Just to link this thread to one I posted on cobalt earlier...

Tannins are iron chelators (which probably accounts for some of their
antimicrobial properties).  Iron chelators can induce HIF-1 expression,
tricking cells into thinking conditions are hypoxic (and that you're low
on iron and need more red blood cells produced).  Triggering this
pathway was recently discovered to block leaky gut syndrome.  These same
gap junction proteins are expressed in the sinuses.  It's just an
educated guess on my part but tannins might shut down the immune
system's exposure to foreign irritants by sealing leaky membranes.

___________
Gastroenterology. 2008 Jan;134(1):156-65. Epub 2007 Oct 10.
 
The hydroxylase inhibitor dimethyloxalylglycine is protective in a
murine model of colitis.

Cummins EP, Seeballuck F, Keely SJ, Mangan NE, Callanan JJ, Fallon PG,
Taylor CT.
UCD Conway Institute, University College Dublin, Belfield, Dublin,
Ireland.

BACKGROUND & AIMS: Prolyl and asparaginyl hydroxylases are key
oxygen-sensing enzymes that confer hypoxic sensitivity to
transcriptional regulatory pathways including the hypoxia inducible
factor 1 (HIF-1) and nuclear factor-kappaB (NF-kappaB). Knockout of
either HIF-1 or (IKKbeta-dependent) NF-kappaB pathways in intestinal
epithelial cells promotes inflammatory disease in murine models of
colitis. Both HIF-1 and NF-kappaB pathways are repressed by the action
of hydroxylases through the hydroxylation of key regulatory molecules.
METHODS: In this study we have investigated the effects of the
hydroxylase inhibitor dimethyloxalylglycine (DMOG) on Caco-2 intestinal
epithelial cells in vitro and in a dextran sodium sulfate-induced model
of murine colitis. RESULTS: DMOG induces both HIF-1 and NF-kappaB
activity in cultured intestinal epithelial cells, and is profoundly
protective in dextran-sodium sulfate colitis in a manner that is at
least in part reflected by the development of an anti-apoptotic
phenotype in intestinal epithelial cells, which we propose reduces
epithelial barrier dysfunction. CONCLUSIONS: These data show that
hydroxylase inhibitors such as DMOG represent a new strategy for the
treatment of inflammatory bowel disease.

Publication Types:
*  Research Support, Non-U.S. Gov't

PMID: 18166353 [PubMed - in process]
------------------------------------------------------------------------
<http://www.ucd.ie/news/2008/01JAN08/011508_idb.html>
Posted: 15 January 2008

Scientists uncover new potential treatment for Inflammatory Bowel Disease

    Irish scientists have discovered a new potential therapeutic
approach to Inflammatory Bowel Disease (IBD), a chronic debilitating
disease involving inflammation of the intestine which affects more than
15,000 people in Ireland and millions of people worldwide.
    People suffering from IBD can experience an array of symptoms
ranging from mild discomfort to debilitating disease requiring surgical
removal of large parts of the intestine. Current therapeutic options in
IBD are very limited and surgery is often the only option.
    In the new discovery published in the scientific journal
Gastroenterology, the Irish scientists have demonstrated that they can
almost completely reverse the symptoms of IBD in a disease model using a
new class of drugs known as hydroxylase inhibitors.
    ³Under normal conditions our gastro-intestinal tract is lined with
cells that block the contents of the gut from leaking into the
intestine,² explains Professor Cormac Taylor from the UCD Conway
Institute, University College Dublin, one of the principal scientists
involved in the discovery. ³However, when a person is suffering from IBD
this barrier is broken and the contents of the gut leak out into
surrounding areas.²
    ³When we applied the new drugs, the gut was tricked into thinking
that it was being deprived of oxygen and this activated protective
pathways which in turn prevented the death of the cells that line the
gastrointestinal tract,² continues Professor Taylor.
    While completing their investigation, the Irish researchers became
aware of a similar study taking place at the University of Colorado,
Denver. This study appears as an accompanying article in the same issue
of Gastroenterology. The US study, while using a different hydroxylase
inhibitor, supports the Irish scientist¹s research findings.
    The Irish and US research groups will now begin a collaborative
investigation to bring the discovery to the next stage which involves
developing a new therapeutic which can be delivered safely to humans.
    ³By working in collaboration with Sigmoid Biotechnologies, a Dublin
based drug delivery company, we intend to focus on developing methods to
safely deliver these drugs to their intended target in the inflamed
gut,² says Professor Taylor.
    ³These findings show that cross-university partnerships adopted by
the new generation of Science Foundation Ireland funded Irish scientists
will help to drive Ireland¹s future knowledge economy,² says Professor
Padraic Fallon, SFI Stokes Professor, TCD School of Medicine, Trinity
College Dublin, the other principal research scientist involved in the
Irish discovery.
    ³If Ireland is to compete at the forefront of scientific
discoveries and to develop partnerships with the international
biotechnology sector, our scientist must work together in synergy,²
continues Professor Fallon.
    The Irish research groups led by Professor Taylor at University
College Dublin and Dr Fallon at Trinity College Dublin have recently
received independent investigator awards from Science Foundation Ireland
totaling over ¤1 million each.
    UCD, Belfield, Dublin 4, Ireland. Tel : 353-1-7167777