Year: 2025
Type: article
Abstract: Description Cholera toxin (CT), an exotoxin produced by Vibrio cholerae, causes severe diarrheal disease and contributes to the third leading cause of death in children under 5. Beyond its pathogenicity, CT possesses potent mucosal adjuvant properties, inducing type 2 immunity in the gastrointestinal tract. However, the immune response to acute oral CT exposure remains poorly characterized. To address this, we intragastrically administered a single nonlethal dose of CT to mice and assessed physiological and immune responses over 24 hours. In C57BL/6 mice, CT induced severe hypothermia, while BALB/c mice exhibited milder effects, with males of both strains showing heightened sensitivity. All treated animals developed diarrhea, and C57BL/6 mice experienced intestinal edema lasting up to 24 hours. Transcriptomic analysis of the small intestine revealed acute upregulation of inflammatory mediators such as IL-1β and IL-33. Immune profiling by full-spectrum flow cytometry showed CT-induced changes in the lamina propria compartment, including increased ILC3, reduced Treg RORγT+ and CD11b+CD103+ dendritic cells. In the epithelial layer, CT slightly elevated neutrophils, eosinophils, monocytes, and ILC3 while reducing CD3+ T lymphocytes and ILC1/ NK cells. These findings emphasize the broader action of CT in pathogenesis and immunity, shedding light on how immune sensing of bacterial toxins can drive protective defenses and adjuvant activity. Funding Sources Supported by Hypothesis Fund Topic Categories Mucosal and Regional Immunology (MUC)
Source: The Journal of Immunology
Institutions: Arizona State University, Mayo Clinic in Arizona
Language: English
Subfield: Endocrinology
Domain: Life Sciences
Open Access status: bronze
OpenAlex ID: W4416451553
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