Journal article

Enteric Glia Modulate Macrophage Phenotype and Visceral Sensitivity following Inflammation

Vladimir Grubisic, Jonathon L McClain, David E Fried, Iveta Grants, Pradeep Rajasekhar, Eva Csizmadia, Olujimi A Ajijola, Ralph E Watson, Daniel P Poole, Simon C Robson, Fievos L Christofi, Brian D Gulbransen

CELL REPORTS | CELL PRESS | Published : 2020

Abstract

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 visc..

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University of Melbourne Researchers

Grants

Awarded by Crohn's and Colitis Foundation Research Fellowship Award


Awarded by National Institutes of Health (NIH)


Awarded by Crohn's and Colitis Foundation Senior Research Award


Awarded by NIH


Awarded by Helmsley Charitable Trust


Funding Acknowledgements

This work was supported by a Crohn's and Colitis Foundation Research Fellowship Award (577598) to V.G., National Institutes of Health (NIH) R01DK103723, R01DK120862, and Crohn's and Colitis Foundation Senior Research Award (327058) to B.D.G., NIH R01DK113943 to F.L.C., a grant from Helmsley Charitable Trust (281574.5069091.0010), and salary support from R01 DK108894 to S.C.R. We acknowledge the University of California Los Angeles Translational Pathology Core laboratory for preparation of paraffin-embedded sections for immunohistochemical studies.