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ARS Home » Plains Area » College Station, Texas » Southern Plains Agricultural Research Center » Food and Feed Safety Research » Research » Publications at this Location » Publication #317936

Title: Effect of Salmonella infection on cecal tonsil regulatory T cell properties in chickens

item SHANMUGASUNDARAM, REVATHI - The Ohio State University
item Kogut, Michael - Mike
item Arsenault, Ryan
item Swaggerty, Christina - Christi
item COLE, KIMBERLY - The Ohio State University
item REDDISH, MARK - The Ohio State University
item SELVARAJ, RAMESH - The Ohio State University

Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/25/2015
Publication Date: 4/19/2015
Publication URL:
Citation: Shanmugasundaram, R., Kogut, M.H., Arsenault, R.J., Swaggerty, C.L., Cole, K., Reddish, M.J., Selvaraj, R.K. 2015. Effect of Salmonella infection on cecal tonsil regulatory T cell properties in chickens. Poultry Science. 94:1828-1835. doi: 10.3382/ps/pev161.

Interpretive Summary: Baby chicks get infected with germs called Salmonella. These germs do not make the baby chick sick, but the germs can move from the chick to humans and make them very sick. The purpose of these experiments was to try to find out why the germs can infect baby chicks but not make them sick. We found that the germs cause the baby chick’s immune system to produce cells that hide the germs from the immune system. This allows the germs to stay in the gut of the baby chick where they can live unnoticed. The results of this experiment are important to the pharmaceutical industry in the United States because we now know which cells are produced by the baby chick’s cells of the immune system when they see Salmonella. Thus, we can now see if there are ways for us to get the baby chick to stop making these cells which will help the chick fight Salmonella infections.

Technical Abstract: Two experiments were conducted to study Regulatory T cell (Treg) properties post-Salmonella infection in broiler birds. Four-day-old broiler chicks were orally infected with 5x106 CFU/ml Salmonella enteritidis or sterile PBS (control). Samples were collected at 4, 7, 10, and 14 d post-infection. There was a significant (P < 0.05) increase in the number of CD4^+CD25^+ cells by day 4 post-infection that increased steadily throughout the course of the 14 days of infection, whereas the number of CD4^+CD25^+ cells in the non-infected controls remained steady throughout the study. CD4^+CD25^+ cells from cecal tonsils of S. enteritidis-infected birds had higher (P < 0.05) amount of IL-10 mRNA content than the CD4^+CD25^+ cells from the non-infected controls at all the time points studied. The amount of IL-2 mRNA content in the cecal tonsil CD4^+CD25^+ cells from the infected birds did not differ significantly (P > 0.05) when compared to that in the non-infected control birds. At a lower effector/responder cell ratio of 0.25:1, CD4^+CD25^+ cells from cecal tonsils of Salmonella-infected birds suppressed T cell proliferation at d 7 and 14 post-S. enteritidis infection while CD4^+CD25^+ cells from non-infected control groups did not suppress T cell proliferation. In the second experiment, day-old chickens were orally infected with 0 (control) or 1.25 X 10^8 CFU/bird S. enteritidis. At 7 and 21 d post Salmonella challenge, CD25^+ cells collected from cecal tonsils of S. enterica infected birds and restimulated in vitro with Salmonella-antigen had significantly higher IL-10 mRNA compared to that in the control group. Spleen CD4^+CD25^+, CD4^+, and CD8^+ cell percentage did not differ significantly between the Salmonella infected and control birds. In conclusion, S. enteritidis infection increased the Treg percentage, suppressive properties, and IL-10 mRNA amounts in the cecal tonsils of broiler birds.