Abstract
Coronavirus disease 2019, or COVID-19, is a major challenge facing scientists worldwide. Alongside the lungs, the system of organs comprising the GI tract is commonly targeted by COVID-19. The dysbiotic modulations in the intestine influence the disease severity, potentially due to the ability of the intestinal microbiota to modulate T lymphocyte functions, i.e., to suppress or activate T cell subpopulations. The interplay between the lungs and intestinal microbiota is named the gut–lung axis. One of the most usual comorbidities in COVID-19 patients is type 2 diabetes, which induces changes in intestinal microbiota, resulting in a pro-inflammatory immune response, and consequently, a more severe course of COVID-19. However, changes in the microbiota in this comorbid pathology remain unclear. Metformin is used as a medication to treat type 2 diabetes. The use of the type 2 diabetes drug metformin is a promising treatment for this comorbidity because, in addition to its hypoglycemic action, it can increase amount of intestinal bacteria that induce regulatory T cell response. This dual activity of metformin can reduce lung damage and improve the course of the COVID-19 disease.
Highlights
The human gastrointestinal (GI) tract is represented by an extremely diverse and complex microbial ecosystem with more than 1014 resident species interacting with the host and actively participating in many physiological processes
The study by Eckburg et al demonstrated that the intestinal microbiota of people with type 2 diabetes (T2D) was characterized by an increase in Bacteroides spp., E. coli, and Desulfovibrio spp
Representatives of the intestinal microbiota can activate different subpopulations of T lymphocytes in the intestinal plate, both directly and indirectly through metabolites, which may lead to enhancement and suppression of certain T lymphocyte subpopulations
Summary
The human gastrointestinal (GI) tract is represented by an extremely diverse and complex microbial ecosystem with more than 1014 resident species interacting with the host and actively participating in many physiological processes. The first lines of defense against SARS-CoV-2 lie within the mucosa-associated lymphoid tissue (MALT)—namely, the nasal-associated lymphoid tissue (NALT) and the gutassociated lymphoid tissue (GALT), which are involved in inducing immune responses towards microorganisms This is accomplished by promoting the differentiation and activation of immune cells, such as T helper 1 (Th1), Th2, dendritic cells (DCs), and macrophages [17]. Th1 cells are characterized by expression of the transcription factor T-bet, signal transducer and activator of transcription (STAT) 4, and the production of IL-2, IFN-γ, and tumor necrosis factor (TNF) β They are involved in the cellular immunity and rejection process. The pathomechanism of GI lesions in SARS-CoV-2 infection was not fully studied, the authors did observe some integral loss of the intestinal barrier and dysbiosis in the microbiota. We focus on these two mechanisms in more detail
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