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Archives de pédiatrie
Volume 14, n° S3
pages 145-151 (octobre 2007)
Doi : S0929-693X(07)80018-2
Physiopathologie de la diarrhée à rotavirus
Physiopathology of Rotavirus diarrhea
 

M. Lorrot l, , M. Vasseur 2
l Service de Pédiatrie Générale, Hôpital Robert Debré 82, Boulevard S~rurier 75019 Paris, France 
2 UnitéINSERM 756, Faculté de Pharmacie de Châtenay-Malabry, Université Paris XI, 5, rue JB Clément 92296 Châtenay-Malabry, France 

*Correspondence
Résumé

Le rotavirus est 1'agent pathogène le plus fréquent des diarrhées de l'enfant de moins de 5 ans dans le monde. L'infection des entérocytes matures des villosités de l'intestin grêle entraîne les anomalies structurales et fonctionnelles complexes de l'épithélium à l'origine de la diarrhée. L'infection diminue les fonctions de digestion (diminution de l'activité des disaccharidases) et d'absorption des nutriments (diminution de l'absorption du glucose via SGLT1 et de l'absorption de la leucine) à l'origine de la diarrhée osmotique. La diarrhée à rotavirus comporte également une hypersécrétion modérée du chlore dans la lumière intestinale. La glycoprotéine non structurale NSP4 du rotavirus est la première entérotoxine virale connue, elle a la capacité d'induire la diarrhée sécrétoire chez le souriceau en l'absence de lésions histologiques. Contrairement à ce qui est observé dans les diarrhées dues à des entérotoxines bactériennes (toxine du cholera ou d'Escherichia coli), la diarrhée à rotavirus s'accompagne d'une augmentation de l'absorption villositaire du chlore alors que la sécrétion de chlore par les cellules cryptiques reste inchangée. Les mécanismes d'action de NSP4 apparaissent très différents de ceux impliqués par les entérotoxines bactériennes. NSP4 pourrait agir en augmentant le calcium intracellulaire par l'intermrdiaire du système nerveux entérique (SNE).

The full text of this article is available in PDF format.
Abstract

The rotavirus is the major cause of infantile gastroenteritis. The virus infects the mature enterocytes of the villus tip of the small intestine and induces a watery diarrhea. Diarrhea can occur in the absence of histological changes in the intestine, and, conversely, the histological changes can be asymptomatic. Rotavirus decreases the activities of digestive enzymes at the apical brush border membrane and inhibits Na+ -solute cotransport systems. Accumulation of carbohydrates in the intestinal lumen as well as malabsorption of nutrients and a concomitant inhibition of water absorption can lead to a malabsorptive component of diarrhea. Since the discovery of the NSP4 enterotoxin, several hypotheses have been proposed in favour of an additional secretion component in the pathogenesis of diarrhea. Rotavirus induces a moderate net chloride secretion at the onset of the diarrhea. The mechanisms appear to different from those used by bacterial enterotoxin that cause pure secretory diarrhea. Rotavirus stimulated C1- reabsorption in villi, and failed to stimulate C1- secretion in crypt. Intestinal villi could secrete chloride as a result of rotavims infection. The chloride secretory response is regulated by a dependant calcium signalling pathway induced by NSP4. The overall response is weak, suggesting that NSP4 may exert both secretory and subsequent antisecretory actions, hence limiting C1- secretion.

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Mots clés : Rotavirus, Gastroentérite, Diarrhée, Physiologie, NSP4




© 2007  Published by Elsevier Masson SAS.
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