Immune responses to oral toxins 9170

Abstract Description Environmental toxins are pervasive and dangerous to human health, yet little is known about their induced immune defenses. This gap is clinically significant, as 1 in 5 deaths worldwide in children below age five is attributed to toxin-induced diarrhea. Mast cells are tissue-resident immune cells capable of rapidly releasing bioactive mediators that drive expulsion reactions such as vomiting and diarrhea. We hypothesize these innate cells are well-suited as toxin sensors and their activation promotes required defense strategies. To investigate this, we exposed bone marrow-derived mast cells to cholera toxin, aconitine, and sennoside A, toxins from Vibrio bacteria, Aconitum, and Senna plant, respectively. Mast cell viability was determined using flow cytometry, degranulation was measured via beta-hexosaminidase release, and cytokine production was assessed with ELISA. None of the toxins induced significant cell death. Cholera toxin and aconitine did not induce degranulation, but sennoside A partially triggered mast cell degranulation. Surprisingly, sennoside A prevented IgE-mediated mast cell degranulation, and both sennoside A and aconitine prevented ionomycin-mediated mast cell degranulation. Our findings suggest that these distinct metabolites may prevent allergic mast cell degranulation. This study can help delineate the path to exploring plant metabolites as novel therapeutics for treating allergies, which continue to affect millions globally. Funding Sources Supported by FASI Topic Categories Immediate Hypersensitivity, Asthma, and Allergic Responses (HYP)