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

<p>Abstract</p> <p>Background</p> <p>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.</p> <p>Methods</p> <p>We surveyed polymorphisms in pig genes encoding PRRs and investigated the relationship between some of the detected polymorphisms and molecular function or disease onset.</p> <p>Results</p> <p>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 <it>TLR2</it> showed an increased tendency to contract pneumonia.</p> <p>Conclusions</p> <p>We propose the possibility of pig breeding aimed at disease resistance by the selection of PRR gene alleles that affect pathogen recognition.</p

Early cytokine response of gnotobiotic piglets to Salmonella enterica serotype Typhimurium

Cytokine response against Salmonella Typhimurium is traditionally studied in conventional animals. Germ-free animals, however, enable to study response against infection without background effect of other microorganisms. Plasma and ileal inflammatory cytokines in germ-free piglets orally infected with virulent LT2 strain or, with a non-virulent SF1591 rough mutant were quantified by ELISA. In plasma and ileal washes, IFN-$\gamma$ levels significantly increased in both infected groups. TNF-$\alpha$ and IL-18 were mostly missing in plasma 24 h after infection. In the ileum, IFN-$\gamma$, TNF-$\alpha$, and IL-1$\beta$ were induced mainly by the virulent strain, whereas IL-18 was induced in highest quantity by non-virulent Salmonella. These data confirmed an important role of IFN-$\gamma$, as well as other inflammatory cytokines in early stage of salmonellosis.La réponse précoce en cytokines contre Salmonella enterica Typhimurium chez des porcelets gnotobiotiques. La réponse en cytokines contre Salmonella Typhimurium est traditionnellement étudiée chez les animaux conventionnels. Les animaux sans germes, cependant, permettent d'étudier la réponse à l'infection sans avoir le bruit de fond dû à d'autres micro-organismes. Les cytokines inflammatoires du plasma et de l'iléon chez des porcelets sans germes, infectés oralement par la souche LT2 ou avec un mutant non virulent de SF1591, ont été quantifiées par ELISA. Dans le plasma et dans les lavages de l'iléon, les taux d'IFN-$\gamma$ ont augmenté significativement chez les animaux des deux groupes infectés. Le TNF-$\alpha$ et l'IL-18 étaient présents en faibles quantités dans le plasma 24 heures après infection. Dans l'iléon, l'IFN-$\gamma$, le TNF-$\alpha$ et l'IL-1$\beta$ ont été induits principalement par la souche virulente, alors que l'IL-18 a été induite en plus grande quantité par les salmonelles non virulentes. Ces données confirment le rôle important de l'IFN-$\gamma$ et des autres cytokines inflammatoires dans les stades précoces de la salmonellose

Expression Cloning of Gamma Interferon-Inducing Antigens of Mycobacterium avium subsp. paratuberculosis

Three recombinant proteins, Map10, Map39, and Map41, produced based on nucleotide sequences obtained from the screening of Mycobacterium avium subsp. paratuberculosis genomic library expressed in Escherichia coli significantly elicited gamma interferon production in peripheral blood mononuclear cells from infected cattle. Two of these proteins were members of the PPE protein family