Intestinal colonization with and mucosal immune response in mice treated with cefoperazone oral antibiotic.

, an emerging multi-drug resistant fungal pathogen, causes invasive infections in humans. The factors regulating the colonization of in host niches are not well understood. In this study, we examined the effect of antibiotic-induced gut dysbiosis on intestinal colonization, dissemination, microbiome composition and the mucosal immune response. Our results indicate that mice treated with cefoperazone alone had a significant increase in intestinal colonization compared to untreated control groups. A significant increase in the dissemination of from the intestine to internal organs was observed in antibiotic-treated immunosuppressed mice. Intestinal colonization of alters the microbiome composition of antibiotic-treated mice. Relative abundance of firmicutes members mainly and were considerably increased in the cefoperazone-treated mice infected with compared to cefoperazone-treated uninfected mice. Next, we examined the mucosal immune response of infected mice and compared the results with infection. The number of CD11b+ CX3CR1+ macrophages was significantly decreased in the intestine of infected mice when compared to infection. On the other hand, both and infected mice had a comparable increase of the number of Th17 and Th22 cells in the intestine. A significant increase in -specific IgA was observed in the serum of but not in the infected mice. Taken together, treatment with broad-spectrum antibiotic increased the colonization and dissemination of from the intestine. Furthermore, findings from this study for the first time revealed the microbiome composition, innate and adaptive cellular immune response to intestinal infection with .