Page Banner

United States Department of Agriculture

Agricultural Research Service

Research Project: AVIAN GENOMIC AND IMMUNOLOGIC APPROACHES FOR CONTROLLING MUCOSAL PATHOGENS Title: Induction of CXC chemokine mRNA expression in chicken oviduct epithelial cells by Salmonella enterica serovar Enteritidis via the type three secretion system-1

Authors
item Lillehoj, Hyun
item Li, Shuhui -
item Zhang, Zhenyu -
item Yan, Lifang -
item Pace, Lanny -
item Zhang, Shuping -

Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: April 19, 2010
Publication Date: June 15, 2010
Citation: Lillehoj, H.S., Li, S., Zhang, Z., Yan, L., Pace, L., Zhang, S. 2010. Induction of CXC chemokine mRNA expression in chicken oviduct epithelial cells by Salmonella enterica serovar Enteritidis via the type three secretion system-1. Avian Diseases. 53(3):396-404.

Interpretive Summary: Salmonella enterica serovar Enteritidis (SE) is an important pathogen for food safety and has a broad range of hosts including mammals and poultry. Intestinal carrier-state is a significant source of horizontal transmission of Salmonella whereas reproductive tract colonization contributes to SE contamination of eggs and hatcheries. To better understand the protective immunity against Salmonella, ARS scientists and scientists at Mississippi State University collaborated on the gene expression analysis of immune response genes following SE. One aspect of this study was on the investigation of the role of two virulence-associated type three secretion systems (T3SS-1 and T3SS-2) encoded by the Salmonella Pathogenicity Island-1 (SPI-1) and SPI-2, respectively since recent studies have demonstrated that T3SS-1 and T3SS-2 are required by Salmonella enterica to colonize chicken intestine and/or reproductive tissues. In this study, the messenger-RNA (mRNA) expression of cytokines in primary chicken oviduct epithelial cells (COEC) was determined using wild type or type three secretion system (T3SS) mutant Salmonella enteritidis (SE) strains. All SE strains examined in this study elicited the expression of pro-inflammatory immune mediators including inducible nitric oxide synthase (iNOS), CXCLi1 (K60), CXCLi2 (IL-8), CCLi3 (K203), and CCLi4 (MIP-1ß). SE also triggered the expression of an anti-inflammatory cytokine, IL-10, but repressed TGF-ß3 transcription. T3SS-1 (sipA and sipB) mutants were significantly impaired in their ability to induce the expression of CXCLi1 and CXCLi2. T3SS-2 mutants displayed a wild type phenotype in terms of modulating the expression of chemokines and cytokines in COEC. Genetic complementation of the sipA mutation restored a wild type phenotype indicating that SE-induction of CXCLi1 and CXCLi2 was sipA-dependent. These results will enhance our understanding of host-pathogen interaction in salmonellosis and will help to guide the future development of novel vaccines against salmonellosis.

Technical Abstract: The messenger-RNA (mRNA) expression of selected cytokines and chemokines in primary chicken oviduct epithelial cells (COEC) was determined following in vitro infection with wild type or type three secretion system (T3SS) mutant Salmonella enteritidis (SE) strains. All SE strains examined in this study elicited the expression of pro-inflammatory immune mediators including inducible nitric oxide synthase (iNOS), CXCLi1 (K60), CXCLi2 (IL-8), CCLi3 (K203), and CCLi4 (MIP-1ß). SE also triggered the expression of an anti-inflammatory cytokine, IL-10, but repressed TGF-ß3 transcription. Both T3SS-1 (sipA and sipB) and T3SS-2 (pipB and ssaV) mutants showed reduced capacity, compared to the wild type SE, to stimulate iNOS mRNA expression in COEC. T3SS-1 (sipA and sipB) mutants were significantly impaired in their ability to induce the expression of CXCLi1 and CXCLi2. T3SS-2 mutants displayed a wild type phenotype in terms of modulating the expression of chemokines and cytokines in COEC. The expression of iNOS, but not CXC chemokines, correlated with the number of intracellular bacteria in COEC. Genetic complementation of the sipA mutation restored a wild type phenotype. Thus, SE-induction of CXCLi1 and CXCLi2 was sipA-dependent.

Last Modified: 11/1/2014
Footer Content Back to Top of Page