The Association of Genetic Variation in Serotonin Receptor and Markers of Inflammation and Stress.

What is it about?

Neuro-immuno-hormones such as serotonin (5-HT) are major mediators within the central nervous system (CNS) that also have the capacity to directly modify the immune response. This dual functionality could be responsible for the ability of stress to influence immune function and predispose individuals to health disparities. The HTR7 SNP genotypes A/A (rs2420367, rs2185706) and C/C (rs7093602) were found to increase the risk for depressed cortisol in males, while A/C (rs2420367) increased the risk of depressed cortisol in females. expression of hsa-miR-425-5p, hsa-miR-1908-3p, and hsa-miR-525-3p were increased by HTR7 activation at physiological 5-HT concentrations while hsa-miR-302d-3p was increased by HTR7 at elevated 5-HT concentrations.

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Why is it important?

HTR7 activation has the ability to modulate an immune response from pro-inflammatory macrophages by miRNA epigenetic regulation of immune-related mRNAs in pro-inflammatory macrophages, and that SNPs in HTR7 result in an improper functioning of the innate and adaptive immune responses which under chronic stress, may be exacerbated to result in a predisposition towards adverse health conditions.

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