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

Thumbnail Image
Kim, Duk
Lillehoj, Hyun
Jang, Seung
Lee, Sung
Hong, Yeong
Major Professor
Committee Member
Journal Title
Journal ISSN
Volume Title
Lamont, Susan
Distinguished Professor
Research Projects
Organizational Units
Organizational Unit
Animal Science

The Department of Animal Science originally concerned itself with teaching the selection, breeding, feeding and care of livestock. Today it continues this study of the symbiotic relationship between animals and humans, with practical focuses on agribusiness, science, and animal management.

The Department of Animal Husbandry was established in 1898. The name of the department was changed to the Department of Animal Science in 1962. The Department of Poultry Science was merged into the department in 1971.

Historical Names

Journal Issue
Is Version Of

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.


This article is from The Journal of Poultry Science 52 (2015): 245, doi:10.2141/jpsa.0140203.