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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE199645 | GEO | 2022/04/01

REPOSITORIES: GEO

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

| PRJNA821057 | ENA

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

Influence of development and dietary phospholipid content and composition on intestinal transcriptome of Atlantic salmon (Salmo salar)

Project description:The inclusion of intact phospholipids in the diet is essential during larval development and can improve culture performance of many fish species. The effects of supplementation of dietary phospholipid from marine (krill) or plant (soy lecithin) sources were investigated in Atlantic salmon, Salmo salar. First feeding fry were fed diets containing either krill oil supplying phospholipid at 2.6% of diet (named K2.6) or soybean lecithin supplying phospholipid at 2.6 % (S2.6), 3.6 % (S3.6) of diet. A control diet (B) without supplemented phospholipid was also supplied. Fish were sampled at ~ 2.5 g (~1990 ˚ day post fertilization, dpf) and ~10 g (2850 ˚dpf). By comparison of the intestinal transcriptome in specifically chosen contrasts, it was determined that by 2850˚dpf fish possessed a profile that resembled that of mature and differentiated intestinal cell types with a number of changes specific to glycerophospholipid metabolism. It was shown that intact phospholipids and particularly phosphatidylcholine are essential during larval development and that this requirement is associated with the inability of enterocytes in young fry to endogenously synthesize sufficient phospholipid for the efficient export of dietary lipid. In the immature phase (~1990 ˚dpf), the dietary phospholipid content as well as its class composition impacted on several biochemical and morphological parameters including growth, but these differences were not associated with differences in intestinal transcriptomes. The results of this study have made an important contribution to our understanding of the mechanisms associated with lipid transport and phospholipid biosynthesis in early life stages of fish.

2015-08-20 | E-MTAB-3673 | biostudies-arrayexpress

Vγ6+ γδ T cells play a critical role in protection against infection by Escherichia coli

Project description:γδ T cells producing interleukin 17A (IL-17A), which are mainly Vγ4 and Vγ6 subsets, are involved in protection against infection by extracellular bacteria. Using a new Vγ6-specific monoclonal antibody (mAb) (1C10-1F7) which we recently developed, we found that IL-17A+ Vγ6+ γδ T cells increased predominantly in the peritoneal cavity compared with IL-17A+ Vγ4+ γδ T cells during intraperitoneal Escherichia coli infection. The number of IL-17A+ Vγ6+ γδ T cells, which rapidly became CD69+ from CD69-, peaked at 12 h after infection. In vivo treatment with 1C10-1F7 mAb significantly inhibited the accumulation of neutrophils and hampered the resolution of E. coli infection. These results suggest that rapid activation of IL-17A+ Vγ6+ γδ T cells contributed to host defence against E. coli infection.

2020-02-28 | GSE144617 | GEO

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

2016-11-27 | GSE2436 | GEO

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. 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).

2011-04-22 | E-GEOD-28726 | biostudies-arrayexpress

CD1d-dependent immune suppression mediated by regulatory B cells through modulations of iNKT cells

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

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

RNA-seq of skin tissues from WT and Cd1d KO B6 mice

Project description:To investigate the effect of iNKT deficiency in the skin, the analysis of global gene expression in the skin tissues from WT and Cd1d KO mice were performed using RNA-seq data obtained from these samples.

2022-11-06 | GSE205602 | GEO

A metabolic function for phospholipid and histone methylation

Project description:S-adenosylmethionine (SAM) is the methyl donor for biological methylation modifications that regulate protein and nucleic acid functions. Here we show that methylation of a phospholipid, phosphatidylethanolamine (PE), is the major consumer of SAM in budding yeast. The induction of phospholipid biosynthetic genes is accompanied by induction of the enzyme that hydrolyzes S-adenosylhomocysteine (SAH), a product and inhibitor of methyltransferases. Beyond its function for the synthesis of phosphatidylcholine (PC), the methylation of PE facilitates the turnover of SAM for the synthesis of cysteine and glutathione. Strikingly, cells that lack PE methylation accumulate SAM, which leads to hypermethylation of histones and the major phosphatase PP2A, dependency on cysteine, and sensitivity to oxidative stress. Without PE methylation, particular sites on histones then become methyl sinks to enable the turnover of SAM. These findings reveal an unforeseen metabolic function for phospholipid and histone methylation intrinsic to the life of a cell.

2017-03-30 | GSE84059 | GEO

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