936 research outputs found

    Activation of Vitamin D3 in Bovine Mastitis Caused by Streptococcus uberis

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    Inflamed mammary tissue of three cows infected with Streptococcus uberis was found to have higher concentrations of 1α-hydroxylase than un-inflamed control mammary glands. Increased levels of 1α−hydroxylase resulted in increased production of 1,25-dihydroxyvitamin D3. Therefore, vitamin D3 may have a role in the inflammation and resolution of bovine mastitis

    1,25-Dihydroxyvitamin D3 Enhances Bovine Mammary Epithelial Innate Immune Responses

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    Bovine mammary epithelial cells that were treated with bacterial lipopolysaccharide and 1,25-dihydroxyvitamin D3 showed an increase in the expression of the genes for inducible nitric oxide synthase (iNOS) and S100 calcium binding protein A12 (S100 A12). iNOS and S100 A12 are part of the innate immune response and expressed in the mammary gland during mastitis. Production of 1,25- dihydroxyvitamin D3 in the mammary gland during mastitis, then, may be an important component of the innate immune response

    Structural geology of southeastern Illinois and vicinity

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    Regulation of Immune Responses to Mycobacteria bovis by a Paracrine Mechanism of Vitamin D Signaling in Cattle

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    We provide evidence that T-cell responses to Mycobacteria bovis are suppressed by the production of 1,25-dihydroxyvitamin D3 in monocytes and B-cells from cattle. Current vitamin D requirements for cattle are solely based on the classical endocrine mechanism of vitamin D signaling that regulates calcium homeostasis and should be re-evaluated to account for vitamin D signaling mechanisms in the immune system

    Timing and mechanism of conceptus demise in a complement regulatory membrane protein deficient mouse

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    PROBLEM: Crry is a widely expressed type 1 transmembrane complement regulatory protein in rodents which protects self-tissue by downregulating C3 activation. Crry METHOD OF STUDY: We investigated the basis of Crry RESULTS: We narrowed the critical period of the complement effect from 6.5 to 8.5 days post-coitus (dpc), which is immediately after the conceptus is exposed to maternal blood. Deposition by 5.5 dpc of maternal C3b on the placental vasculature lacking Crry CONCLUSION: Our data are most consistent with the deposition of C3b being responsible for the failure of the allantois to fuse to the chorion leading to subsequent conceptus demise
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