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Title:   Author  item
                                            CHEESEMAN, JENNIFER - IOWA STATE UNIVERSITY,AMEitem
                                            LEVY, NYASA - IOWA STATE UNIVERSITY,AMEitem
                                            KAISER, PETE - BERKSHIRE UKitem
                                            Lillehoj, Hyunitem
                                            LAMONT, SUSAN - IOWA STATE UNIVERSITY,AME
  Submitted to: Avian Diseases
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 9/20/2007
                                    Publication  Date: 9/1/2008
                                    Citation: Cheeseman, J.H., Levy, N.A., Kaiser, P., Lillehoj, H.S., Lamont, S.J. 2008. Salmonella enteritidis-induced alteration of inflammatory CXCL chemokine messenger-RNA expression and histologic changes in the ceca of infected chicks. Avian Diseases. 52:229-34.Interpretive Summary: There is a critical need to better understand 
host-pathogen immunology for many of poultry pathogens of economic 
importance.  Poultry eggs and meat contaminated with food pathogens such as Salmonella enteritidis (SE) continue to be very significant sources of human food poisoning in the United States.  Antimicrobial resistance in SE strains is widespread, with more than 90% being resistant to at least one antimicrobial drug, and over 50% of SE strains isolated from poultry have been found to be multi-drug resistant. A more thorough understanding of the avian immune response to SE may provide novel insights for vaccine 
development as well as enhancing host immunity to this problematic 
bacterial pathogen, with an overall goal of reducing human illness. There is limited information on the role of various host lymphocytes and their secreted products called cytokines in infections caused by many poultry enteric pathogens inclduing Salmonella and coccidia. Cytokines which are secreted upon pathogen invasion of host play a very important role in the 
immunoregulation of mucosal response and macrophages are very important cells in host defense against pathogens. In this report, ARS scientists collaborated with scientists at Iowa State University and Compton Animal Health Institute in UK in a study to investigate the role of cytokines, antimicrobial peptide  and lymphocyte subsets in young chickens infected with Salmonella enteritidis using a new molecular biological method.  The results of this study clearly provided new evidence that local interaction of host lymphocytes and Salmonella is important to understand 
immunopathology mediated by Salmonella. Understanding cecum-specific immune response of young chicks infected with Salmonella enteritidis and other enteric pathogens of poultry may provide insight to explain the persistent colonization of this organ, and open avenues to reduce the incidence of contamination in eggs and meat products as well as giving direction to future studies.
                                Technical Abstract:  To better understand the avian host immune response 
to Salmonella enteritidis, we examined mRNA expression for 8 genes: CXCLi1[K60], CXCLi2 [IL-8/CAF], Interferon [IFN]-y Interleukin [IL] -1, IL-6, IL-12, IL-12, and Gallinacin [Gal] -2 in the cecum of young chicks one week post-inoculation with Salmonella enteritidis [SE].  Cecum tissue sections were stained and evaluated for the presence of macrophages, lymphocytes, heterophils, and apoptotic cells following SE infection.  Using quantitative RT-PCR, Salmonella enteritidis infection was associated with a significant (P < 0.01) up-regulation of cecal 
CXCLi1 and CXCLi2 mRNA expression.  Bacterial infection with SE was also associated (P < 0.05) with increased staining for macrophages and decreased apoptosis (ssDNA) in cecal tissue sections when compared to uninfected animals.  Changes in hemokine expression and cell population dynamics are a direct result of SE infection, as uninfected animals do not show these alterations.  Thus, these SE induced changes reflect the host immune response to this bacterial pathogen in young chickens.


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