title: Role of the W07-toxin on Vibrio cholerae-induced diarrhoea.
abstract: Vibrio cholerae W07 strain isolated from a cholera epidemic in South India, lacked the ctx gene but could still secrete a novel toxin, the W07-toxin that could cause fluid accumulation in ligated rabbit ileal loop. The important intracellular messengers implicated in this study were Ca(2+), cyclic AMP, inositol triphosphate and protein kinase C (PKC). A number of inhibitors/channel blockers have further shown the major role of [Ca(2+)](i) in modulation of the toxin-induced cellular response. An increase in the level of reactive oxygen species (ROS) in the W07-toxin-stimulated enterocytes correlated with the decrease in the levels of antioxidant enzymes, catalase and superoxide dismutase (SOD). The reactive nitrogen intermediates (RNI) detected by measuring the levels of nitrite and citrulline, were found to be high in the enterocytes triggered with the W07-toxin, thereby indicating their role in toxin-mediated change in mucosal permeability. The precise role of the toxin has also been authenticated by conducting the experiments with W07-toxin preincubated in the presence of IgG(WT) (IgG isolated from antitoxin sera) or GM(1). Thus, a significant increase in the levels of second messengers and a decrease in antioxidant defenses appear to be important in mediating the fluid secretion caused by this novel toxin from V. cholerae W07.
authors.affiliation: Department of Experimental Medicine and Biotechnology, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India. Shalmoli@glide.net.in
authors.forename: Shalmoli
authors.initials: S
authors.lastname: Bhattacharyya
authors.forename: Sujata
authors.initials: S
authors.lastname: Ghosh
authors.forename: Jasleen
authors.initials: J
authors.lastname: Shant
authors.forename: Nirmal K
authors.initials: NK
authors.lastname: Ganguly
authors.forename: Siddhartha
authors.initials: S
authors.lastname: Majumdar
mesh_terms: D000818:Animals; D001427:Bacterial Toxins / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D002478:Cells, Cultured; D002956:Citrulline / Q000032:analysis; D003967:Diarrhea / Q000209:etiology / Q000382:microbiology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D020895:Enterocytes / Q000187:drug effects* / Q000378:metabolism; D007295:Inositol Phosphates / Q000378:metabolism; D007421:Intestine, Small / Q000187:drug effects* / Q000378:metabolism; D008163:Luminescent Measurements; D051379:Mice; D008807:Mice, Inbred BALB C; D009573:Nitrites / Q000032:analysis; D051966:Phospholipase C gamma; D011493:Protein Kinase C / Q000378:metabolism; D015398:Signal Transduction; D013997:Time Factors; D010738:Type C Phospholipases / Q000378:metabolism; D014734:Vibrio cholerae / Q000472:pathogenicity
chemical_list: D001427:Bacterial Toxins; D007295:Inositol Phosphates; D009573:Nitrites; C420689:Vibrio cholerae WO7 toxin; D002956:Citrulline; D002374:Catalase; D011493:Protein Kinase C; D010738:Type C Phospholipases; D051966:Phospholipase C gamma; D002118:Calcium