Transcriptional Profiles of Host-Pathogen Responses to Necrotic Enteritis and Differential Regulation of Immune Genes in Two Inbreed Chicken Lines Showing Disparate Disease Susceptibility

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.

Effects of cLFchimera, a recombinant antimicrobial peptide, on intestinal morphology, microbiota, and gene expression of immune cells and tight junctions in broiler chickens challenged withC. perfringens

“…Results of the present study showed that while C. perfringens challenged upregulated the expression of TRAF3 in the jejunum of chickens, antibiotic and AMP significantly decreased the expression of this cytokine in the challenged birds. To the best of our knowledge, this is the first experiment that reports the expression of TRAF3 under AMP and antibiotic treatments in C. perfringens challenged chickens, while there is consistency between the current results and previous ones regarding the effects of C. perfringens challenge on TRAF3 expression [62, 64].…”

“…TRAF3 is a cytoplasmic protein that controls signal transduction from different receptor families, especially TLRs [61]. Following the activation of TLR4 with pathogen attachment, TRAF3 is recruited into signaling complexes, and its activation increases vital pro-inflammatory cytokines production [62, 63]. Results of the present study showed that while C. perfringens challenged upregulated the expression of TRAF3 in the jejunum of chickens, antibiotic and AMP significantly decreased the expression of this cytokine in the challenged birds.…”

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

“…The genes were selected from the transcripts significantly altered by NE induction (＞2.0-fold differential expression) in the IELs of broilers in our previous report (Kim et al, 2014), and also identified as the biological functions related with immune response by functional genomics. Interestingly, most genes analyzed in this study showed the decreased expression in both NE-infected Fayoumi chicken lines compared with non-infected control chickens (Table 2).…”

“…In our previous study (Kim et al, 2014), transcriptome profiling was applied to elucidate molecular mechanisms underlying the pathogenesis of NE and obtain further insights on host immune responses to NE infection. Therefore, based on the report, this study was conducted to compare the differences in the resistance to NE and the expression levels of immune related genes between two Fayoumi chickens, M5.1 and M15.2 lines following NE induction by functional genomics to identify host genes associated with NE disease resistance.…”

Systems Perspective of Morbillivirus Replication

“…Although comprehensive information about all the host factors is lacking, one of the elements that has been identified and which makes water buffalo resistant to PPR (compared to goats) is the higher basal level expression of Toll-like receptors 3/7 [Dhanasekaran et al, 2014]. Systems virology can unravel all the host factors that may be responsible for disease resistance, like those identified for chicken flocks, differently susceptible for necrotic enteritis [Kim et al, 2014].…”