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Publication : Enteric Glia Modulate Macrophage Phenotype and Visceral Sensitivity following Inflammation.

First Author  Grubišić V Year  2020
Journal  Cell Rep Volume  32
Issue  10 Pages  108100
PubMed ID  32905782 Mgi Jnum  J:315958
Mgi Id  MGI:6714731 Doi  10.1016/j.celrep.2020.108100
Citation  Grubisic V, et al. (2020) Enteric Glia Modulate Macrophage Phenotype and Visceral Sensitivity following Inflammation. Cell Rep 32(10):108100
abstractText  Mechanisms resulting in abdominal pain include altered neuro-immune interactions in the gastrointestinal tract, but the signaling processes that link immune activation with visceral hypersensitivity are unresolved. We hypothesized that enteric glia link the neural and immune systems of the gut and that communication between enteric glia and immune cells modulates the development of visceral hypersensitivity. To this end, we manipulated a major mechanism of glial intercellular communication that requires connexin-43 and assessed the effects on acute and chronic inflammation, visceral hypersensitivity, and immune responses. Deleting connexin-43 in glia protected against the development of visceral hypersensitivity following chronic colitis. Mechanistically, the protective effects of glial manipulation were mediated by disrupting the glial-mediated activation of macrophages through the macrophage colony-stimulating factor. Collectively, our data identified enteric glia as a critical link between gastrointestinal neural and immune systems that could be harnessed by therapies to ameliorate abdominal pain.
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