Transcriptional profiles of host-pathogen responses to necrotic enteritis and differential regulation of immune genes in two inbreed chicken lines showing disparate disease susceptibility.

Duk Kyung Kim,Seung I Jang,Yeong Ho Hong,Sung Hyen Lee,Hans H Cheng,Hyun S Lillehoj,Shu-Biao Wu

doi:10.1371/journal.pone.0114960

Abstract

Necrotic enteritis (NE) is an important intestinal infectious disease of commercial poultry flocks caused by Clostridium perfringens. Using an experimental model of NE involving co-infection with C. perfringens and Eimeria maxima, transcriptome profiling and functional genomics approaches were applied to identify the genetic mechanisms that might regulate the host response to this disease. Microarray hybridization identified 1,049 transcripts whose levels were altered (601 increased, 448 decreased) in intestinal lymphocytes from C. perfringens/E. maxima co-infected Ross chickens compared with uninfected controls. Five biological functions, all related to host immunity and inflammation, and 11 pathways were identified from this dataset. To further elucidate the role of host genetics in NE susceptibility, two inbred chicken lines, ADOL line 6 and line 7 which share an identical B2 major histocompatibility complex haplotype but differ in their susceptibility to virus infection, were compared for clinical symptoms and the expression levels of a panel of immune-related genes during experimental NE. Line 6 chickens were more susceptible to development of experimental NE compared with line 7, as revealed by decreased body weight gain and increased E. maxima oocyst shedding. Of 21 immune-related genes examined, 15 were increased in C. perfringens/E. maxima co-infected line 6 vs. line 7 chickens. These results suggest that immune pathways are activated in response to experimental NE infection and that genetic determinants outside of the chicken B complex influence resistance to this disease.

Highlights

Necrotic enteritis (NE) is an acute clostridial disease of economic importance to the poultry industry [1]
Effects of Necrotic Enteritis on Genetically Different Chicken Lines perfringens/E. maxima co-infected line 6 vs. line 7 chickens. These results suggest that immune pathways are activated in response to experimental NE infection and that genetic determinants outside of the chicken B complex influence resistance to this disease
Chickens were infected with E. maxima strain 41A (1.06104 oocysts/bird) by oral gavage on day 14 post-hatch followed by infection with C. perfringens strain Del-1 (1.06109 colony forming units/bird) by oral gavage on day 18 [11]

Summary

Introduction

Necrotic enteritis (NE) is an acute clostridial disease of economic importance to the poultry industry [1]. C. perfringens is a normal component of the chicken gut microbiota and the alterations in the hostpathogen relationship that regulate the development of NE remain to be determined [3]. A variety of predisposing factors, are known to promote disease, including diets containing high levels of wheat, barley, or poorly digestible proteins and co-infection by the apicomplexan protozoa, Eimeria, the etiologic agent of avian coccidiosis [4, 5]. Because of the risk of transmission to humans through the food chain, C. perfringens is important for public health [4, 6]. Prophylactic in-feed antibiotics have proven effective for control of clostridial field infections in chickens. NE has recently emerged as a significant problem as a result of decreased antibiotic usage amid concerns over the appearance of antibiotic-resistant human pathogens [4, 7]

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Results