Genetically Disparate Fayoumi Chicken Lines Show Different Response to Avian Necrotic Enteritis

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  • Kim Duk K.
    Animal Biosciences and Biotechnology Laboratory, Beltsville Agricultural Research Center, United States Department of Agriculture, USA C&K Genomics Inc., South Korea
  • Lillehoj Hyun S.
    Animal Biosciences and Biotechnology Laboratory, Beltsville Agricultural Research Center, United States Department of Agriculture, USA
  • Jang Seung I.
    Animal Biosciences and Biotechnology Laboratory, Beltsville Agricultural Research Center, United States Department of Agriculture, USA Institute of Health and Environment, Daejeon Metropolitan City, South Korea
  • Lee Sung H.
    Animal Biosciences and Biotechnology Laboratory, Beltsville Agricultural Research Center, United States Department of Agriculture, USA National Academy of Agricultural Science, Rural Development Administration, South Korea
  • Hong Yeong H.
    Department of Animal Science and Technology, Chung-Ang University, South Korea
  • Lamont Susan J.
    Department of Animal Science, Iowa State University, USA

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Necrotic enteritis (NE) has reemerged as a significant problem as a result of growing restrictions of antibiotics in agricultural animal production and increasing concerns over antibiotic resistance in human pathogens. To enhance our understanding of host-pathogen immunobiology in NE, transcriptional analysis was conducted to compare changes in NE-induced intestinal transcripts and to identify immune-related genes whose expression are associated with NE disease resistance using two genetically disparate Fayoumi chicken lines, M5.1 and M15.2. NE was induced by co-infection of Eimeria maxima and Clostridium perfringens using an established disease model and two major NE-induced clinical signs, body weight loss and intestinal lesions, were measured in two inbred Fayoumi chicken lines, M5.1 and M15.2. In the clinical criteria, line M5.1 chickens were more resistant to NE compared to line 15.2 birds. Although they have the same genetic background, these two chicken lines are genetically disparate at their major histocompatibility complex (MHC) and this difference was reflected in the differential expression patterns of several inflammatory genes such as suppressor of cytokine signaling 3 (SOCS3), interleukin 8 (IL8), nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, zeta (NFKBIZ), serpin peptidase inhibitor, clade F (alpha-2 antiplasmin, pigment epithelium derived factor), member 1 (SERPINF1), and gap junction protein, alpha 1, 43kDa (GJA1) between NE-afflicted and uninfected chickens. These results will lead to increased insights on the NE disease resistance mechanisms and the role of host genes controlling host immune response to C. perfringens.

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