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These substances interact with EP3 receptors in MCs and prevent degranulation, limiting the release of histamine and minimizing allergic response.

This led to changes in the expression levels of the IgE-receptor, which ultimately inhibited degranulation in MCs.

Additional experiments revealed that non-steroidal anti-inflammatory drugs suppressed the anti-allergic effects of SCFAs, and that vitamin B-3, which interacts with the GPR109A receptor, also inhibited MC degranulation.

LAT1-dependent calcium signals required for mast cell degranulation were dampened, but the role of LAT2 in chemokine production was enhanced, altering immune cell recruitment at the site of inflammation.

In vitro studies demonstrate that serum AAT coordinates TNF-α intracellular signaling and neutrophil degranulation of tertiary and secondary granules via modulation of ligand-receptor interactions.