Effect of W07-toxin on gut physiological response in mice
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Updated: Jan 19, 2026

Investigating the Alleviating Effects of Bacillus cereus Administration on Colitis through Gut Microbiota Modulation
Published on: July 27, 2022
Shalmoli Bhattacharyya1, Sujata Ghosh, Jasleen Shant
1Department of Experimental Medicine and Biotechnology, Post Graduate Institute of Medical Education and Research, Chandigarh 160012, India. shalmoli@glide.net.in
Abstract:
A number of unknown secretogenic factor(s) from Vibrio cholerae have been implicated to play a role in inducing cholera-like symptoms observed in patients. The present study has been carried out on the novel W07-toxin (pI 5.2) from V. cholerae W07, an epidemic cholera strain devoid of the ctx gene. The toxin showed maximum binding to GM(1) and interacted with a 20 kDa glycoprotein present on the cell membrane of mice enterocytes in a GM(1) specific manner. The analysis of biochemical parameters in enterocytes triggered with this toxin revealed a significant increase in intracellular calcium concentration and a massive secretion of Cl(-). However, no absorption of Na(+) was observed under the same condition. This toxin also elevated the level of cyclic adenosine 3',5'-monophosphate (cAMP) as well as protein kinase A (PKA). Thus, the novel toxin, although distinct from cholera-toxin, showed some functional homology to it and may be one of the key players inducing electrolyte imbalance within intestinal cells in the cholera-like symptoms associated with V. cholerae W07.
Insights
A novel W07-toxin from Vibrio cholerae induces cholera-like symptoms by increasing chloride secretion and intracellular calcium in intestinal cells. This secretogenic factor, distinct from cholera toxin, disrupts electrolyte balance.
Area of Science:
- Microbiology
- Molecular Biology
- Pathogenesis
Background:
- Vibrio cholerae secretes factors causing cholera-like symptoms.
- The ctx gene is typically associated with cholera toxin production.
- An epidemic V. cholerae strain W07 lacks the ctx gene but causes similar symptoms.
Purpose of the Study:
- To investigate a novel toxin from V. cholerae W07.
- To characterize the mechanism of action of this new toxin.
- To understand its role in electrolyte imbalance and cholera-like symptoms.
Main Methods:
- Isolation and characterization of W07-toxin.
- Toxin binding assays with GM(1) and enterocyte membranes.
- Biochemical analysis of intracellular calcium, chloride, and sodium transport.
- Measurement of cyclic adenosine 3',5'-monophosphate (cAMP) and protein kinase A (PKA) levels.
Main Results:
- The novel W07-toxin binds to GM(1) and a 20 kDa glycoprotein on mouse enterocytes.
- Toxin exposure significantly increased intracellular calcium and chloride secretion.
- Sodium absorption was not affected.
- Elevated levels of cyclic adenosine 3',5'-monophosphate (cAMP) and protein kinase A (PKA) were observed.
Conclusions:
- The W07-toxin is a novel secretogenic factor from V. cholerae.
- It induces cholera-like symptoms through mechanisms involving increased intracellular calcium and chloride secretion.
- Despite functional similarities to cholera toxin, it is biochemically distinct.
- This toxin may be a key factor in electrolyte imbalance caused by V. cholerae W07.
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