|He, Louis - Haiqi|
|Genovese, Kenneth - Ken|
|Swaggerty, Christina - Christi|
|Kogut, Michael - Mike|
Submitted to: Foodborne Pathogens and Disease
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/23/2012
Publication Date: 10/15/2012
Citation: He, L.H., Genovese, K.J., Swaggerty, C.L., Nisbet, D.J., Kogut, M.H. 2012. A comparative study on invasion, survival, modulation of oxidative burst, and nitric oxide responses of macrophages (HD11), and systemic infection in chickens by prevalent poultry Salmonella serovars. Foodborne Pathogens and Disease. 9:1104-1110.
Interpretive Summary: Poultry is a major reservoir for the food poisoning bacteria Salmonella. Many Salmonella species colonize and infect chickens and cause contamination of eggs and meat products with Salmonella, which is a main cause of human Salmonellosis. Macrophage cells are one of the white blood cells that can produce chemicals to kill bacteria and play an important role in controlling infections. In this study, we investigated the interactions between different Salmonella species and chicken macrophage cells. We found that one of the Salmonella species, S. Enteritidis, is highly resistant to macrophage killing, and this evidence suggests that S. Enteritidis is more likely to cause contamination in chicken products. Additionally, we also found that many poultry Salmonella species are able to inhibit macrophage cells to produce anti-bacterial chemicals and survive inside the macrophage cells. This information is important to the pharmaceutical and poultry industries in the United States because it offers ideas to develop new methods to control Salmonella in poultry and reduce food poisoning in humans.
Technical Abstract: Poultry is a major reservoir for foodborne Salmonella serovars. Salmonella Typhimurium, S. Enteritidis, S. Heidelberg, S. Kentucky, and S. Senftenberg are the most prevalent serovars in poultry. Information concerning the interactions between different Salmonella species and host cells in poultry is lacking. In the present study, the above mentioned Salmonella serovars were examined for invasion, intracellular survival, and their ability to modulate oxidative burst and nitric oxide responses in chicken macrophage HD-11 cells. All Salmonella serovars demonstrated similar capacity to invade HD-11 cells. At 24 hour post infection, a 36-43% reduction of intracellular bacteria, in log10(cfu), was observed for S. Typhimurium, S. Heidelberg, S. Kentucky, and S. Senftenberg; whereas a significantly lower reduction (16%) was observed for S. Enteritidis, indicating its higher resistance to the killing by HD-11 cells. Production of nitric oxide was completely diminished in HD-11 cells infected with S. Typhimurium and S. Enteritidis, but remained intact when infected with S. Heidelberg, S. Kentucky, and S. Senftenberg. Phorbol myristate acetate-stimulated oxidative burst in HD-11 cells was greatly impaired after infection by each of the five serovars. When newly hatched chickens were challenged orally, a high rate (86-96%) of systemic infection (Salmonella positive in liver/spleen) was observed in birds challenged with S. Typhimurium, S. Enteritidis, S. Heidelberg, and S. Kentucky, while only 14% of the birds were S. Senftenberg-positive. However, there was no direct correlation between systemic infection and in vitro differential cellular survival and modulation of nitric oxide response among the tested serovars.