Datta Abhishek, Hernandez-Franco Juan F, Park Sungtae, Olson Matthew R, HogenEsch Harm, Thangamani Shankar
Department of Comparative Pathobiology, College of Veterinary Medicine, Purdue University, West Lafayette, IN 47906, USA.
Department of Biological Sciences, Purdue University, West Lafayette, IN 47906, USA.
J Fungi (Basel). 2022 Jun 7;8(6):610. doi: 10.3390/jof8060610.
Invasive () infections often arise from the intestine and cause life-threatening infections in immunocompromised individuals. The role of gut commensal microbiota, metabolites, and host factors in the regulation of CA colonization in the intestine is poorly understood. Previous findings from our lab indicate that taurocholic acid (), a major bile acid present in the intestine, promotes CA colonization and dissemination. Here, we report that oral administration of TCA to CA-infected mice significantly decreased the number of mononuclear phagocytes and CD4+ IL17A+ T helper 17 cells that play a critical role in controlling CA in the intestine. Collectively, our results indicate that TCA modulates mucosal innate and adaptive immune responses to promote CA colonization in the intestine.
侵袭性()感染通常源于肠道,并在免疫功能低下的个体中引发危及生命的感染。肠道共生微生物群、代谢产物和宿主因素在调节肠道中CA定植方面的作用尚不清楚。我们实验室之前的研究结果表明,牛磺胆酸()是肠道中存在的一种主要胆汁酸,可促进CA的定植和传播。在此,我们报告,给感染CA的小鼠口服TCA可显著减少在控制肠道CA中起关键作用的单核吞噬细胞和CD4+ IL17A+辅助性T细胞17的数量。总体而言,我们的结果表明,TCA可调节黏膜固有免疫和适应性免疫反应,以促进肠道中CA的定植。