Source:http://linkedlifedata.com/resource/pubmed/id/10978752
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2-3
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pubmed:dateCreated |
2001-1-22
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pubmed:abstractText |
Several studies have documented the involvement of both Clostridium difficile, toxins, A and B in the pathogenesis of antibiotic-associated diarrhea. Recently, we demonstrated that IL-1 beta is the intestinal secretory factor released by macrophages stimulated with toxin A. The aim of this study was to evaluate the importance of macrophages stimulated with toxin B on rabbit ileal ion transport. The changes in ion transport were analyzed by studying the short-circuit current of the rabbit ileal mucosa mounted in Ussing chambers. The supernatants of macrophages treated with toxin B (3.6 x 10(-7) M) had no effect on the ion transport (change in short-circuit current =28.0+/-9.2 vs. control=26.8+/-3.6 microA cm(-2)). Supernatants of macrophages stimulated with toxin A (3.2 x 10(-7) M), our positive control, induced a significant change in ileal ion transport (delta I(sc)=55.2+/-5.7 mA cm(-2)). It was also observed that, like toxin A, toxin B stimulated macrophages to produce TNF-alpha (555.0+/-37.9 pg/ml vs. control=182.0+/-39.8 pg/ml; p<0.05). Nevertheless, in contrast to toxin A, toxin B did not stimulate IL-1 beta synthesis (28.0+/-7.5 pg/ml vs. control=40. 0+/-14.4 pg/ml; p>0.05). We conclude that the supernatants of macrophages stimulated with toxin B are not able to stimulate ion transport and that both toxins stimulate the genesis of TNF-alpha, but only toxin A induces the synthesis of IL-1 beta, which, we have earlier reported, causes an electrogenic intestinal response in rabbit ileum.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Bacterial Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Bacterial Toxins,
http://linkedlifedata.com/resource/pubmed/chemical/Enterotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/tcdA protein, Clostridium difficile,
http://linkedlifedata.com/resource/pubmed/chemical/toxB protein, Clostridium difficile
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pubmed:status |
MEDLINE
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pubmed:issn |
0041-0101
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
39
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
335-40
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10978752-Animals,
pubmed-meshheading:10978752-Bacterial Proteins,
pubmed-meshheading:10978752-Bacterial Toxins,
pubmed-meshheading:10978752-Enterotoxins,
pubmed-meshheading:10978752-Female,
pubmed-meshheading:10978752-Ileum,
pubmed-meshheading:10978752-Interleukin-1,
pubmed-meshheading:10978752-Ion Transport,
pubmed-meshheading:10978752-Macrophages,
pubmed-meshheading:10978752-Male,
pubmed-meshheading:10978752-Rabbits,
pubmed-meshheading:10978752-Rats,
pubmed-meshheading:10978752-Tumor Necrosis Factor-alpha
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pubmed:articleTitle |
Absence of intestinal secretion on supernatants from macrophages stimulated with Clostridium difficile toxin B on rabbit ileum.
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pubmed:affiliation |
Department of Physiology and Pharmacology, School of Medicine, Federal University of Ceará, Fortaleza, CE, Brazil.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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