Abstract :
Vibrio cholerae is a Gram-negative bacterium that causes the life-threatening diarrheal disease cholera, which remains a major global health concern despite significant advances in understanding its epidemiology and molecular pathogenesis. The disease predominantly affects populations in developing regions with inadequate sanitation and limited access to clean water. Infection by V. cholerae primarily stimulates humoral immune responses, with CD4⁺ T-helper cell differentiation serving as a central determinant of both disease progression and vaccine efficacy. Among these responses, the Th2 subset and its signature cytokine, interleukin-13 (IL-13), play crucial roles in mucosal defense by inducing goblet cell differentiation, mucus hypersecretion, and antibody production. This coordinated mucosal response facilitates bacterial clearance but can also contribute to excessive fluid loss characteristic of cholera. The balance between Th1, Th2, and Th17 pathways therefore represents a key immunological checkpoint that shapes host protection and the quality of vaccine-induced immunity. This review synthesizes current knowledge on the role of IL-13 and Th2-mediated immunity in V. cholerae infection, emphasizing how cytokine regulation and mucosal antibody responses contribute to protection. Furthermore, it explores how these mechanisms can be leveraged to design next-generation cholera vaccines with enhanced and long-lasting immunogenicity. A deeper understanding of IL-13–driven mucosal mechanisms provide critical insight into host–pathogen interactions and offers promising directions for improving both prophylactic and therapeutic strategies against cholera.
