Microarray analysis of CD14+ CD163high CD160high cells in human intestinal lamina propria and CX3CR1high CD11b+ CD11c+ cells in murine intestinal lamina propria
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ABSTRACT:
ORGANISM(S): Mus musculus Homo sapiens
PROVIDER: GSE79629 | GEO | 2016/07/17
SECONDARY ACCESSION(S): PRJNA316473
REPOSITORIES: GEO
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2016-07-17 | E-GEOD-79629 | biostudies-arrayexpress
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.
2016-07-17 | GSE79628 | GEO
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.
2016-07-17 | E-GEOD-79628 | biostudies-arrayexpress
Project description:Microarray analysis of CD14+ CD163high CD160high cells in human intestinal lamina propria and CX3CR1high CD11b+ CD11c+ cells in murine intestinal lamina propria
| PRJNA316473 | ENA
Project description:Mouse intestinal innate immune cells have been identified as inducing Th17 cell differentiation. However, few studies have investigated innate immune cells that are involved in CD (Crohn's disiease) pathogenesis in humans. The present study aimed to identify a human intestinal lamina propria cell subset that induces Th17 cells, and to clarify its role in CD pathogenesis. Intestinal mucosa samples were obtained from patients who underwent resection of colorectal cancer or CD. Lamina propria cells (LPCs) were obtained by enzymatic digestion, and were analyzed for expression of HLA-DR, lineage markers (Lin), CD14, and CD163 using flow cytometry. Among HLA-DRhigh Lin- cells, we identified a CD14+ CD163low cell subset that was selectively present in intestinal LPCs. We identified CD14+ CD163low cells as having a potent capacity to induce Th17 cell differentiation in human intestinal lamina propria. The Th17-inducing activity of these cells was enhanced in CD patients.
2013-08-24 | GSE49066 | GEO
Project description:Mouse intestinal innate immune cells have been identified as inducing Th17 cell differentiation. However, few studies have investigated innate immune cells that are involved in CD (Crohn's disiease) pathogenesis in humans. The present study aimed to identify a human intestinal lamina propria cell subset that induces Th17 cells, and to clarify its role in CD pathogenesis. Intestinal mucosa samples were obtained from patients who underwent resection of colorectal cancer or CD. Lamina propria cells (LPCs) were obtained by enzymatic digestion, and were analyzed for expression of HLA-DR, lineage markers (Lin), CD14, and CD163 using flow cytometry. Among HLA-DRhigh Lin- cells, we identified a CD14+ CD163low cell subset that was selectively present in intestinal LPCs. We identified CD14+ CD163low cells as having a potent capacity to induce Th17 cell differentiation in human intestinal lamina propria. The Th17-inducing activity of these cells was enhanced in CD patients. The Cy3-labeled cDNAs were hybridized on Agilent-039494 SurePrint G3 Human GE v2 8x60K Microarray (G4845A) in one color experiments, resulting in four individual microarrays.
2013-08-24 | E-GEOD-49066 | biostudies-arrayexpress
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.
2016-07-17 | GSE79627 | GEO
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 pooled lamina propria cells (LPCs) (n=12) and human blood CD14+ monocytes (n=7) were performed using Whole Human Genome Microarray Kit, 4x44K (G4112F) as one-color experiments.
2016-07-17 | E-GEOD-79627 | biostudies-arrayexpress
Project description:Signal regulatory protein alpha (SIRP?/CD172a) is a conserved transmembrane protein thought to play an inhibitory role in immune function by binding the ubiquitous ligand CD47. SIRP? expression has been used to identify dendritic cell subsets across species and here we examined its expression and function on intestinal DCs in mice. Normal mucosa contains four subsets of DCs based on their expression of CD103 and CD11b and three of these express SIRP?. However, loss of SIRP? signaling in mice leads to a selective reduction in the CD103(+) CD11b(+) subset of DCs in the small intestine, colon, and among migratory DCs in the mesenteric lymph node. In parallel, these mice have reduced numbers of TH 17 cells in steady-state intestinal mucosa, and a defective TH 17 response to Citrobacter infection. Identical results were obtained in CD47KO mice. DC precursors from SIRP? mutant mice had an enhanced ability to generate CD103(+) CD11b(+) DCs in vivo, but CD103(+) CD11b(+) DCs from mutant mice were more prone to die by apoptosis. These data show a previously unappreciated and crucial role for SIRP? in the homeostasis of CD103(+) CD11b(+) DCs in the intestine, as well as providing further evidence that this subset of DCs is critical for the development of mucosal TH 17 responses.
| S-EPMC4284040 | biostudies-literature
Project description:Organic dust exposure in the agricultural industry results in significant lung disease. Macrophage infiltrates are increased in the lungs after organic dust exposures, yet the phenotype and functional importance of these cells remain unclear. Using an established intranasal inhalation murine model of dust-induced lung inflammation, animals were treated once or daily for 3 weeks with swine confinement organic dust extract (DE). Repetitive DE treatment for 3 weeks resulted in significant increases in CD11c(+)/CD11b(+) macrophages in whole lung-associated tissue. These cells displayed increased costimulatory molecule (CD80 and CD86) expression, enhanced phagocytic ability, and an increased production of IL-6, CXCL1, and CXCL2. Similar findings were observed with the CD11c(+)/CD11b(+) macrophage infiltrate after repetitive exposure to peptidoglycan, a major DE component. To determine the functional importance of macrophages in mediating DE-induced airway inflammation, lung macrophages were selectively depleted using a well-established intranasal clodronate liposome depletion/suicide strategy. First, macrophage depletion by clodronate liposomes resulted in significant reductions in airway neutrophil influx and TNF-? and IL-6 production after a single exposure to DE. In contrast, after repetitive 3-week exposure to DE, airway lavage fluid and lung tissue neutrophils were significantly increased in clodronate liposome-treated mice compared with control mice. A histological examination of lung tissue demonstrated striking increases in alveolar and bronchiolar inflammation, as well as in the size and distribution of cellular aggregates in clodronate-liposome versus saline-liposome groups repetitively exposed to DE. These studies demonstrate that DE elicits activated CD11c(+)/CD11b(+) macrophages in the lung, which play a critical role in regulating the outcome of DE-induced airway inflammation.
| S-EPMC3547108 | biostudies-literature