Submitted to: Meeting Abstract
Publication Type: Abstract only
Publication Acceptance Date: 5/17/2007
Publication Date: 10/20/2007
Citation: Zhang, S., Lillehoj, H.S., Kim, C.H., Keeler, C.L., Zhang, M. 2007. Transcriptional Response of Chicken Macrophages to Salmonella enterica serovar Enteritidis Infection. International Symposium on Animal Genomics for Animal Health. Oct 20-27, Paris, France. Interpretive Summary: Many enteric pathogens such as Salmonella invade the intestine of chicken host causing inflammatory response resulting in poor performance. Ability to develop a new vaccine against salmonellosis will benefit poultry industry and will reduce Salmonella-borne food poisoning for humans. In this paper, ARS scientists collaborated with scientists at Mississippi State University to investigate host immune response against Salmonella using new molecular genomics technology. The results demonstrated important immune mechanisms that Salmonella employ to evade host immune response. The new information will help poultry industry to develop a better management strategy against salmonellosis.
Technical Abstract: Salmonella enterica serovar Enteritidis (SE) continues to be the predominant etiologic agent of salmonellosis, with contaminated egg products being the primary source of infection. At the present time, the molecular and immunological mechanisms involved in SE colonization of chicken hosts are not well understood. The aims of this study were (1) to investigate the innate immune response of chicken macrophages to SE infection and (2) to investigate the role of the type III secretion systems encoded by Salmonella pathogenicity islands 1 and 2 (TTSS-1 and TTSS-2) in modulating host immune responses. The transcriptional profiles of HD11 macrophages infected with SE were analyzed using an avian macrophage microarray and real time RT-PCR. Of 4,906 array elements interrogated, 338 genes from infected macrophages exhibited 2-fold altered expression compared with uninfected macrophages (P < 0.001) within 24 hours post infection. Genes encoding proinflammatory cytokines, CC and CXC chemokines, and chemokine ligands were up-regulated; whereas genes associated with transcription, cell adhesion, and proliferation were down-regulated. Most transcriptional changes occurred at 5 hours post infection, with more genes down-regulated than up-regulated. SE infection suppressed the expression of gallinacin 1 and lymphotactin, two important host defense molecules. In addition, SE infection transiently blocked the expression of MHC I '-2 microglobulin and activated MHC II B-L'. Infection of HD11 cells with mutant SE strains carrying inactivated TTSS-1 or TTSS-2 induced significantly higher levels of CC chemokines than wild type SE. In conclusion, persistence of SE in chickens may involve a mechanism of selective modulation of certain innate immune response genes.