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Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: N-Oleoyl dopamine induces IL-10 via central nervous system TRPV1 and improves endotoxemia and sepsis outcomes

Fig. 7

Hypothetical model of OLDA’s anti-inflammatory effects mediated by CNS TRPV1 neurons, and TRPV1-independent actions on leukocytes and endothelial cells. Left panel: Under inflammatory conditions, the activation of central nervous system TRPV1 neurons by OLDA triggers a neuro-immune inflammatory reflex, that culminates in the acute upregulation of IL-10 production in the peripheral circulation. Monocytic myeloid cells are required for the upregulation of IL-10 and are speculated to be the cellular source of the upregulated IL-10. The link between neuronal TRPV1 activation in the CNS and the effector myeloid cells remains unknown. Potential mechanistic mediators include neuromodulators released by TRPV1 neurons, or bone marrow innervation. Right panel: In addition to the neuro-immune upregulation of IL-10, OLDA acts directly upon monocytes/macrophages and/or non-conventional immune cells, such as endothelial cells and glial cells, to reduce their production of pro-inflammatory cytokines and chemokines. Therefore, the endovanilloid system has a multi-pronged ability to limit the amplification of acute inflammation and promote its resolution

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