Document Detail


Diclofenac enhances allergic responses in a mouse peanut allergy model.
MedLine Citation:
PMID:  20718777     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Cite this as: M. Bol-Schoenmakers, R. Bleumink, M. Marcondes Rezende, E. Mouser, I. Hassing, I. Ludwig, J. J. Smit and R. H. H. Pieters, Clinical & Experimental Allergy, 2011 (41) 424-433. SUMMARY: Background Diclofenac and other non-steroidal anti-inflammatory drugs (NSAIDs) interfere with cyclo-oxygenase-mediated synthesis of prostaglandins, resulting in the inhibition of inflammatory immune responses. In contrast, it is known that NSAIDs are able to induce gastrointestinal damage. Objective Our aim was to investigate whether NSAIDs are able to enhance sensitization or abrogate tolerance to food antigens. Methods Mice were exposed to diclofenac and sensitized to peanut using cholera toxin as a mucosal adjuvant. In a tolerance model, oral tolerance was induced via feeding of peanut 3 weeks before sensitization with peanut. Diclofenac was administered before peanut feeding. After 4 weeks, peanut-specific antibodies in the serum and cytokine production in the spleen were measured. Induction of intestinal damage after oral exposure with diclofenac and peanut + cholera toxin was examined microscopically. Results Diclofenac-exposed animals showed increased levels of peanut-specific IgG1, IgG2a and IgE in the serum compared with vehicle-treated animals. Furthermore, peanut-induced cytokine production in the spleen was elevated upon diclofenac treatment. Importantly, diclofenac did not induce peanut-allergic responses in the absence of the cholera toxin, although exposure to diclofenac and peanut + cholera toxin resulted in intestinal epithelial damage. Reduced peanut-specific antibody production in the case of oral tolerance was not reversed after diclofenac exposure. However, oral tolerance, as measured by inhibition of peanut-specific cytokine responses, was reverted by diclofenac. Conclusions These data point towards an increased risk for induction of food-allergic responses by diclofenac, when other circumstances are also in favour of induction of allergy.
Authors:
M Bol-Schoenmakers; R Bleumink; M Marcondes Rezende; E Mouser; I Hassing; I Ludwig; J J Smit; R H H Pieters
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Publication Detail:
Type:  Journal Article     Date:  2010-08-16
Journal Detail:
Title:  Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology     Volume:  41     ISSN:  1365-2222     ISO Abbreviation:  Clin. Exp. Allergy     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-02-07     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8906443     Medline TA:  Clin Exp Allergy     Country:  England    
Other Details:
Languages:  eng     Pagination:  424-33     Citation Subset:  IM    
Copyright Information:
© 2010 Blackwell Publishing Ltd.
Affiliation:
Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands Utrecht Center for Food Allergy, Utrecht, The Netherlands TIPharma, Leiden, The Netherlands.
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