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Vitamin D suppresses staphylococcus mediated inflammation by inhibiting NR4A2 activity in human mesenchymal stem cells
Author(s) -
Maiti Aparna,
Jiranek William
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.952.3
Subject(s) - calcitriol receptor , mesenchymal stem cell , staphylococcus aureus , vitamin d and neurology , inflammation , stromal cell , stem cell , proinflammatory cytokine , vitamin , microbiology and biotechnology , biology , immunology , cancer research , chemistry , endocrinology , bacteria , genetics
Mesenchymal stem cells (MSCs) are multipotent cells found in many tissues of the body, could differentiate into stromal tissue such as bone. Staphylococci, particularly Staphylococcus aureus are the predominant cause of bone disease worldwide. In our previous stududies we observed that S. aureus as TLR ligands augmented nuclear factor kB (p65‐NF‐kappaB), pro‐inflammatory cytokines IL‐6, IL8, and NR4A2, a nuclear receptor is emerging as key regulator in disease like prolonged inflammatory responses in MSCs which leads to reduced osteoblast differentiation and increase mesenchymal stem cells proliferations. The active form of Vitamin D [1,25 dihydroxyvitamin D3] has potent immunomodulatory properties which promotes its potential use in prevention of various infectious diseases. Vitamin D mediates its actions by binding to the vitamin D receptor (VDR). This study was aimed to examine the antimicrobial effect of Vitamin D during staphylococcus infection in MSCs. Quantitative realtime PCR data indicated that Vitamin D treatment increased VDR, 1‐alpha hydroxylase, and cathelicidine mRNA levels. Interestingly, Vitamin D treatment along with Staphylococcus aureus infection of MSCs demonstrated significant suppression of NR4A2 expression. Thus Vitamin D is an important contributor to host protection from Staphylococcus infection by inhibiting NR4A2‐mediated inflammation in MSCs.