{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["He Q"],"funding":["NCRR NIH HHS","NIAID NIH HHS","NIMHD NIH HHS","PHS HHS"],"pagination":["7-14"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4065015"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["135"],"pubmed_abstract":["Vitamin D hormone (1,25-dihydroxyvitamin D) is involved in innate immunity and induces host defense peptides in epithelial cells, suggesting its involvement in mucosal defense against infections. Chlamydia trachomatis is a major cause of bacterial sexually transmitted disease worldwide. We tested the hypothesis that the vitamin D endocrine system would attenuate chlamydial infection. Vitamin D receptor knock-out mice (VDR(-/-)) and wild-type mice (VDR(+/+)) were infected with 10(3) inclusion forming units of Chlamydia muridarum and cervical epithelial cells (HeLa cells) were infected with C. muridarum at multiplicity of infection 5:1 in the presence and absence of 1,25-dihydroxyvitamin D3. VDR(-/-) mice exhibited significantly higher bacterial loading than wild-type VDR(+/+) mice (P<0.01) and cleared the chlamydial infection in 39 days, compared with 18 days for VDR(+/+) mice. Monocytes and neutrophils were more numerous in the uterus and oviduct of VDR(-/-) mice than in VDR(+/+) mice (P<0.05) at d 45 after infection. Pre-treatment of HeLa cells with 10nM or 100nM 1,25-dihydroxyvitamin D3 decreased the infectivity of C. muridarum (P<0.001). Several differentially expressed protein spots were detected by proteomic analysis of chlamydial-infected HeLa cells pre-treated with 1,25-dihydroxyvitamin D3. Leukocyte elastase inhibitor (LEI), an anti-inflammatory protein, was up-regulated. Expression of LEI in the ovary and oviduct of infected VDR(+/+) mice was greater than that of infected VDR(-/-) mice. We conclude that the vitamin D endocrine system reduces the risk for prolonged chlamydial infections through regulation of several proteins and that LEI is involved in its anti-inflammatory activity."],"journal":["The Journal of steroid biochemistry and molecular biology"],"pubmed_title":["Chlamydial infection in vitamin D receptor knockout mice is more intense and prolonged than in wild-type mice."],"pmcid":["PMC4065015"],"funding_grant_id":["RR03062","S21 MD000101","U54 RR026137","G12 RR003034","G12 RR003062","G12 MD007602","C06 RR018386","08247","1 C06 RR18386","U54 MD007588","1 U54 RR026137","SC1 AI103041","G12-RR03034"],"pubmed_authors":["Ananaba GA","Lyn D","Yi Y","Black CM","Patrickson J","Pitts S","Eko FO","He Q","Yan F","Igietseme JU","Thierry-Palmer M"],"additional_accession":[]},"is_claimable":false,"name":"Chlamydial infection in vitamin D receptor knockout mice is more intense and prolonged than in wild-type mice.","description":"Vitamin D hormone (1,25-dihydroxyvitamin D) is involved in innate immunity and induces host defense peptides in epithelial cells, suggesting its involvement in mucosal defense against infections. Chlamydia trachomatis is a major cause of bacterial sexually transmitted disease worldwide. We tested the hypothesis that the vitamin D endocrine system would attenuate chlamydial infection. Vitamin D receptor knock-out mice (VDR(-/-)) and wild-type mice (VDR(+/+)) were infected with 10(3) inclusion forming units of Chlamydia muridarum and cervical epithelial cells (HeLa cells) were infected with C. muridarum at multiplicity of infection 5:1 in the presence and absence of 1,25-dihydroxyvitamin D3. VDR(-/-) mice exhibited significantly higher bacterial loading than wild-type VDR(+/+) mice (P<0.01) and cleared the chlamydial infection in 39 days, compared with 18 days for VDR(+/+) mice. Monocytes and neutrophils were more numerous in the uterus and oviduct of VDR(-/-) mice than in VDR(+/+) mice (P<0.05) at d 45 after infection. Pre-treatment of HeLa cells with 10nM or 100nM 1,25-dihydroxyvitamin D3 decreased the infectivity of C. muridarum (P<0.001). Several differentially expressed protein spots were detected by proteomic analysis of chlamydial-infected HeLa cells pre-treated with 1,25-dihydroxyvitamin D3. Leukocyte elastase inhibitor (LEI), an anti-inflammatory protein, was up-regulated. Expression of LEI in the ovary and oviduct of infected VDR(+/+) mice was greater than that of infected VDR(-/-) mice. We conclude that the vitamin D endocrine system reduces the risk for prolonged chlamydial infections through regulation of several proteins and that LEI is involved in its anti-inflammatory activity.","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 May","modification":"2020-10-29T14:00:05Z","creation":"2019-03-27T01:30:31Z"},"accession":"S-EPMC4065015","cross_references":{"pubmed":["23201171"],"doi":["10.1016/j.jsbmb.2012.11.002"]}}