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Expression data of kidneys from Wild-type (WT) or Mincle-deficient (KO) mouse subjected to renal ischemia-reperfusion injury.

ABSTRACT: Mincle (Macrophage inducible C-type lectin) is a pattern recognition receptor expressed in innate immune cells and can sense cell death, suggesting a role in sterile inflammation. We induced renal ischemia–reperfusion injury to KO and WT mice and collected the kidneys to compare the gene expression. Microarray analysis revealed that the overlap between the genes upregulated in injured kidney vs. sham kidney in WT mice and the genes downregulated in injured kidney in KO mice vs. WT mice included inflammation-related pathways on day 3.

ORGANISM(S): Mus musculus

PROVIDER: GSE153321 | GEO | 2020/07/15

REPOSITORIES: GEO

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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

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

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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

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

Project description: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.

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Combined phosphoproteome and transcriptome analysis of the macrophage response to mycobacterial cord factor reveals a dichotomy of MINCLE-dependent and -independent signaling

Project description:Immune sensing of Mycobacterium tuberculosis relies on recognition by macrophages. Mycobacterial cord factor, trehalose-6,6’-dimycolate (TDM), is the most abundant cell wall glycolipid and binds to the C-type lectin receptor (CLR) MINCLE. To explore the kinase signaling linking the TDM-MINCLE interaction to gene expression, we employed quantitative phosphoproteome analysis. TDM caused upregulation of 6.7% and suppressed 3.8% of the 14,000 phospho-sites identified on 3727 proteins. MINCLE-dependent phosphorylation was observed for canonical players of CLR signaling (e.g. PLCg, PKCd), and was enriched for PKCd and GSK3 kinase motifs. MINCLE-dependent activation of the PI3K-AKT-GSK3 pathway contributed to inflammatory gene expression and required the PI3K regulatory subunit p85a. Unexpectedly, a substantial fraction of TDM-induced phosphorylation was MINCLE-independent, a finding paralleled by transcriptome data. Bioinformatic analysis of both datasets concurred in the requirement for MINCLE for innate immune response pathways and processes. In contrast, MINCLE-independent phosphorylation and transcriptome responses were linked to cell cycle regulation. Collectively, our global analyses show substantial reprogramming of macrophages by TDM and reveal a dichotomy of MINCLE-dependent and -independent signaling linked to distinct biological responses.

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

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

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

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2023-02-03 | GSE202711 | GEO

Combined phosphoproteome analysis of the response to mycobacterial cord factor reveals a dichotomy of Mincle-dependent and -independent signaling in macrophages

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2019-01-17 | PXD009513 | Pride

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

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