Document Detail

Role of TNF-α in the mechanisms responsible for preterm delivery induced by Stx2 in rats.
MedLine Citation:
PMID:  23043728     Owner:  NLM     Status:  MEDLINE    
BACKGROUND AND PURPOSE: Infections with a strain of Escherichia coli producing Shiga toxins could be one of the causes of fetal morbidity and mortality in pregnant women. We have previously reported that Shiga toxin type 2 (Stx2) induces preterm delivery in pregnant rats. In this study, we evaluate the role of TNF-α, PGs and NO in the Stx2-induced preterm delivery.
EXPERIMENTAL APPROACH: Pregnant rats were treated with Stx2 (0.7 ng g(-1)) and killed at different times after treatment. Placenta and decidua were used to analyse NOS activity by the conversion of L-[(14)C]arginine into L-[(14)C]citrulline, levels of PGE(2) and PGF(2α) assessed by radioimmunoassay, and cyclooxygenase (COX) proteins by Western blot. TNF-α level was analysed in serum by ELISA and by cytotoxicity in L929 cells. The inhibitor of inducible NOS, aminoguanidine, the COX-2 inhibitor, meloxicam, and the competitive inhibitor of TNF-α, etanercept, were used alone or combined to inhibit NO, PGs and TNF-α production respectively, to prevent Stx2-induced preterm delivery.
KEY RESULTS: Stx2 increased placental PGE(2) and decidual PGF(2α) levels as well as COX-2 expression in both tissues. Aminoguanidine and meloxicam delayed the preterm delivery time but did not prevent it. Etanercept blocked the TNF-α increase after Stx2 treatment and reduced the preterm delivery by approximately 30%. The combined action of aminoguanidine and etanercept prevented Stx2-induced preterm delivery by roughly 70%.
CONCLUSION AND IMPLICATIONS: Our results demonstrate that the increased TNF-α and NO induced by Stx2 were the predominant factors responsible for preterm delivery in rats.
Juliana Burdet; Flavia Sacerdoti; Maximiliano Cella; Ana M Franchi; Cristina Ibarra
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  British journal of pharmacology     Volume:  168     ISSN:  1476-5381     ISO Abbreviation:  Br. J. Pharmacol.     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-01-25     Completed Date:  2013-07-16     Revised Date:  2014-02-04    
Medline Journal Info:
Nlm Unique ID:  7502536     Medline TA:  Br J Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  946-53     Citation Subset:  IM    
Copyright Information:
© 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.
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MeSH Terms
Cyclooxygenase 2 / biosynthesis
Decidua / drug effects,  enzymology,  metabolism
Dinoprost / biosynthesis*
Dinoprostone / biosynthesis*
Drug Therapy, Combination
Guanidines / administration & dosage,  therapeutic use
Immunoglobulin G / administration & dosage,  therapeutic use
Nitric Oxide / biosynthesis
Placenta / drug effects,  enzymology,  metabolism
Premature Birth / blood,  chemically induced*,  metabolism,  prevention & control
Rats, Sprague-Dawley
Receptors, Tumor Necrosis Factor / administration & dosage,  therapeutic use
Shiga Toxin 2 / toxicity*
Tumor Necrosis Factor-alpha / blood*
Reg. No./Substance:
0/Guanidines; 0/Immunoglobulin G; 0/Receptors, Tumor Necrosis Factor; 0/Shiga Toxin 2; 0/Tumor Necrosis Factor-alpha; 185243-69-0/TNFR-Fc fusion protein; 31C4KY9ESH/Nitric Oxide; B7IN85G1HY/Dinoprost; EC 2; EC protein, rat; K7Q1JQR04M/Dinoprostone; SCQ4EZQ113/pimagedine

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