Future work to expand our observations could include assessing leptin levels during other bacterial intestinal infections, assessing possible association with leptin and antibody maturation and class switching, assessing a possible role of leptin to T cell–dependent and T cell–independent antigens beyond those used in this study, assessing whether leptin levels predispose to cholera itself or to severity of disease, assessing leptin levels in mucosal tissues during intestinal infection, and addressing potential mechanisms of leptin involvement in immune responses during cholera. The gene discussed is LEP; the disease is bacterial infectious disease.