Avaliação da disbiose intestinal causada pela vancomicina durante a infecção pela bactéria Pseudomonas aeruginosa

Abstract

P. aeruginosa is one of the most common opportunistic bacteria causing lung infections in hospitals, and vancomycin is widely used in hospitalized patients, influencing their intestinal microbiota. Given the relevance of P. aeruginosa bacteria in infectious and inflammatory processes and stimulated by the need for new treatment strategies, the objective of this study was to analyze how the effect of vancomycin on the murine intestinal microbiota may or may not favor the infection caused by opportunistic P bacteria. aeruginosa and how the use of TMF can affect this response. It was demonstrated in this work that the fecal bacterial content is altered in the animals using vancomycin and that the intestinal dysbiosis caused alteration in the animals weight. Murine bone marrow-derived macrophages (BMDMs) stimulated with cecal content of dysbiosis mice showed higher levels of expression of proinflammatory cytokine genes, such as TNF-α, while IL-10 expression was decreased. Since it was confirmed that intestinal bacterial dysbiosis was caused by vancomycin and that this change differentially stimulates macrophages, it was evaluated whether this change in the intestinal bacterial microbiota alters the host response to lung infection by the opportunistic bacterium P. aeruginosa. The amount of viable P. aeruginosa in the lungs, spleens, and livers of dysbiosis mice showed higher levels, more damage to the lung and cecum, and increased IL10 expression and increased recruitment of CD11b + cells in bronchial lavage. alveolar. Susceptible phenotype and tissue damage were reversed when dysbiosis mice received fecal microbiota transplantation. Taken together, the results show that vancomycin alters the intestinal microbiota, inducing murine intestinal dysbiosis, and TMF has proved to be an excellent strategy for restoring the intestinal microbial community and assisting in the control and prevention of nosocomial opportunistic bacterial infections. However, although our results may shed light on the crosstalk between the lungs and intestines, further investigation is needed to understand the immune response within the lungs, as well as the influence of intestinal dysbiosis in this context