GTPases and Actin as Targets for Bacterial Toxins

Author(s):  
K. Aktories ◽  
I. Just
Keyword(s):  
2003 ◽  
Vol 23 (4) ◽  
pp. 267-299 ◽  
Author(s):  
Ulrich Grandel ◽  
Friedrich Grimminger
Keyword(s):  

2014 ◽  
Vol 21 (4) ◽  
pp. 374-381 ◽  
Author(s):  
Laszlo Otvos ◽  
Helen Flick-Smith ◽  
Marc Fox ◽  
Eszter Ostorhazi ◽  
Raymond Dawson ◽  
...  

2010 ◽  
Vol 3 (2) ◽  
pp. 1-2
Author(s):  
Holger Barth ◽  
Brad Stiles
Keyword(s):  

1938 ◽  
Vol 32 (10) ◽  
pp. 1718-1728 ◽  
Author(s):  
Walter Reginald Wooldridge ◽  
Constance Higginbottom

2006 ◽  
Vol 140 (3) ◽  
pp. 439-444 ◽  
Author(s):  
Muktadir S. Hossain ◽  
Hiroshi Hamamoto ◽  
Yasuhiko Matsumoto ◽  
Iony M. Razanajatovo ◽  
Jorge Larranaga ◽  
...  

2005 ◽  
Vol 88 (3) ◽  
pp. 157-202 ◽  
Author(s):  
Anthony K. Campbell ◽  
Jonathan P. Waud ◽  
Stephanie B. Matthews

A staggering 4000 million people cannot digest lactose, the sugar in milk, properly. All mammals, apart from white Northern Europeans and few tribes in Africa and Asia, lose most of their lactase, the enzyme that cleaves lactose into galactose and glucose, after weaning. Lactose intolerance causes gut and a range of systemic symptoms, though the threshold to lactose varies considerably between ethnic groups and individuals within a group. The molecular basis of inherited hypolactasia has yet to be identified, though two polymorphisms in the introns of a helicase upstream from the lactase gene correlate closely with hypolactasia, and thus lactose intolerance. The symptoms of lactose intolerance are caused by gases and toxins produced by anaerobic bacteria in the large intestine. Bacterial toxins may play a key role in several other diseases, such as diabetes, rheumatoid arthritis, multiple sclerosis and some cancers. The problem of lactose intolerance has been exacerbated because of the addition of products containing lactose to various foods and drinks without being on the label. Lactose intolerance fits exactly the illness that Charles Darwin suffered from for over 40 years, and yet was never diagnosed. Darwin missed something else – the key to our own evolution – the Rubicon some 300 million years ago that produced lactose and lactase in sufficient amounts to be susceptible to natural selection.


Blood ◽  
2006 ◽  
Vol 109 (8) ◽  
pp. 3325-3332 ◽  
Author(s):  
Anders Woetmann ◽  
Paola Lovato ◽  
Karsten W. Eriksen ◽  
Thorbjørn Krejsgaard ◽  
Tord Labuda ◽  
...  

AbstractBacterial toxins including staphylococcal enterotoxins (SEs) have been implicated in the pathogenesis of cutaneous T-cell lymphomas (CTCLs). Here, we investigate SE-mediated interactions between nonmalignant T cells and malignant T-cell lines established from skin and blood of CTCL patients. The malignant CTCL cells express MHC class II molecules that are high-affinity receptors for SE. Although treatment with SE has no direct effect on the growth of the malignant CTCL cells, the SE-treated CTCL cells induce vigorous proliferation of the SE-responsive nonmalignant T cells. In turn, the nonmalignant T cells enhance proliferation of the malignant cells in an SE- and MHC class II–dependent manner. Furthermore, SE and, in addition, alloantigen presentation by malignant CTCL cells to irradiated nonmalignant CD4+ T-cell lines also enhance proliferation of the malignant cells. The growth-promoting effect depends on direct cell-cell contact and soluble factors such as interleukin-2. In conclusion, we demonstrate that SE triggers a bidirectional cross talk between nonmalignant T cells and malignant CTCL cells that promotes growth of the malignant cells. This represents a novel mechanism by which infections with SE-producing bacteria may contribute to pathogenesis of CTCL.


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