Transcriptional profiling avian beta-defensins in chicken oviduct epithelial cells before and after infection with <it>Salmonella enterica </it>serovar Enteritidis

• Main Authors: Bailey R Hartford, Zhang M Zhenyu, Zhang C Yan, Ebers Katie L, Zhang Shuping
• Format: Article
• Language: English
• Published: BMC 2009-07-01
• Series: BMC Microbiology
• Online Access: http://www.biomedcentral.com/1471-2180/9/153

<p>Abstract</p> <p>Background</p> <p><it>Salmonella enterica </it>serovar Enteritidis (SE) colonizes the ovary and oviduct of chickens without causing overt clinical signs which can lead to SE-contamination of the content and membrane of shell-eggs as well as hatchery eggs. The organism utilizes the <it>Salmonella </it>Pathogenicity Island-2 encoded type III secretion system (T3SS-2) to promote persistence in the oviduct of laying hens. In this study, reverse transcriptase-polymerase chain reaction (RT-PCR) was carried out to determine the expression profiles of 14 known avian beta defensins (AvBDs) in primary chicken oviduct epithelial cells (COEC) before and after infections with a wild type SE strain and T3SS mutant SE strains carrying an inactivated <it>sipA </it>or <it>pipB </it>gene.</p> <p>Results</p> <p>Based on the expression levels in uninfected COEC, AvBDs can be loosely grouped into three categories with AvBD4-5 and AvBD9-12 being constitutively expressed at high levels; AvBD1, AvBD3, and AvBD13-14 at moderate levels; and AvBD2 and AvBD6-8 at minimal levels. Infection with the wild type SE strain temporarily repressed certain highly expressed AvBDs and induced the expression of minimally expressed AvBDs. The <it>pipB </it>mutant, compared to the wild type strain, had reduced suppressive effect on the expression of highly expressed AvBDs. Moreover, the <it>pipB </it>mutant elicited significantly higher levels of the minimally expressed AvBDs than the wild type SE or the <it>sipA </it>mutant did.</p> <p>Conclusion</p> <p>Chicken oviduct epithelial cells express most of the known AvBD genes in response to SE infection. PipB, a T3SS-2 effector protein, plays a role in dampening the β-defensin arm of innate immunity during SE invasion of chicken oviduct epithelium.</p>