An estrogen-sensitive neuroimmune interaction as a potential mechanism for sex differences in pain
Sex differences in the immune system may contribute to higher pain prevalence in women. Serotonin (5HT) released in the periphery contributes to pain signaling in sensory neurons. Immune cells, like macrophages, can release 5HT at sites of injury to affect immune cell activity. Macrophages express estrogen receptors and may respond to gonadal hormones. We hypothesized that 17β−estradiol (E2) triggers inflammatory responses in macrophages. To test this hypothesis we quantified 5HT release from murine macrophage culture supernatant collected before and after 1-hour treatment with various E2 concentrations. Inflammatory cytokine production was evaluated from supernatants collected before and after E2 and 5HT treatments. 5HT release was dependent on concentration of E2 treatment and release of several cytokines was significantly increased with combined treatments. These data indicate that E2 alters 5HT and cytokine release from macrophages. Further studies are warranted to determine if this estrogen-sensitive neuroimmune interaction contributes to sex differences in pain.
Presented at the 2021 Student Creative Arts and Research Symposium
Creative Arts and Research Symposium