Date:   4/9/2007 12:30:59 AM ( 17 y ago)
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URL:   https://www.curezone.org/forums/fm.asp?i=842759

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Immunology. 2006 Aug;118(4):509-19.

Control of the innate epithelial antimicrobial response is cell-type
specific and dependent on relevant microenvironmental stimuli.
I remember Duane bring Butyrate to the attention of the group as being one of the ways Glyconutrients could improve health. I found this on Alt. Life Extention.
RO



Schauber J, Dorschner RA, Yamasaki K, Brouha B, Gallo RL.

Division of Dermatology, University of California, San Diego and VA San
Diego Healthcare System, San Diego, CA, USA.

Immune defence against microbes depends in part on the production of
antimicrobial peptides, a process that occurs in a variety of cell types
but is incompletely understood. In this study, the mechanisms
responsible for the induction of cathelicidin and beta-defensin
antimicrobial peptides were found to be independent and specific to the
cell type and stimulus. Vitamin D3 induced cathelicidin expression in
keratinocytes and monocytes but not in colonic epithelial cells.
Conversely, butyrate induced cathelicidin in colonic epithelia but not
in keratinocytes or monocytes. Distinct factors induced beta-defensin
expression. In all cell types, vitamin D3 activated the cathelicidin
promoter and was dependent on a functional vitamin D responsive element.
However, in colonic epithelia butyrate induced cathelicidin expression
without increasing promoter activity and vitamin D3 activated the
cathelicidin promoter without a subsequent increase in transcript
accumulation. Induction of cathelicidin transcript correlated with
increased processed mature peptide and enhanced antimicrobial activity
against Staphylococcus aureus. However, induction of beta-defensin-2
expression did not alter the innate antimicrobial capacity of cells in
culture. These data suggest that antimicrobial peptide expression is
regulated in a tissue-specific manner at transcriptional,
post-transcriptional and post-translational levels. Furthermore, these
data show for the first time that innate antimicrobial activity can be
triggered independently of the release of other pro-inflammatory
molecules, and suggest strategies for augmenting innate immune defence
without increasing inflammation.

Publication Types:
* Research Support, N.I.H., Extramural
* Research Support, Non-U.S. Gov't

PMID: 16895558
 

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