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Subject:
From:
Roy Jamron <[log in to unmask]>
Reply To:
Roy Jamron <[log in to unmask]>
Date:
Sun, 25 Jan 2004 16:33:45 -0500
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<<Disclaimer: Verify this information before applying it to your situation.>>

Paneth cells, located at the base of the crypts of intestinal villi, have
long been an object of study in celiac disease research, especially during
the late 1960's into the 1980's.  However, a review of PubMed abstracts
turns up a conflicting body of research that has the number and size and
granules of Paneth cells both increasing and decreasing in CD patients.  A
new study (hopefully accurate this time) shows Paneth cell granule
depletion occuring in intestinal disorders.  Recent research has been
demonstrating more and more the importance, function and role of Paneth
cells in maintaining intestinal health and in destroying harmful microbes.
One thing for sure, CD has an effect on Paneth cells.  Here are a few
articles of interest on Paneth cells.  (You will need to paste the web
addresses together on one line.)

----------
Paneth cells:
http://arbl.cvmbs.colostate.edu/hbooks/pathphys/digestion/smallgut/paneth.ht
ml

Photographic image of Paneth cells (in red):
http://home.primus.com.au/royellis/smint.jpg

Tales from the crypts: Cells battle germs
http://www.findarticles.com/cf_dls/m1200/9_158/65368554/p1/article.jhtml

Gut Bacteria Interact with Intestine to Regulate Blood Supply (Nov. 4, 2002)
http://mednews.wustl.edu/medadmin/PAnews.nsf/0/B14C4FCB1C4037CA86256C67007DF
1A2
http://mednews.wustl.edu/medadmin/PAnews.nsf/Archives?OpenForm&yr=2002

Search and Destroy: Newly Identified Gut Protein Kills Bacteria (Jan. 26,
2003)
http://mednews.wustl.edu/medadmin/PAnews.nsf/0/7BF498C3BA91B68586256CB8007C7
B81
http://mednews.wustl.edu/medadmin/PAnews.nsf/Archives?OpenForm&yr=2003

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Clin Exp Immunol. 2004 Feb; 135(2): 303-309

Paneth cell granule depletion in the human small intestine under infective
and nutritional stress.

Kelly P, Feakins R, Domizio P, Murphy J, Bevins C, Wilson J, McPhail G,
Poulsom R, Dhaliwal W.

Institute of Cell and Molecular Science, Bart's and The London School of
Medicine, London, Institute of Human Nutrition, University of Southampton,
Southampton, Department of Medical Microbiology and Immunology, University
of California Davis School of Medicine, Davis, CA, USA, and Cancer Research
UK, London Research Institute, Lincoln's Inn Fields, London, UK.

Paneth cells are important contributors to the intestinal antimicrobial
barrier through synthesis and release of antimicrobial peptides and
proteins. Animal studies indicate that Paneth cell numbers, location and
granule morphology are altered by infection and zinc status. We examined
human tissue to determine whether Paneth cell numbers, distribution or
granule morphology are altered in infective, inflammatory and nutritional
disorders. Archival sections from infective disorders (giardiasis,
cryptosporidiosis, HIV, helminth infection) were compared with active
inflammatory conditions (coeliac, Crohn's and graft-versus-host diseases)
and histologically normal tissues. A subset of tissues was studied by
electron microscopy and TUNEL staining for apoptosis. Human defensin-5
(HD5) peptide and mRNA was analysed by immunohistochemistry, in situ
hybridization and quantitative reverse transcription polymerase chain
reaction. Sections from a tropical population cohort study were then
analysed to determine the relationship of granule depletion to infection,
nutritional status and plasma zinc concentration. In HIV-related
cryptosporidiosis, but not other disorders, Paneth cells were reduced in
number and markedly depleted of granules. Paneth cell granule depletion was
associated with reduced HD5 immunoreactivity, but this was not due to
apoptosis and there was no reduction in mRNA transcripts. In the tropical
population studied, depletion of granules was associated with reduced body
mass index, reduced plasma zinc levels and HIV infection. Paneth cell
granules in human small intestine may be depleted in response to infective
and nutritional stress. We postulate that this is one mechanism through
which zinc status influences host susceptibility to intestinal infection.

PMID: 14738460 [PubMed - as supplied by publisher]

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