Public Release:  New study helps explain how botulism-causing toxin can enter circulation

Rockefeller University Press

New research in the Journal of Cell Biology helps explain how the toxic protein responsible for botulism can enter circulation from the digestive system. The study appears online May 10 (www.jcb.org).

Botulism, a rare but serious paralytic illness, is caused by botulinum neurotoxin (BoNT), an extremely toxic protein that is produced by the bacterium Clostridium botulinum. In food-borne botulism, the nontoxic components of BoNT--including hemagglutinin (HA)--protect the toxin from the low pH and enzymes encountered in the digestive tract. BoNT then passes through the intestinal epithelial barrier to enter circulation from the gut.

Although studies have examined how BoNT crosses the intestinal epithelial barrier, the mechanism by which it accomplishes this feat has remained a mystery. In this study, a team of Japanese researchers led by Yukako Fujinaga shows that HA plays a role. HA binds epithelial cadherin (E-cadherin), disrupting E-cadherin-mediated cell-to-cell adhesion and thereby disrupting the epithelial barrier.

Interestingly, the research demonstrates a species-specific interaction between HA and E-cadherin. Although HA binds human, bovine, and mouse E-cadherin, for instance, it does not bind rat or chicken.

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About The Journal of Cell Biology

Founded in 1955, The Journal of Cell Biology (JCB) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by active scientists in conjunction with our in-house scientific editors. JCB content is posted to PubMed Central, where it is available to the public for free six months after publication. Authors retain copyright of their published works and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit www.jcb.org.

Sugawara, Y., et al. 2010. J. Cell Biol. doi:10.1083/jcb.200910119.

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