What question did this study set out to answer?

To determine whether genetic loss or pharmacological activation of the innate immune sensor STING modulates intestinal inflammation severity in an experimental colitis model.

October 3, 2019Scientific ReportsOpen Access

Stimulator of interferon genes (STING) activation exacerbates experimental colitis in mice

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Authors

GMGary R. Martin CBCharlene M. Blomquist KHKimiora Henare

Discussion

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Overview

Experimental study reveals that STING activation worsens intestinal inflammation in mice, suggesting STING inhibition may alleviate acute colitis severity.

Key Points

To determine whether genetic loss or pharmacological activation of the innate immune sensor STING modulates intestinal inflammation severity in an experimental colitis model.
Administered dextran sodium sulphate (DSS) to induce acute colitis in STING-mutant (Tmem173 gt) mice and in wild-type mice co-treated with DSS and a STING agonist.
Assessed STING expression and immune responses in colonic tissue, murine bone marrow-derived macrophages (BMDMs), and human THP-1 monocytes under M1 and M2 polarization conditions.
DSS-induced colitis severity was markedly reduced in STING-deficient Tmem173 gt mice, whereas wild-type mice receiving the STING agonist exhibited greatly exacerbated disease.
STING expression was selectively elevated in pro-inflammatory M1-polarized murine and human macrophages, and STING agonist exposure actively repolarized anti-inflammatory M2 macrophages toward an M1-like phenotype.

Cite This Study

Martin et al. (2019) studied this question.

synapsesocial.com/papers/6a6f6447f44fa9f079dcd2ac https://doi.org/10.1038/s41598-019-50656-5

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October 3, 2019Scientific ReportsOpen Access

Stimulator of interferon genes (STING) activation exacerbates experimental colitis in mice

View Full Paper

Ask AI

Bookmark

Authors

GMGary R. Martin CBCharlene M. Blomquist KHKimiora Henare

Discussion

Member takes

Overview

Experimental study reveals that STING activation worsens intestinal inflammation in mice, suggesting STING inhibition may alleviate acute colitis severity.

Key Points

To determine whether genetic loss or pharmacological activation of the innate immune sensor STING modulates intestinal inflammation severity in an experimental colitis model.
Administered dextran sodium sulphate (DSS) to induce acute colitis in STING-mutant (Tmem173 gt) mice and in wild-type mice co-treated with DSS and a STING agonist.
Assessed STING expression and immune responses in colonic tissue, murine bone marrow-derived macrophages (BMDMs), and human THP-1 monocytes under M1 and M2 polarization conditions.
DSS-induced colitis severity was markedly reduced in STING-deficient Tmem173 gt mice, whereas wild-type mice receiving the STING agonist exhibited greatly exacerbated disease.
STING expression was selectively elevated in pro-inflammatory M1-polarized murine and human macrophages, and STING agonist exposure actively repolarized anti-inflammatory M2 macrophages toward an M1-like phenotype.

Cite This Study

Martin et al. (2019) studied this question.

synapsesocial.com/papers/6a6f6447f44fa9f079dcd2ac https://doi.org/10.1038/s41598-019-50656-5

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