Dr. Michael KOGUT
BIOGRAPHY
Dr. Kogut is a Research Microbiologist and Lead Scientist within the Food and Feed Safety research Unit at the Southern Plains Agricultural Research Center. Dr. Kogut’s research is centered on alternatives to antibiotics to control disease and increase production; specifically, the development of cost-effective, pre-harvest immunological interventions to improve gut health by studying: the role of the microbiota in immunity to infection; role of dietary metabolites in promoting immune regulation and immune responses to pathogens; tissue specific regulatory responses to infection; novel molecular characterization of dietary compounds and botanicals in inflammation and immunity.
Company
USDA ARS
Southern Plains Agricultural Research Center
Food and Feed Safety Research Unit
Country
USA 🇺🇸
Presentation
Chinese version 🇨🇳
Spanish version 🇪🇸
Portuguese version 🇵🇹
Salmonella Mechanisms of Persistence in Gut
The gastrointestinal ecosystem involves interactions between the host, gut microbiota, and external environment. To colonize the gut of poultry, Salmonella must surmount barriers levied by the intestine including mucosal innate immune responses and microbiota-mediated niche restrictions.
Salmonella intestinal colonization in poultry requires an understanding of the pathogen interacts with the intestinal ecosystem. In chickens, Salmonella survive the initial innate immune response and persist in the avian ceca without clinical signs.
Persistence involves a complex balance of antagonistic and cooperative host defense strategies. The initial phase is typically an innate pro-inflammatory response that controls bacterial invasion. The second phase involves an expansion of the T regulatory cell population followed by distinct alterations of the immune and metabolic pathways that dramatically changes the local immunometabolic phenotype.
Thus, Salmonella in chickens have evolved a unique survival strategy in poultry that minimizes host defenses (disease resistance) during the initial infection and then exploits and/or induces a dramatic immunometabolic reprogramming in the cecum (disease tolerance).