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Stop taking Vitamin D already
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<blockquote data-quote="Phil Goodman" data-source="post: 229661" data-attributes="member: 42777"><p>Vitamin does a lot more than just reduce or prevent inflammation.</p><p></p><p></p><p>The beneficial effects of vitamin D on protective immunity are due in part to its effects on the innate immune system. It is known that macrophages recognize lipopolysacharide LPS, a surrogate for bacterial infection, through toll like receptors (TLR). Engagement of TLRs leads to a cascade of events that produce peptides with potent bacterialcidal activity such as cathelocidin and beta defensin 4[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/#R16" target="_blank">16</a>]. These peptides colocalize within phagosomes with injested bacteria where they disrupt bacterial cell membranes and have potent anti-microbacterial activity [<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/#R17" target="_blank">17</a>].</p><p>Vitamin D plays an important part in the innate antimicrobial response. TLR binding leads to increased expression of both the 1-α-hydroxylase and the VDR[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/#R17" target="_blank">17</a>-<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/#R18" target="_blank">18</a>]. This results in binding of the 1,25 D-VDR-RXR heterodimer to the VDREs of the genes for cathelocidin and beta defensin 4 and subsequent transcription of these proteins. Transcription of cathelocidin is absolutely dependent on sufficient 25 D[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/#R17" target="_blank">17</a>]. It is now clear that transcription of beta defensin 4 requires binding of NFkB to appropriate response elements on the beta defensin 4 RNA[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/#R19" target="_blank">19</a>]. TLR 2-1 signaling facilitates IL-1 receptor engagement which results in translocation of NFkB to its binding site[<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/#R19" target="_blank">19</a>].</p><p></p><p></p><p><strong>[URL unfurl="true"]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/[/URL]</strong></p></blockquote><p></p>
[QUOTE="Phil Goodman, post: 229661, member: 42777"] Vitamin does a lot more than just reduce or prevent inflammation. The beneficial effects of vitamin D on protective immunity are due in part to its effects on the innate immune system. It is known that macrophages recognize lipopolysacharide LPS, a surrogate for bacterial infection, through toll like receptors (TLR). Engagement of TLRs leads to a cascade of events that produce peptides with potent bacterialcidal activity such as cathelocidin and beta defensin 4[[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/#R16']16[/URL]]. These peptides colocalize within phagosomes with injested bacteria where they disrupt bacterial cell membranes and have potent anti-microbacterial activity [[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/#R17']17[/URL]]. Vitamin D plays an important part in the innate antimicrobial response. TLR binding leads to increased expression of both the 1-α-hydroxylase and the VDR[[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/#R17']17[/URL]-[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/#R18']18[/URL]]. This results in binding of the 1,25 D-VDR-RXR heterodimer to the VDREs of the genes for cathelocidin and beta defensin 4 and subsequent transcription of these proteins. Transcription of cathelocidin is absolutely dependent on sufficient 25 D[[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/#R17']17[/URL]]. It is now clear that transcription of beta defensin 4 requires binding of NFkB to appropriate response elements on the beta defensin 4 RNA[[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/#R19']19[/URL]]. TLR 2-1 signaling facilitates IL-1 receptor engagement which results in translocation of NFkB to its binding site[[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/#R19']19[/URL]]. [B][URL unfurl="true"]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3166406/[/URL][/B] [/QUOTE]
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