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The new ‘connexin’ to the pathogenesis of E coli diarrhoea
  1. Alastair J M Watson
  1. Correspondence to Professor Alastair Watson, School of Clinical Sciences, The Henry Wellcome Laboratory, Nuffield Building, University of Liverpool, Crown Street Liverpool L69 3GE, UK; alastair.watson{at}liv.ac.uk

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Infectious diarrhoea is a major cause of morbidity and mortality causing 1.5 million deaths worldwide in 2005.1 Thus the pathobiology of diarrhoea is of considerable interest. However, despite considerable research over the last 50 years, significant gaps remain in our knowledge of the pathogenic diarrhoea mechanisms of specific microorganisms.

Diarrhoea can be regarded simply as an excess of water in faeces. The healthy adult intestine must absorb approximately 7 litres per 24 h to produce a normal stool. Failure of absorption or, alternatively, secretion of water into the intestine or a combination of the two will cause diarrhoea.

Vibrio cholerae or enterotoxogenic Escherichia coli (ETEC) secrete toxins which cause the accumulation of the second messenger cyclic AMP or, in the case of ETEC, cyclic GMP in intestinal epithelial cells. These second messengers cause secretion of water into the intestinal lumen through a couple of mechanisms. Secretion occurs predominately in the intestinal crypts. They can directly open an anion channel on the apical membrane of epithelial cells called cystic fibrosis transmembrane conductance regulator (CFTR) allowing the efflux of chloride ions resulting in osmotic gradients that pull water into the intestinal lumen; a process called electrogenic chloride secretion.2 They also activate a neural reflex within …

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