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Cholera toxin and intestinal neurotransmitters modulate dendritic cell phenotype and function.

Principal Investigator: Bonny L. Dickinson, Ph.D.

Abstract

Mucosal vaccines targeted to the gut generate immune protection against pathogens that infect via mucosal surfaces of the gastrointestinal, respiratory, and genitourinary tract. Most replication incompetent oral vaccines, however, are poorly immunogenic and require inclusion of mucosal adjuvants to generate a robust immune response. Cholera toxin (CT) is the most potent oral adjuvant examined to date, and yet its enterotoxicity precludes its use in humans. A detailed understanding of how CT acts as an adjuvant would set the stage for development of adjuvants that exploit the toxin pathway without causing disease. It is already known that CT gains access into the intestine where it interacts with resident immune cells to affect immune function and acts on enteroendocrine cells and enteric neurons to elicit the local release of vasoactive intestinal peptide, acetylcholine and serotonin. We hypothesize that the transient accumulation of neuropeptides and neurotransmitters in the gut in the presence of intact toxin influences the function of a key resident immune cell, the dendritic cell (DC). We are currently characterizing the effects of intestinal neuropeptides and neurotransmitters on dendritic cell phenotype and function.