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Vancomycin‐induced gut dysbiosis during Pseudomonas aeruginosa pulmonary infection in a mice model
Author(s) -
Rosa Caio Pupin,
Pereira Jéssica Assis,
Cristina de Melo Santos Natália,
Brancaglion Gustavo Andrade,
Silva Evandro Neves,
Tagliati Carlos Alberto,
Novaes Rômulo Dias,
Corsetti Patrícia Paiva,
Almeida Leonardo Augusto
Publication year - 2020
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.4ab0919-432r
Subject(s) - dysbiosis , proinflammatory cytokine , pseudomonas aeruginosa , biology , immunology , bronchoalveolar lavage , microbiology and biotechnology , gut flora , lung , inflammation , medicine , bacteria , genetics
Pseudomonas aeruginosa is one of the most common opportunistic pathogens causing respiratory infections in hospitals. Vancomycin, the antimicrobial agent usually used to treat bacterial nosocomial infections, is associated with gut dysbiosis. As a lung‐gut immunologic axis has been described, this study aimed to evaluate both the immunologic and histopathologic effects on the lungs and the large intestine resulting from vancomycin‐induced gut dysbiosis in the P. aeruginosa pneumonia murine model. Metagenomic analysis demonstrated that vancomycin‐induced gut dysbiosis resulted in higher Proteobacteria and lower Bacteroidetes populations in feces. Given that gut dysbiosis could augment the proinflammatory status of the intestines leading to a variety of acute inflammatory diseases, bone marrow‐derived macrophages were stimulated with cecal content from dysbiotic mice showing a higher expression of proinflammatory cytokines and lower expression of IL‐10 . Dysbiotic mice showed higher levels of viable bacteria in the lungs and spleen when acutely infected with P. aeruginosa , with more lung and cecal damage and increased IL‐10 expression in bronchoalveolar lavage. The susceptible and tissue damage phenotype was reversed when dysbiotic mice received fecal microbiota transplantation. In spite of higher recruitment of CD11b+ cells in the lungs, there was no higher CD80+ expression, DC+ cell amounts or proinflammatory cytokine expression. Taken together, our results indicate that the bacterial community found in vancomycin‐induced dysbiosis dysregulates the gut inflammatory status, influencing the lung‐gut immunologic axis to favor increased opportunistic infections, for example, by P. aeruginosa .