Location: Food and Feed Safety ResearchTitle: Mitogen-activated protein kinase p38, not ERK1/2 and JNK, regulates nitric oxide response to Salmonella Heidelberg infection in chicken macrophage HD11 cells Author
|He, Louis - Haiqi|
|Genovese, Kenneth - Ken|
|Swaggerty, Christina - Christi|
|Nisbet, David - Dave|
|Kogut, Michael - Mike|
Submitted to: International Journal of Bacteriology & Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/24/2018
Publication Date: 6/4/2018
Citation: He, L.H., Genovese, K.J., Swaggerty, C.L., Nisbet, D.J., Kogut, M.H. 2018. Mitogen-activated protein kinase p38, not ERK1/2 and JNK, regulates nitric oxide response to Salmonella Heidelberg infection in chicken macrophage HD11 cells. International Journal of Bacteriology & Parasitology. 2018(2):1-5. doi: 10.29011/IJBP-107.000007.
DOI: https://doi.org/10.29011/IJBP-107.000007 Interpretive Summary: Salmonella Heidelberg is one of the most prevalent poultry Salmonella strains and is an important human pathogen responsible for salmonellosis. Macrophage cells are one type of white blood cells found in chickens; the macrophage cells can produce nitric oxide, a chemical that can kill bacteria. The nitric oxide is a very important bacteria-killing chemical that protects chickens from infection by pathogenic bacteria such as Salmonella. We have performed experiments to see if and how the macrophage cells produce bacteria-killing nitric oxide when they are exposed to S. Heidelberg. We found that the chicken macrophage can produce nitric oxide after infected with S. Heidelberg; we also found that a very important protein called p38 MAP kinase controls the processes for the macrophage cells to produce the nitric oxide. This information is important to the pharmaceutical and poultry industries in the United States because it help us to better understand the interactions between pathogen and host cells and enables us to develop new ways to produce healthy poultry and reduce foodborne disease.
Technical Abstract: Salmonella Heidelberg is one of the most prevalent poultry Salmonella strains. Infection with S. Heidelberg strongly stimulates nitric oxide (NO) response in the chicken macrophage HD11 cells. In the present study, regulation of NO response to S. Heidelberg infection by the host mitogen-activated protein (MAP) kinases (p38, ERK1/2, and JNK) was investigated using the selective pharmaceutical inhibitors, SB203580, PO98059, and SP600125, respectively. At the concentrations used, the p38 inhibitor strongly inhibited the NO productions in S. Heidelberg infected cells (61-80% reduction; p less than or equal to 0.05); whereas ERK1/2 inhibitor produced a much less inhibition (14-20% reduction; p less than or equal to 0.05) and JNK inhibitor showed no inhibitory effect (4-6% increase). The total MAP kinases p38 and JNK were not changed by Salmonella infection, with mild increase detected in ERK1/2. However, large changes were observed in phopho-p38 (100% increase) and JNK (45% increase), with a minor change detected in phospho-ERK1/2 (9% increase). Although both p38 and JNK phosphorylation can be significantly inhibited (p less than or equal to 0.05) by their inhibitors, only inhibition of p38 produced a significant reduction of NO. Together, these results indicated that p38 MAP kinase, not JNK and ERK1/2, plays a significant role in regulating the NO response of HD11 cells to Salmonella infection.