Elucidating the role of carbon metabolism genes chiA and yjiY in Salmonella pathogenesis

Abstract

Salmonella is a foodborne pathogen that causes debilitating enteric diseases in a wide range of hosts. While Salmonella Typhimurium causes self-limiting gastroenteritis in human beings, Salmonella Typhi causes typhoid fever that has plagued through history and continues to be a major threat to public health even after tremendous advancements in the field of medicine. A related but evolutionarily distinct serovar Salmonella Paratyphi serotype A is the etiological agent of a similar enteric fever known as paratyphoid. While Salmonella Typhimurium can cause gastroenteritis like disease in a broad range of hosts, what makes Salmonella Typhi and S. Paratyphi strict human pathogens, is not clearly understood. When contaminated food is ingested, Salmonella passes through the acidic gastric environment and reaches the intestine. The pathogen crosses intestinal mucus layer and invades enterocytes by engaging SPI1 encoded T3SS mediated effectors that triggers membrane ruffling. Some bacteria are taken up directly by the specialized microfold or M cells present on the Peyer s patches. This induces IL8 production by the epithelial cells, leading to infiltration of the perimorphonuclear cells and localized inflammation. Once the bacteria transcytose through the epithelial cells, tissue resident macrophages and dendritic cells engulf the bacteria by macropinocytosis. This step marks the beginning of systemic dissemination of the pathogen in the host. Bacterial infections accounts for approximately 80-90% of all food-borne disease outbreaks every year, with Escherichia coli, Salmonella enterica and Listeria monocytogenes infections being the primary ones. Thus studying host-pathogen interaction is critical in understanding the interaction between a pathogenic microorganism and its broad host range... newline