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Title: Wild-type and mutant AvrA- Salmonella induce broadly similar immune pathways in the chicken ceca with key differences in signaling intermediates and inflammation

item ARSENAULT, RYAN - University Of Delaware
item Genovese, Kenneth - Ken
item He, Louis
item WU, XUIXIAN - Emory University, School Of Medicine
item NEISH, ANDREW - Emory University, School Of Medicine
item Kogut, Michael - Mike

Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/2/2015
Publication Date: 2/1/2016
Publication URL:
Citation: Arsenault, R.J., Genovese, K.J., He, H., Wu, H., Neish, A.S., Kogut, M.H. 2016. Wild-type and mutant AvrA- Salmonella induce broadly similar immune pathways in the chicken ceca with key differences in signaling intermediates and inflammation. Poultry Science. 95:354-363.

Interpretive Summary: During the first week of life after hatching, the immune system of the baby chick is not very good at fighting bacterial infections such as Salmonella. In this paper, we tried to understand why the baby chicks can get infected with Salmonella. We found that Salmonella produces substances that they can release inside the baby chick that prevent the chicks’ immune system from working. Thus, the immune cells cannot attack this bug and kill it. These results are important to the pharmaceutical industry because we have identified a specific target to stimulate the bird’s immune system and provide protection against infection.

Technical Abstract: Salmonella enterica serovar Typhimurium (ST) is a serious infectious disease throughout the world, and a major reservoir for Salmonella is chicken. Chicken infected with Salmonella do not develop clinical disease, this may be the result of important host interactions with key virulence proteins. To study this, we inoculated chicken with mutant Salmonella Typhimurium that lacked the virulence protein AvrA (AvrA^-). AvrA is referred to as an avirulence factor as it moderates the host immune response. The lack of the AvrA virulence gene in ST resulted in reduced weight gain, enhanced persistence, and greater extraintestinal organ invasion in chickens, as compared to WT ST. Kinome analysis was performed on inoculated cecal tissue. The majority of the signal transduction pathways induced by AvrA^- and wild-type (WT) ST were similar; however, we observed alterations in innate immune system signaling. In addition, a leukocyte migration pathway was altered by AvrA^- ST that may allow greater gut barrier permeability and invasion by the mutant. Cytokine expression did not appear significantly altered at 7 days post-inoculation; at 14 days post-inoculation, there was an observed increase in the expression of anti-inflammatory IL-10 in the WT inoculated ceca. This study is the first to describe mutant AvrA^- ST infection of chicken and provides further insight into the Salmonella responses observed in chicken relative to other species such as humans and cattle.