Polymorphisms in pattern recognition receptors and their relationship to infectious disease susceptibility in pigs

Pattern recognition receptors (PRRs), including Toll-like receptors (TLRs), are censoring receptors for molecules derived from bacteria, viruses, and fungi. The PRR system is a prerequisite for proper responses to pathogens, for example by cytokine production, resulting in pathogen eradication. Many...

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Veröffentlicht in:BMC proceedings 2011-06, Vol.5 Suppl 4 (S4), p.S27-S27, Article S27
Hauptverfasser: Uenishi, Hirohide, Shinkai, Hiroki, Morozumi, Takeya, Muneta, Yoshihiro, Jozaki, Kosuke, Kojima-Shibata, Chihiro, Suzuki, Eisaku
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Sprache:eng
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Zusammenfassung:Pattern recognition receptors (PRRs), including Toll-like receptors (TLRs), are censoring receptors for molecules derived from bacteria, viruses, and fungi. The PRR system is a prerequisite for proper responses to pathogens, for example by cytokine production, resulting in pathogen eradication. Many cases of polymorphisms in PRR genes affecting the immune response and disease susceptibility are known in humans and mice. We surveyed polymorphisms in pig genes encoding PRRs and investigated the relationship between some of the detected polymorphisms and molecular function or disease onset. Nonsynonymous polymorphisms abounded in pig TLR genes, particularly in the region corresponding to the ectodomains of TLRs expressed on the cell surface. Intracellular TLRs such as TLR3, TLR7, and TLR8, and other intracellular PRRs, such as the peptidoglycan receptor NOD2 and viral RNA receptors RIG-I and MDA5, also possessed nonsynonymous polymorphisms. Several of the polymorphisms influenced molecular functions such as ligand recognition. Polymorphisms in the PRR genes may be related to disease susceptibility in pigs: pigs with a particular allele of TLR2 showed an increased tendency to contract pneumonia. We propose the possibility of pig breeding aimed at disease resistance by the selection of PRR gene alleles that affect pathogen recognition.
ISSN:1753-6561
1753-6561
DOI:10.1186/1753-6561-5-S4-S27