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

Collection:
Clark Atlanta University Faculty Publications
Title:
Chlamydial Infection in Vitamin D Receptor Knockout Mice is More Intense and Prolonged than in Wild-type Mice
Creator:
He, Qing,
Ananaba, Godwin A.
Patrickson, John
Pitts, Sidney
Yi, Yeming
Yan, Fengxia
Eko, Francis O.
Lyn, Deborah
Black, Carolyn M.
Igietseme, Joseph U.
Thierry-Palmer, Myrtle
Date of Original:
2013-05-01
Subject:
African Americans--Education (Higher)--Georgia
Clark Atlanta University
Location:
United States, Georgia, Fulton County, Atlanta, 33.749, -84.38798
Medium:
articles
Type:
Text
Format:
application/pdf
Description:
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 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 less than 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)
Source: The Journal of Steroid Biochemistry and Molecular Biology
DOI: 10.1016/j.jsbmb.2012.11.002
URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4065015/
Metadata URL:
http://hdl.handle.net/20.500.12322/cau.ir:2013_ananaba
Language:
eng
Original Collection:
Clark Atlanta University Faculty Publications
Holding Institution:
Clark Atlanta University
Rights:

Locations