Chlamydial Infection in Vitamin D Receptor Knockout Mice is More Intense and Prolonged than in Wild-type Mice

He, Qing, Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine
Ananaba, Godwin A., Department of Biological Sciences, Clark Atlanta University
Patrickson, John, Department of Anatomy and Neuroscience, Morehouse School of Medicine
Pitts, Sidney, Department of Anatomy and Neuroscience, Morehouse School of Medicine
Yi, Yeming, Centers for Disease Control and Prevention
Yan, Fengxia, Clinical Research Center, Morehouse School of Medicine
Eko, Francis O., Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine
Lyn, Deborah, Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine
Black, Carolyn M., Centers for Disease Control and Prevention
Igietseme, Joseph U., Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine
Thierry-Palmer, Myrtle, Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine

2013-05-01

2010-2019

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 103 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 (PP< 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.

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articles

The Journal of Steroid Biochemistry and Molecular Biology

Clark Atlanta University

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4065015/

10.1016/j.jsbmb.2012.11.002

http://hdl.handle.net/20.500.12322/cau.ir:2013_ananaba

http://rightsstatements.org/vocab/InC/1.0/