Authors:

Michael Tran

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About Paper:

Salmonella enterica serovar Typhimurium is an enteric, facultative intracellular bacterial pathogen known for causing gastroenteritis in humans. Invasion of the intestinal epithelium by Salmonella is driven primarily by the Type III Secretion System 1 (T3SS-1), a syringe-like apparatus that translocates effector proteins into epithelial cells to manipulate the cytoskeleton to facilitate bacterial entry. Recent studies suggest a novel interplay between Salmonella and the gut commensal fungal opportunist, Candida albicans. Notably, a T3SS-1 dependent interaction tied to the upregulation of L-arginine in C. albicans by Salmonella has been observed in both in vitro & in vivo co-culture models. This increase in L-arginine correlated with enhanced gene expression of the T3SS-1 and increased epithelial invasion of Salmonella within the host. To investigate this mechanism, this study examined gene knockouts of arginine transporters and' regulators in Salmonella. Results have indicated that co-culture with C. albicans or supplementation with L-arginine increased T3SS-1 gene expression and further propagated invasion into the host. Gene knockouts of arginine transporters and regulators in Salmonella reduced T3SS-1 activity and impaired invasion of the host, supporting the notion that fungal-derived arginine can act as a key signal promoting Salmonella virulence in the gut. This study aims to elucidate the precise role of L-arginine on Salmonella Typhimurium virulence in vitro. These findings could offer insight into how fungal-derived metabolites influence bacterial pathogenesis and provide a framework for future studies on fungal-bacterial interactions.

Source:

University of Illinois Chicago

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Co-authors:

Michael Tran