of the bacteria present in the lungs in different states of health or disease, that knowledge has advanced to an understanding of the interaction of this microbiota with the local and systemic immune systems, through which it modulates the immune response. Given this intrinsic relationship between the microbiota and the lungs, studies have put forth new concepts about the pathophysiological mechanisms of homeostasis in the respiratory system and the potential dysbiosis in some diseases, such as cystic fibrosis, COPD, asthma, and interstitial lung disease. This departure from the paradigm regarding knowledge of the lung microbiota has made it imperative to improve understanding of the role of the microbiome, in order to identify possible therapeutic targets and to develop innovative clinical approaches. Through this new leap of knowledge, the results of preliminary studies could translate to benefits for our patients.

Environmental Risk Factors for Sarcoidosis

“…Human microbiotica regulate several physiological processes including metabolic functions and immune homeostasis (79). Alterations in the gut and respiratory microbiome have been associated with several inflammatory diseases including autoimmune diseases and cancer (80)(81)(82)(83). It is plausible that sarcoidosis may be associated with specific changes in the composition of lung or gut microbiotica.…”

Victoria

“…While some are associated with immune impairment, others are allergic or even idiopathic. The pathogenesis of these diseases is not fully elucidated; the exaggeration of the host's immune response, which acts as a continuous stimulant to the alveolar epithelium, may be a triggering mechanism of the disease [19]. The pathogenesis of pulmonary fibrosis is complex and may be specific for different agents, with the destruction of pulmonary architecture [20] Few studies have been carried out on the microbiome in interstitial lung disease.…”

“…Precisely from this more accurate identification of IPF, the pulmonary microbiome was further studied in the context of exacerbation of IPF, which does not yet have a definite conclusion. Some studies incriminate Staphylococcus and Streptococcus in aggravating the underlying disease [19].…”

Host-microbe interactions in the pathogenesis and clinical course of sarcoidosis

“…Human microbiota composition is functionally implicated in the regulation of several physiological processes, including metabolic functions and immune homeostasis. Although gut microbiota is the most studied human microbiota niche, well-defined microbiota communities have been identified in virtually any body niche, including the skin and the respiratory tract [24, 53, 111]. In addition, the use of novel microbiome analysis techniques has shown that even internal structures such as the blood vessels, may have their own microbiota niche [51].…”