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Cited 7 time in webofscience Cited 7 time in scopus
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Genetically Disparate Fayoumi Chicken Lines Show Different Response to Avian Necrotic Enteritisopen access

Authors
Kim, Duk K.Lillehoj, Hyun S.Jang, Seung I.Lee, Sung H.Hong, Yeong H.Lamont, Susan J.
Issue Date
Oct-2015
Publisher
JAPAN POULTRY SCIENCE ASSOC
Keywords
disease resistance; Fayoumi; gene expression; NE; necrotic enteritis
Citation
JOURNAL OF POULTRY SCIENCE, v.52, no.4, pp 245 - 252
Pages
8
Journal Title
JOURNAL OF POULTRY SCIENCE
Volume
52
Number
4
Start Page
245
End Page
252
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/9050
DOI
10.2141/jpsa.0140203
ISSN
1346-7395
1349-0486
Abstract
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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