Moreover, IL-1β can cause depression by upregulating indolamine-2,3-dioxygenase (IDO), thus activating the catabolism of tryptophan to kynurenine (Cattaneo et al., 2013), reducing brain serotonin (5-HT), and increasing the N-methyl-D-aspartate receptor agonist quinolinic acid (Belzeaux et al., 2012; Cattaneo et al., 2016); and by activating the HPA axis and inducing glucocorticoid receptors resistance (Powell et al., 2013; Guilloux et al., 2015). This evidence concerns the gene HTR5A and depressive symptom measurement.