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RNA sequencing of the stomachs of H. pylori-infected WT and Mincle–/– mice after 8 weeks

ABSTRACT: Helicobacter pylori (H. pylori) causes assorted gastrointestinal disorders. H. pylori-specific T cells develop during infection, which is a prerequisite for the induction of gastritis and malignancy. How the innate immune system senses H. pylori to prime T cells remains unclear. We report that cholesteryl glucosides in H. pylori activate innate immunity through C-type lectin receptors (CLRs). Cholesteryl acyl α-glucoside (αCAG) was identified as a ligand for Mincle (Clec4e). Upon H. pylori infection, T cell responses and gastritis were ameliorated in Mincle-deficient mice, although bacterial numbers were comparable.Thus the cholesteryl lipid–CLR axis exacerbates H. pylori-induced gastric inflammation with limited contribution to protective immunity.

ORGANISM(S): Mus musculus

PROVIDER: GSE136203 | GEO | 2020/09/19

REPOSITORIES: GEO

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The role of Clec4e (Mincle) in microglia response to transient ischemic injury

Project description:This data set shows dramatic changes in gene expression in microglia isolated from C57Bl6/J mice subjected to transient middle cerebral artery occlusion, as compared to those subjected to sham surgery. Mice deficient in Mincle (Clec4e-/-) showed significantly improved injury outcomes 3 and 7 days after transient middle cerebral artery occlusion. However, when comparing changes in gene expression in microglia 24 hours after blood reperfusion, there were no differences between wild-type and Clec4e-/- mice, indicating that Mincle does not participate in early microglial activation. Wild type and Mincle knock-out (Clec4e-/-) mice. After 1 h of transient middle cerebral artery occlusion (tMCAO) and 24 h of reperfusion, mice were perfused with PBS, their brains dissected, and 2 ipsilesional hemispheres (with cerebellum and brainstem removed) pooled for microglia isolation. For sham-operated animals, the whole forebrain was used and brains were not pooled. After myelin separation by Percoll gradient centrifugation, around 80,000 CD45intermediate, CD11b+ microglial cells were sorted from each sample. Sham samples n=3, tMCAO samples n=5.

2016-03-24 | E-GEOD-77986 | biostudies-arrayexpress

The role of Clec4e (Mincle) in microglia response to transient ischemic injury

2016-03-24 | GSE77986 | GEO

Expression data from peritoneal macrophages stimulated with trehalose-6,6'-dimycolate (TDM)

Project description:Macrophage-inducible C-type lectin (Mincle, Clec4e) is a pathogen sensor that recognizes pathogenic fungi and Mycobactrium tuberculosis. We perfomed microarray analysis using peritoneal macrophages stimulated with TDM, a mycobacterial cell wall glycolipid that is known to be a Mincle ligand. Many chemokine and cytokine genes were upregulated in wildtype macrophages stimulated with TDM. Upregulation of these genes were completely abolishd in Mincle KO macrophages. Peritoneal macrophages from WT and Mincle KO mice were stimulated with TDM or vehicle for 24 h (3 samples each). Microarray analysis was performed using Affymetrix Mouse 430 2.0.

2013-11-14 | E-GEOD-52338 | biostudies-arrayexpress

Transcriptional and translational analysis of wild-type and Mincle-KO macrophages

Project description:Analysis of total RNAs from wild-type and Mincle-KO macrophages stimulated with TLR2 ligand and co-stimulated with TLR2 ligand and Mincle ligand. And analysis of total and polysomal RNAs from wild-type macrophages co-stimulated with TLR2 ligand and Mincle ligand in the presence or absence of DHS inhibitor (GC7). Mincle is a C-type lectin receptor for trehalose dimycolate, a mycobacterial cell wall component. And results provide insight into the crosstalk between the TLR2 and Mincle signaling pathways by RNA-seq assay and identifying potential targets of Mincle-mediated translational control by polysome profiling assay.

2016-07-10 | GSE70793 | GEO

Role of Mincle overexpression in pneumococcal pneumonia

Project description:Macrophage-inducible C-type lectin (Mincle) dependent sensing of pathogens trig-gers proinflammatory immune responses in professional phagocytes that contribute to protect the host against pathogen invasion. Here, we examined whether overex-pression of Mincle designed to improve early pathogen sensing by professional phagocytes would improve lung protective immunity against Streptococcus pneu-moniae in mice. Proteomic profiling of alveolar macrophages (AM) of Mincle trans-genic (tg) mice stimulated with the Mincle-specific pneumococcal ligand glucosyl-diacylglycerol (Glc-DAG) revealed increased Nlrp3 inflammasome activation and downstream IL-1 cytokine release that was not observed in Glc-DAG stimulated Mincle KO or Nlrp3 KO macrophages. Along this line, Mincle tg mice also responded with a stronger Nlrp3 expression and early proinflammatory cytokine release after challenge with S. pneumoniae, ultimately leading to fatal pneumonia in the Mincle tg mice. Importantly, Nlrp3 inhibitor treatment of Mincle tg mice significantly mitigated the observed hyperinflammatory response to pneumococcal challenge. Together, we show that overexpression of the pattern recognition receptor Mincle triggers in-creased Glc-DAG dependent Nlrp3 inflammasome activation in professional phago-cytes leading to fatal pneumococcal pneumonia in mice, which is amenable to Nlrp3 inhibitor treatment. These data show that ectopic expression of Mincle receptor con-fers increased susceptibility rather than resistance to S. pneumoniae in mice, thus highlighting the importance of an inducible Mincle receptor expression in response to microbial challenge.

2020-10-05 | PXD018752 | Pride

Expression data from peritoneal macrophages stimulated with trehalose-6,6'-dimycolate (TDM)

2013-11-14 | GSE52338 | GEO

Cholesteryl α-D-glucoside 6-acyltransferase enhances the adhesion of Helicobacter pylori to gastric epithelium

Project description:Cellular locations of (Cholesteryl α-D-glucoside 6-acyltransferase) CGAT To study the cellular location of CGAT, based on our pervious experiments, the CGAT activity was observed in the outer membrane vesicles (OMVs), rather than in the culture medium, suggesting that CGAT resided in the outer membrane can be enclosed in the OMVs and secreted to the extracellular space. We then performed proteomic analysis for OMVs. Based on proteomic analysis, we found CGAT was present in the OMVs isolated from the strains of H. pylori 26695 and ΔCGT-knock-out, instead of ΔCGAT-knock-out strain.

2020-03-19 | PXD017518 | Pride

RNA sequencing of the stomachs of H. pylori-infected WT and Mincle–/– mice after 8 weeks

Project description:RNA sequencing of the stomachs of H. pylori-infected WT and Mincle–/– mice after 8 weeks

| PRJNA561590 | ENA

The protective effect of inflammatory monocytes during systemic C. albicans infection is dependent on collaboration between C-type lectin-like receptors

Project description:Invasive candidiasis, mainly caused by Candida albicans, is a serious healthcare problem with high mortality rates, particularly in immunocompromised patients. Innate immune cells express pathogen recognition receptors (PRRs) including C-type lectin-like receptors (CLRs) that bind C. albicans to initiate an immune response. Multiple CLRs including Dectin-1, Dectin-2 and Mincle have been proposed individually to contribute to the immune response to C. albicans. However how these receptors collaborate to clear a fungal infection is unknown. Herein, we used novel multi-CLR knockout (KO) mice to decipher the individual, collaborative and collective roles of Dectin-1, Dectin-2 and Mincle during systemic C. albicans infection. These studies revealed an unappreciated and profound role for CLR co-operation in anti-fungal immunity. The protective effect of multiple CLRs was markedly greater than any single receptor, and was mediated through inflammatory monocytes via recognition and phagocytosis of C. albicans, and production of C. albicans-induced cytokines and chemokines. These CLRs were dispensable for mediating similar responses from neutrophils, likely due to lower expression of these CLRs on neutrophils compared to inflammatory monocytes. Concurrent deletion of Dectin-1 and Dectin-2, or all three CLRs, resulted in dramatically increased susceptibility to systemic C. albicans infection compared to mice lacking a single CLR. Multi-CLR KO mice were unable to control fungal growth due to an inadequate early inflammatory monocyte-mediated response. In response to excessive fungal growth, the multi-CLR KO mice mounted a hyper-inflammatory response, likely leading to multiple organ failure. Thus, these data reveal a critical role for CLR co-operation in the effective control of C. albicans and maintenance of organ function during infection.

2019-06-20 | E-MTAB-8030 | biostudies-arrayexpress

Mincle-mediated signaling leads to characteristic gene expressions in rat mast cells

Project description:Rat mast cell line RBL-2H3 was analyzed to investigate the molecular mechanism of Mincle-mediated activation and responses of mast cells. Mincle-mediated signaling stimulated characteristic gene expression, such as IL-3, IL-4, IL-9, IL-13, IL-31 and TNFα.

2016-04-20 | GSE80416 | GEO

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