Bacterial toxin interaction with the developing intestine
- PMID: 8382647
- DOI: 10.1016/0016-5085(93)91032-d
Bacterial toxin interaction with the developing intestine
Abstract
An important approach to the major health problem of bacterial infection in young children has been to examine bacterial toxin binding to microvillus membrane receptors, the signal transduction produced by that interaction and the mechanisms of fluid secretion in the developing intestine as a basis for toxigenic diarrhea in the infant population. These studies indicate that receptor binding and effector responses may be subjected to developmental regulation. This regulation process of toxin interaction with the developing intestine may have an enhanced or harmful effect or, under some circumstances, may have a beneficial effect and be protective to the vulnerable child. Specific mechanisms for the developmental control of receptor expression may involve the regulation of individual glycosyltransferases responsible for the addition of receptor sugar sequences to glycolipids and/or glycoproteins, presumably at the transcriptional level. Furthermore, although highly speculative at this point, the differential expression of signal transducers (e.g., guanine nucleotide-regulatory proteins or G proteins) and ion transporters (e.g., Na+,K(+)-stimulated adenosine triphosphatase, the Cl- channels, etc.) during development may also alter the neonatal host's responsiveness. Therefore, the developmental control of microvillus membrane receptors, signal transduction mechanisms, and ion transport systems in the gastro-intestinal tract may in part contribute to the altered host sensitivity in toxigenic diarrhea of infancy.
Similar articles
-
Gangliosides as receptors for bacterial enterotoxins.Adv Lipid Res. 1993;25:165-87. Adv Lipid Res. 1993. PMID: 8396312 Review. No abstract available.
-
Modulation of enterotoxin binding and function in vitro and in vivo.J Infect Dis. 1988 Mar;157(3):557-64. doi: 10.1093/infdis/157.3.557. J Infect Dis. 1988. PMID: 2830346
-
A gradient in expression of the Escherichia coli heat-stable enterotoxin receptor exists along the villus-to-crypt axis of rat small intestine.Biochem Biophys Res Commun. 1992 Jul 15;186(1):483-90. doi: 10.1016/s0006-291x(05)80833-2. Biochem Biophys Res Commun. 1992. PMID: 1378729
-
STa receptors: physiological and pathophysiological regulation of intestinal secretion by 5'-cyclic guanosine monophosphate.Gastroenterology. 1995 Jul;109(1):325-7. doi: 10.1016/0016-5085(95)90304-6. Gastroenterology. 1995. PMID: 7541001 No abstract available.
-
Receptors for cholera toxin and Escherichia coli heat-labile enterotoxin revisited.Prog Brain Res. 1994;101:163-77. doi: 10.1016/s0079-6123(08)61947-0. Prog Brain Res. 1994. PMID: 8029448 Review. No abstract available.
Cited by
-
Developmental differences in the expression of the cholera toxin sensitive subunit (Gs alpha) of adenylate cyclase in the rat small intestine.Gut. 1996 Jun;38(6):853-8. doi: 10.1136/gut.38.6.853. Gut. 1996. PMID: 8984023 Free PMC article.
-
Inflammation in the developing human intestine: A possible pathophysiologic contribution to necrotizing enterocolitis.Proc Natl Acad Sci U S A. 2000 May 23;97(11):6043-8. doi: 10.1073/pnas.97.11.6043. Proc Natl Acad Sci U S A. 2000. PMID: 10823949 Free PMC article.
-
Role of intestinal mucins in innate host defense mechanisms against pathogens.J Innate Immun. 2009;1(2):123-35. doi: 10.1159/000163037. Epub 2008 Oct 8. J Innate Immun. 2009. PMID: 20375571 Free PMC article. Review.
-
Mini-review: microbiota have potential to prevent PEDV infection by improved intestinal barrier.Front Immunol. 2023 Jul 12;14:1230937. doi: 10.3389/fimmu.2023.1230937. eCollection 2023. Front Immunol. 2023. PMID: 37503350 Free PMC article. Review.
-
Hydrocortisone induces changes in gene expression and differentiation in immature human enterocytes.Am J Physiol Gastrointest Liver Physiol. 2011 Mar;300(3):G425-32. doi: 10.1152/ajpgi.00011.2010. Epub 2010 Dec 9. Am J Physiol Gastrointest Liver Physiol. 2011. PMID: 21148402 Free PMC article.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources