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

Kelly, P., Feakins, R., Domizio, P., Murphy, J.L., Bevins, C., Wilson, J., McPhail, G., Poulsom, R. and Dhaliwal, W. (2004) Paneth cell granule depletion in the human small intestine under infective and nutritional stress Clinical and Experimental Immunology, 135, (2), pp. 303-309. (doi:10.1111/j.1365-2249.2004.02374.x).

Record type: Article


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.

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Published date: 2004
Keywords: defensins, hiv, innate immunity, mucosal immunology, paneth cells, zinc


Local EPrints ID: 25706
ISSN: 0009-9104
PURE UUID: ef4d5ff1-d457-4ee5-b955-884236180fb2

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Date deposited: 21 Apr 2006
Last modified: 17 Jul 2017 16:09

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

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