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Phospholipid Metabolites of the Gut Microbiota Promote Hypoxia-induced Intestinal Injury via CD1d-dependent gd T Cells

ABSTRACT: Phospholipid Metabolites of the Gut Microbiota Promote Hypoxia-induced Intestinal Injury via CD1d-dependent gd T Cells

PROVIDER: PRJNA821057 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18516200_1.fastq.gz	Fastqsanger.gz
	SRR18516200_2.fastq.gz	Fastqsanger.gz
	SRR18516201_1.fastq.gz	Fastqsanger.gz
	SRR18516201_2.fastq.gz	Fastqsanger.gz
	SRR18516202_1.fastq.gz	Fastqsanger.gz

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Phospholipid Metabolites of the Gut Microbiota Promote Hypoxia-induced Intestinal Injury via CD1d-dependent gd T Cells

Project description:Phospholipid metabolites PE and PC are presented by intestinal epithelial CD1d to induce the proliferation of IL-17A-producing γδ T cells, which aggravates intestinal injury.

2022-04-01 | GSE199645 | GEO

Phospholipid metabolites of the gut microbiota promote hypoxia-induced intestinal injury via CD1d-dependent γδ T cells.

Project description:Gastrointestinal dysfunction is a common symptom of acute mountain sickness (AMS). The gut microbiota and γδ T cells play critical roles in intestinal disease. However, the mechanistic link between the microbiota and γδ T cells in hypoxia-induced intestinal injury remains unclear. Here, we show that hypoxia-induced intestinal damage was significantly alleviated after microbiota depletion with antibiotics. Hypoxia modulated gut microbiota composition by promoting antimicrobial peptides angiogenin-4 secretions. The abundance of Clostridium in the gut of mice after hypoxia significantly decreased, while the abundance of Desulfovibrio significantly increased. Furthermore, Desulfovibrio-derived phosphatidylethanolamine and phosphatidylcholine promoted γδ T cell activation. In CD1d-deficient mice, the levels of intraepithelial IL-17A and γδ T cells and intestinal damage were significantly decreased compared with those in wild-type mice under hypoxia. Mechanistically, phospholipid metabolites from Desulfovibrio are presented by intestinal epithelial CD1d to induce the proliferation of IL-17A-producing γδ T cells, which aggravates intestinal injury. Gut microbiota-derived metabolites promote hypoxia-induced intestinal injury via CD1d-dependent γδ T cells, suggesting that phospholipid metabolites and γδ T cells can be targets for AMS therapy.

| S-EPMC9336479 | biostudies-literature

SortaseA cleavable CD1d and H2Kb

Project description:Identification of SortaseA cleavable MHC class I proteins (CD1d, H2Kb) for shotgun lipidomics

2022-07-08 | PXD034366 | Pride

PBS vs. LPS stimulation of gd T cells

Project description:gd T cells recognize unprocessed or non-peptide antigens, respond rapidly to infection, and localize to mucosal surfaces. We have hypothesized that the innate functions of gd T cells may be more similar to those of cells of the myeloid lineage than to other T cells. To begin to test this assumption, we have analyzed the direct response of cultured human and peripheral blood bovine gd T cells to pathogen associated molecular patterns (PAMPs) in the absence of APCs using microarray, real time RT-PCR, proteome array, and chemotaxis assays. Our results indicate that purified gd T cells respond directly to PAMPs by increasing expression of chemokine and activation related genes. The response was distinct from that to known gd T cell antigens and different from the response of myeloid cells to PAMPs. In addition, we have analyzed the expression of a variety of PAMP receptors in gd T cells. Freshly purified bovine gd T cells responded more robustly to PAMPs than did cultured human cells and expressed measurable mRNA encoding a variety of PAMP receptors. Our results suggest that rapid response to PAMPs through the expression of PAMP receptors may be another innate role of gd T cells. Keywords: parallel sample

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CD1d orchestrates skin cell survival and inflammation in response to UV linking the etiology of sunburn to skin cancer

Project description:Solar UV represents a ubiquitous environmental physical insult. Thus, to maintain its integrity as an effective barrier, skin must be unusually resistant to cell death. However, UV overexposure causes sunburn1,2 (necrosis and inflammation) and cells that survive harbour damaged DNA, which if not repaired or removed by apoptosis can lead to skin cancer development3-10. CD1d, a transmembrane protein identified in glycolipid antigen presentation11,12 to invariant natural killer T (NKT) cells13,14 is expressed by epithelial cells of most tissues including skin15-17, and shares close homology between humans and mice12. Since CD1d and NKT cells are implicated in regulating UV skin carcinogenesis4,18, we studied susceptibility to UV-induced sunburn in mice either lacking expression of both CD1d and NKT cells or expressing CD1d without NKT cells. Here we show that CD1d, but not NKT cells is necessary for UV to cause sunburn. CD1d causes cells to resist apoptosis in response to UV overexposure as the means to promote cell survival and directs the expression of inflammatory response genes, resulting in tissue destruction and skin inflammation. This previously unknown action of CD1d links the etiology of sunburn to skin cancer. Keywords = CD1d knockout, UV, sunburn, cancer Keywords: other

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Project description:Microarray analysis was performed to determine the transcriptional profiles of NKT, CD1d-aGC+ Va24-, and CD4 T cells. Clones of NKT, CD1d-aGC+ Va24-, and CD4 T cells were generated using peripheral blood drawn from two healthy individuals. RNA was extracted from cells that had been either rested (18 days post-stimulation) or stimulated (3 days post-stimulation).

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Project description:Regulatory B cells (Breg) express high levels of CD1d that presents lipid antigens to invariant natural killer T (iNKT) cells. The function of CD1d in Breg biology and iNKT cell activity during inflammation remains unclear. Here we show, using chimeric mice, cell depletion and adoptive cell transfer, that CD1d-lipid presentation by Bregs induces iNKT cells to secret IFN-γ to contribute, partially, to the down-regulation of T helper (Th)1 and Th17 adaptive immune responses for ameliorating experimental arthritis. Mice lacking CD1d-expressing B cells develop exacerbated diseases compared to wild-type mice, and fail to respond to α-galactosylceramide treatment. Absence of lipid presentation by B cells causes altered activation of iNKT cells, with disruption of regulatory pathways including those involved in metabolism and cytokine responses. Thus, we identify an IL-10-independent mechanism by which Bregs restrain excessive inflammation via lipid presentation.

2018-01-25 | E-MTAB-6381 | biostudies-arrayexpress

Differential Gene Expression Profiles in Broiler Chickens with Gangrenous Dermatitis (GD)

Project description:This study utilized comparative global gene expression microarray analysis of GD-affected and clinically healthy chickens from a recent GD outbreak to glean insights into the molecular and cellular changes associated with this disease process. Two-condition experiment, GD-affected vs. Healthy chickens. Biological replicates: 2 control replicates, 2 GD-infected replicates with dye-switching.

2010-10-27 | E-GEOD-24939 | biostudies-arrayexpress

NKT, CD1d-aGC+ Va24-, and CD4 T cell clones from human peripheral blood

Project description:Microarray analysis was performed to determine the transcriptional profiles of NKT, CD1d-aGC+ Va24-, and CD4 T cells.

2011-04-22 | GSE28726 | GEO

Angiogenesis study of Gd@C82(OH)22 nanoparticle

Project description:we report a novel nanomedicine (Gd@C82(OH)22 ) effectively inhibit human breast tumor growth by antiangiogenesis in vivo. To further identify which angiogenic factor(s) were affected on mRNA level, the "RT² Profiler™ PCR Array Mouse Angiogenesis (APMM-024, SuperArray Bioscience Corporation)" was used. Keywords: nanomedicine, Gd@C82(OH)22, angiogenesis, MCF-7, breast cancer

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