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Title:   Author  item
                                            PARK, SOON - USDA,ARS,BELTSVILLE MDitem
                                            Allen, Patriciaitem
                                            Lillehoj, Hyunitem
                                            PARK, DONG WOON - USDA,ARS,BELTSVILLE MDitem
                                            FITZCOY, STEVE - MILLSBORO, DELAWAREitem
                                            BAUTISTA, DANIEL - U DELAWARE, GEORGETOWNitem
                                            LILLEHOJ, ERIK - U MARYLAND BALTIMORE
  Submitted to: Avian Diseases
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 8/9/2007
                                    Publication  Date: 4/1/2008
                                    Citation: Park, S.S., Allen, P., Lillehoj, H.S., Park, D., Fitzcoy, S., Bautista, D.A., Lillehoj, E.P. 2008. Immunopathology and Cytokine Responses in Broiler Chickens Coinfected with Eimeria maxima and Clostridium perfringens Using an Animal Model of Necrotic Enteritis. Avian Diseases. 52:14-22.Interpretive Summary: With the withdrawl of several growth promoting drugs in poultry production, there is an increasing incidence of necrotic enteritis which causes severe inflammatory response in the gut in poultry. Understanding of basic host-pathogen interaction and the fundamental immune mechanisms leading to necrotic enteritis is important to reduce economic losses due to this infection. In this paper, ARS scientists in collaboration with scientists at Shering Plough Animal Health and the Lashed Poultry Diagnostic lab developed a chicken disease model to replicate necrotic enteritis using a co-infection model of Eimeria maxima and Clostridium perfringene.  To better understand the disease interaction leading to necrotic enteritis, real time RT-PCR was used to investigate local gene expression changes of several immune-related genes. The results indicate that this disease model is suitable to study field necrotic enteritis and represents a replicable disease model for laboratory study. Molecular analysis of several host immune related genes and local macrophage immune response in this necrotic enteritis disease model showed a clear interaction of these two pathogens and the role of Eimeria in inducing necrotic inflammatory response upon Clostridium infection. Thios model will be useful for detailed analysis of host-pathogen interaction and studies like this will lead to the development of logical control strategy against necrotic enteritis in poultry.
                                Technical Abstract: The incidence of necrotic enteritis (NE) due to Clostridium perfringens (CP) infection in commercial poultry has been increasing at an alarming rate.  While pre-exposure of chickens to coccidia infections is believed to be one of the major risk factors leading to NE, the underlying mechanisms of CP virulence remain undefined.  The objectives of this study were to utilize an experimental model of NE produced by Eimeria maxima (EM) and CP coinfection to investigate the pathological and immunological parameters of the disease.  Broilers coinfected with EM plus CP exhibited more severe gut pathology compared with animals given EM or CP alone.  Additionally, EM/CP coinfection increased the numbers of intestinal CP bacteria compared with chickens exposed to an identical challenge of CP alone.  Coinfection with EM and CP repressed nitric oxide synthase gene expression that was induced by EM alone, leading to lower plasma NO levels.  Intestinal expression of a panel of cytokine and chemokine genes following EM/CP coinfection showed a mixed response depending on the transcript analyzed and the time following infection.  In general, IFN-', IFN-', IL-1', IL-2, IL-12, IL-13, IL-17, and TGF-'4 were repressed, while IL-8, IL-10, IL-15, and LITAF were increased during coinfection compared with challenge by EM or CP alone.  These results are discussed in the context of probable synergistic host responses to EM and CP infections that create a more severe disease phenotype leading to altered cytokine/chemokine responses different from those produced by infection with the individual pathogens.


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