| First Author | Haque TT | Year | 2023 |
| Journal | Sci Signal | Volume | 16 |
| Issue | 802 | Pages | eabc9089 |
| PubMed ID | 37699080 | Mgi Jnum | J:358233 |
| Mgi Id | MGI:7779715 | Doi | 10.1126/scisignal.abc9089 |
| Citation | Haque TT, et al. (2023) Fluoxetine restrains allergic inflammation by targeting an FcvarepsilonRI-ATP positive feedback loop in mast cells. Sci Signal 16(802):eabc9089 |
| abstractText | There is a clinical need for new treatment options addressing allergic disease. Selective serotonin reuptake inhibitors (SSRIs) are a class of antidepressants that have anti-inflammatory properties. We tested the effects of the SSRI fluoxetine on IgE-induced function of mast cells, which are critical effectors of allergic inflammation. We showed that fluoxetine treatment of murine or human mast cells reduced IgE-mediated degranulation, cytokine production, and inflammatory lipid secretion, as well as signaling mediated by the mast cell activator ATP. In a mouse model of systemic anaphylaxis, fluoxetine reduced hypothermia and cytokine production. Fluoxetine was also effective in a model of allergic airway inflammation, where it reduced bronchial responsiveness and inflammation. These data show that fluoxetine suppresses mast cell activation by impeding an FcvarepsilonRI-ATP positive feedback loop and support the potential repurposing of this SSRI for use in allergic disease. |
