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The IL-10/IL-10Ra axis in fibroblasts limits large intestinal pathology by suppressing type I interferon signaling [RNA-Seq]

ABSTRACT: In the intestines, stromal cells are essential for epithelial homeostasis, supplying both stem cell niche signals and differentiation factors. Recent studies have shown that they play crucial roles not only in epithelial maintenance, but also in the immune system. However, the molecular mechanisms that control inflammatory response by stromal cells are poorly understood. We showed that stromal cells from Rag2 knock out (KO) mice highly express inflammatory cytokines and chemokines, and the IL10-IL10R axis is a key suppressor for those inflammatory mediators in fibroblasts. Fibroblast-specific Il10ra KO mice developed spontaneous colitis in aged mice. We performed (sc)RNA-seq on stromal cells from these mice and 16s rDNA-seq on the feces from those mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE306433 | GEO | 2026/05/17

REPOSITORIES: GEO

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The IL-10/IL-10Ra axis in fibroblasts limits large intestinal pathology by suppressing type I interferon signaling

Project description:In the intestines, stromal cells are essential for epithelial homeostasis, supplying both stem cell niche signals and differentiation factors. Recent studies have shown that they play crucial roles not only in epithelial maintenance, but also in the immune system. However, the molecular mechanisms that control inflammatory response by stromal cells are poorly understood. We showed that stromal cells from Rag2 knock out (KO) mice highly express inflammatory cytokines and chemokines, and the IL10-IL10R axis is a key suppressor for those inflammatory mediators in fibroblasts. Fibroblast-specific Il10ra KO mice developed spontaneous colitis in aged mice. We performed (sc)RNA-seq on stromal cells from these mice and 16s rDNA-seq on the feces from those mice.

2026-05-17 | GSE325756 | GEO

The IL-10/IL-10Ra axis in fibroblasts limits large intestinal pathology by suppressing type I interferon signaling [scRNA-Seq]

2026-05-17 | GSE306432 | GEO

The IL-10/IL-10Ra axis in fibroblasts limits large intestinal pathology by suppressing type I interferon signaling [RNA-Seq, part2]

2026-05-17 | GSE306443 | GEO

The IL-10/IL-10Ra axis in fibroblasts limits large intestinal pathology by suppressing type I interferon signaling [scRNA-Seq, part2]

2026-05-17 | GSE306442 | GEO

IL10RA signaling deficiency change the anti-inflammatory signature of Ccr2-independent resident macrophages

Project description:In adult mice the majority of intestinal macrophages exhibit a mature phenotype and are derived from blood monocytes. In the steady state replenishment of these cells is reduced in the absence of the chemokine receptor Ccr2. Within the intestine of mice with colitis there is marked increase in the accumulation of immature macrophages that demonstrate an inflammatory phenotype. However, whether Ccr2 is necessary for the accumulation of these immature macrophages and further for the development of colitis in susceptible mouse models is incompletely defined. Here, we ask whether Ccr2 is necessary for the development of colitis in mice lacking the receptor for IL10. We compared the development of intestinal inflammation in mice lacking IL10RA or both IL10RA and Ccr2. The absence of Ccr2 interfered with the accumulation of immature macrophages in IL10R-deficien mice, including a novel population of rounded submucosal Iba1+ cells and reduced the severity of colitis in these mice. In contrast, the absence of Ccr2 did not reduce augmented inflammatory gene expression observed in mature intestinal macrophages isolated from mice lacking IL10RA. These data suggest that both newly recruited Ccr2-dependent immature macrophages and Ccr2-independent residual mature macrophages contribute to the development of intestinal inflammation observed in IL10R-deficient mice.

2022-01-19 | GSE183960 | GEO

Interleukin-10 signaling complex with IL-10RA and IL-10RB

Project description: Not available

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Autonomous and non-autonomous functions of IL10RA in intestinal macrophages

Project description:To investigate the effects of cell-intrinsic loss of IL10RA on inflammatory macrophage function we performed gene expression profiling analysis using data from sorted lamina propria macrophages from bone marrow chimeric mice.

2022-12-22 | GSE211841 | GEO

Tregs stimulate intestinal repair by integrating epithelial IFNy/IL-10 signaling

Project description:To understand the transcriptional changes on cellular level within the murine intestinal epithelial tissue, we generated small intestinal organoids from wild type mice, co-cultured them with Treg cells +/- rIL10/rIFNg or anti-IFNg/IL10R, dissagregated the samples, sorted into single cells and profiled them by single-cell RNA-seq

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Monocyte-derived IL-10 drives sex differences in pain duration

Project description:Women frequently experience longer-lasting pain than men, indicating delayed pain resolution. While we understand that pain can be orchestrated by the close interplay between the sensory nervous system and the immune system, it remains unclear whether this interaction contributes to the longer duration of pain in women. Here, we demonstrate that interleukin (IL)-10+ monocytes resolve inflammatory pain by signaling to IL-10R1+ sensory neurons in a mouse model of skin inflammation. A higher number of IL-10+ monocytes in males enables faster resolution of inflammatory pain compared to females. In both sexes, pain resolution was impaired by deleting Il10 from monocytes or Il10ra from sensory neurons. Similarly, in humans, men’s pain resolved faster than women’s after traumatic injury, which was associated with higher levels of circulating monocytes and IL-10 in men. In mice, androgen signaling promotes IL-10 production by monocytes, resulting in sex differences in the number of IL-10+ monocytes. Enhancing IL-10+ monocytes in the inflamed skin through Resolvin D1 treatment accelerated pain resolution in both sexes of mice. Our findings uncover a novel role for peripheral IL-10+ monocytes in driving sex differences in pain resolution. These results reveal a previously underappreciated contribution of immune cells to resolving pain and preventing the transition to chronic pain.

2026-01-14 | GSE316149 | GEO

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