A mutation in the NLRC5 promoter limits NF-κB signaling after Salmonella Enteritidis infection in the spleen of young chickens

• cNLRC5 was first cloned and a mutation in A-1017G of cNLRC5 promoter was detected.
• Chickens respond to Samonella Enteritidis by upregulating NLRC5 mRNA expression.
• An A1017G of cNLRC5 polymorphism is associated with infection by S. Salmonella Enteritidis.
• AA chickens had stronger immune response and resistance to Salmonella Enteritidis than GG chicken.

To date, the functions of the NLRC5 in chickens remain undefined. In the current study, chicken NLRC5 was cloned and an A1017G mutation was detected in its promoter region. The relative expression levels of the NLRC5 and key NF-κB pathway genes, IKKα, IKKβ, NF-κB, IL-6, IL-1β and IFN-γ, in the spleens of wild and mutant type birds, AA and GG, were determined using FQ-PCR at 7 day post-infection (DPI) with Salmonella Enteritidis. Additionally, the bacterial burden in the caecum and various immune response parameters were measured to evaluate immune responses. All of the examined immune response parameters were significantly different between the AA chickens and the GG chickens. Specifically, the mRNA expression levels of IKKα, NF-κB, IL-6, IL-1β and IFN-γ were higher in AA chickens than those in GG chickens, while the mRNA expression levels of NLRC5 were lower in AA chickens than those in GG chickens (P < 0.05). Moreover, the mRNA expression levels of TLR4 and MyD88 were not affected in either group. Collectively, considering former NLRC5 functional study in vitro, the wild genotype birds presented with better resistance to Salmonella Enteritidis through the actions of the NLRC5 and subsequent inhibition of the NF-κB pathway in chickens.