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The enteric glia—looking at the gut healing from a different prospective
Progatzky F, Shapiro M, Chng SH, et al. Regulation of intestinal immunity and tissue repair by enteric glia. Nature 2021; 5997883:125–130. doi: 10.1038/s41586-021-04006-z.
The role of other cell types in intestinal tissue repair and homeostasis is well known, but the one for enteric glia cells (EGCs) is yet to be uncovered. In this paper, Progatzky et al demonstrate the pathway involving EGC in tissue repair after infection.
Seven days after infecting with helminthic larvae, the duodenal tunica muscularis (TM) of mice expressing red tomato (tdT) fluorescence for EGC, proliferation and reactive gliosis of EGC was demonstrated. RNA sequencing was employed in tdT+ and tdT− cells in infected and naive mice demonstrating increased expression of interferon (IFNγ) genes in tdT+ cells. Using single-cell RNA sequencing for EGCs, Progatzky et al identified two clusters of EGC: with high levels of EGC type 2 in infected mice expressing glial fibrillar acidic protein (associated with mitosis) and IFNγ genes. Similar cell clusters and gene expressions were identified on transcriptomic analysis of healthy and ulcerative colitis human colons. When cultured in IFNγ, EGCs expressed genes encoding the IFNγ receptor and if ablated, infected mice showed reduction of the TM EGCs proliferation, increased granulomas formation, abnormal gut peristalsis and serositis. Even in naive mice, the ablation of IFNγ signalling in EGCs induced proinflammatory responses in TM cell (including immune cells). The authors demonstrated the role of chemokine ligand 10 (CXCL10) in IFNγ–EGCs axis in TM, by ablating this in infected mice and showing same effect as in IFNγ receptor ablated mice.
These findings illustrate the pivotal role of EGCs and IFNγ in repair and homeostasis of the gut, suggesting IFNγ signalling pathway to be a potential therapeutic target in inflammatory bowel conditions.
Steatotic liver disease selects for specific non-carcinogenic mutations
Ng S, Rouhani F, Brunner S, et al. Article: Convergent somatic mutations in …
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Not commissioned; internally peer reviewed.
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