CD11c+ myeloid cell exosomes regulate intestinal inflammation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA788743 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17226630_1.fastq.gz | Fastqsanger.gz | |||
| SRR17226630_2.fastq.gz | Fastqsanger.gz | |||
| SRR17226631_1.fastq.gz | Fastqsanger.gz | |||
| SRR17226631_2.fastq.gz | Fastqsanger.gz | |||
| SRR17226632_1.fastq.gz | Fastqsanger.gz |
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Project description:Intercellular communication is critical for maintaining homeostasis in mammalian organ systems, including the gastrointestinal (GI) tract. Exosomes are small nanoscale lipid extracellular vesicles that mediate communication between a wide variety of cell types. Notably, the roles played by immune cell exosomes in regulating homeostasis and inflammation in the GI tract are largely uncharacterized. By generating novel mouse strains deficient in cell-specific exosome production, we demonstrate that specific disruption of exosome signaling via the deletion of Rab27a in myeloid cells exacerbates colitis, which is reversed through administration of dendritic cell (DC)-derived exosomes. Profiling small, non-coding RNAs within exosomes from colonic tissues revealed a distinct subset of microRNAs (miRNAs) carried by both colon- and DC-derived exosomes. Among the DC-enriched exosomal miRNAs, miR-146a was transferred from gut immune cells to myeloid and T cells through a Rab27-dependent mechanism to regulate macrophage phenotypes during colitis. Upon assessing clinical samples, RAB27A was also expressed at lower levels in a cohort of ulcerative colitis patients. Together, this work reveals an exosome-mediated regulatory mechanism underlying gut inflammation, and paves the way for potential use of exosomes containing miRNA cargo as a novel therapeutic for inflammatory bowel disease.
2022-06-13 | GSE190854 | GEO
Project description:Intercellular communication is critical for homeostasis in mammalian systems, including the gastrointestinal (GI) tract. Exosomes are nanoscale lipid extracellular vesicles that mediate communication between many cell types. Notably, the roles of immune cell exosomes in regulating GI homeostasis and inflammation are largely uncharacterized. By generating mouse strains deficient in cell-specific exosome production, we demonstrate deletion of the small GTPase Rab27A in CD11c+ cells exacerbated murine colitis, which was reversible through administration of DC-derived exosomes. Profiling RNAs within colon exosomes revealed a distinct subset of miRNAs carried by colon- and DC-derived exosomes. Among antiinflammatory exosomal miRNAs, miR-146a was transferred from gut immune cells to myeloid and T cells through a Rab27-dependent mechanism, targeting Traf6, IRAK-1, and NLRP3 in macrophages. Further, we have identified a potentially novel mode of exosome-mediated DC and macrophage crosstalk that is capable of skewing gut macrophages toward an antiinflammatory phenotype. Assessing clinical samples, RAB27A, select miRNAs, and RNA-binding proteins that load exosomal miRNAs were dysregulated in ulcerative colitis patient samples, consistent with our preclinical mouse model findings. Together, our work reveals an exosome-mediated regulatory mechanism underlying gut inflammation and paves the way for potential use of miRNA-containing exosomes as a novel therapeutic for inflammatory bowel disease.
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Project description:Several innate immune cell subsets have recently been identified to maintain gut homeostasis in both human and mice. Among these subsets, CX3CR1high CD11b+ CD11c+ cells contribute to intestinal tolerance through various mechanisms in mice. However, whether tolerogenic innate myeloid cells are present in the human intestine is not clearly defined. In this manuscript, we identified an intestinal myeloid cell subset possessing tolerogenic ability. HLA-DRhigh CD14+ CD163high cells in the human colon were divided into two subsets based on CD160 expression: CD163high CD160high and CD163high CD160low cells. Both cell subsets exhibited high levels of IL-10 production and high phagocytic activities. CD163high CD160high cells suppressed effector CD4+ T cell proliferation by a Foxp3+ Treg cell induction-independent mechanism. We further observed that the number and suppressive activity of these cells were profoundly decreased in patients with ulcerative colitis (UC). In addition, CD163high CD160high cells in the UC patients showed inflammatory phenotype, such as increased expression of IL6, CD80, and CD86, accompanied with decreased IL10RB expression. Our results highlight that a tolerogenic CD163high CD160high cell subset might be implicated in the prevention of UC development. Gene expression analysis of murine CX3CR1high cells (n=10) and murine blood Ly6c+ CD11b+ monocytes (n=6) were performed using Whole Mouse Genome Microarray Kit, 4x44K V2 (G4846A) as dye-swapped experiments.
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Project description:Several innate immune cell subsets have recently been identified to maintain gut homeostasis in both human and mice. Among these subsets, CX3CR1high CD11b+ CD11c+ cells contribute to intestinal tolerance through various mechanisms in mice. However, whether tolerogenic innate myeloid cells are present in the human intestine is not clearly defined. In this manuscript, we identified an intestinal myeloid cell subset possessing tolerogenic ability. HLA-DRhigh CD14+ CD163high cells in the human colon were divided into two subsets based on CD160 expression: CD163high CD160high and CD163high CD160low cells. Both cell subsets exhibited high levels of IL-10 production and high phagocytic activities. CD163high CD160high cells suppressed effector CD4+ T cell proliferation by a Foxp3+ Treg cell induction-independent mechanism. We further observed that the number and suppressive activity of these cells were profoundly decreased in patients with ulcerative colitis (UC). In addition, CD163high CD160high cells in the UC patients showed inflammatory phenotype, such as increased expression of IL6, CD80, and CD86, accompanied with decreased IL10RB expression. Our results highlight that a tolerogenic CD163high CD160high cell subset might be implicated in the prevention of UC development.
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