Card9 protects zymosan-induced peritonitis through regulating autophagy in macrophage
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ABSTRACT:
PROVIDER: PRJNA691233 | ENA |
REPOSITORIES: ENA
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Project description:CARD9 is an adapter protein, which plays a critical role in anti-fungal immunity. However, the role of CARD9 in fungal-induced autophagy remains unknown. In this study, we demonstrated that Card9-/- mice displayed more severe phenotype of zymosan-induced peritonitis, presenting as multiple organs injury and increased systemic inflammation. Moreover, the number of macrophage in spleen was increased in Card9-/- mice. Further studies revealed that autophagy was impaired in peritoneal macrophages of Card9-/- -peritonitis mice. Notably, the autophagy agonist, rapamycin, ameliorated peritonitis in Card9-/- mice. Moreover, Card9 mediates the interaction of Malt1 and P62 upon zymosan stimulation. Together, our results confirmed the protective role of Card9 in the development of peritonitis via regulates autophagy in macrophage cells. The study indicates Card9 may be a potential therapeutic target for peritonitis.
2024-01-01 | GSE164572 | GEO
Project description:Nanostring analysis of macrophage subsets following zymosan-induced peritonitis
| PRJNA693010 | ENA
Project description:Total RNA was extracted from monocyte and macrophages isolated from the peritoneal cavity of un-inflamed mice or 4, 24, 48 an 72h after mice had been injected with 0.1 or 10mg zymosan
2011-07-30 | E-MEXP-3189 | biostudies-arrayexpress
Project description:Resident macrophages from naïve mice or resident/inflammatory macrophages from mice treated with zymosan(10ug) 3 days prior were purified from C57BL/6 CD45.2+ donor mice. Purified populations were transferred into mirroring CD45.1/2+ recipient mice or clodronate pre-treated recipient mice. Donor populations were purified 8 weeks following transfer for Nanostring analysis.
2021-01-28 | GSE165036 | GEO
Project description:Macrophage-mediated innate immune responses contribute to the initiation, progression and complications of atherosclerosis. However, the underlying pathways linking activation of macrophages to atherosclerotic plaque develoment are still poorly understood. We hypothesized that activation of caspase recruitment-domain containing protein 9 (CARD9) plays a determinant role in pro-atherogenic responses in macrophages. Transcriptomic analysis of human monocytes isolated from CARD9-deficient patients confirmed the pathogenic signature identified in several murine models: increased production of pro-inflammatory cytokines, improved lipid uptake, higher cell death susceptibility and defective autophagy.
2023-04-01 | GSE221782 | GEO
Project description:Impact of mPGES-1 on the resolution of zymosan-induced peritonitis in mice
| PRJNA690115 | ENA
Project description:Despite the progress to understand inflammatory reactions, mechanisms causing their resolution remain poorly understood. Prostanoids, especially prostaglandin E2 (PGE2), are well characterized mediators of inflammation. PGE2 is produced in an inducible manner in macrophages (Mf) by microsomal PGE2-synthase-1 (mPGES-1), with the notion that it also conveys pro-resolving properties. We aimed to characterize the role of mPGES-1 during resolution of acute, zymosan-induced peritonitis. Experimentally, we applied the mPGES-1 inhibitor compound III (CIII) once the inflammatory response was established and confirmed its potent PGE2-blocking efficacy. mPGES-1 inhibition resulted in an incomplete removal of neutrophils and a concomitant increase in monocytes and Mf during the resolution process. mRNA-seq analysis identified enhanced C-X3-C motif receptor 1 (CX3CR1) expression in resident and infiltrating Mf upon mPGES-1 inhibition. Besides elevated Cx3cr1 expression, its ligand CX3CL1 was enriched in the peritoneal lavage of the mice, produced by epithelial cells upon mPGES-1 inhibition. CX3CL1 not only increased adhesion and survival of Mf, but its neutralization also completely reversed elevated inflammatory cell numbers, thereby normalizing the cellular, peritoneal composition during resolution. Our data suggest that mPGES-1-derived PGE2 contributes to resolution of inflammation by preventing CX3CL1-mediated retention of activated myeloid cells at sites of injury.
2021-02-10 | GSE164364 | GEO
Project description:Bone marrow derived macrophages from wt and card9 KO mice were stimulated with CpG, Curdlan or TDB, an analogon to the mycobacterial cord factor TDM for 48h, respectively. Keywords: card9 knockout, macropphage, TDB wt or card9 KO macrophages stimulated for 48h
2009-01-31 | E-GEOD-10530 | biostudies-arrayexpress
Project description:With murine zymosan peritonitis, repetitive dosing of a SPM panel (RvD1, RvD2, RvD5, MaR1 and RvE2 at 1 ng/mouse, i.p.) was given to mice, followed by zymosan challenge to initiate peritonitis. Leukocyte composition and resolution indices were calculated. RNA-sequencing was carried out
2024-10-09 | GSE270972 | GEO
Project description:It is crucial to decipher the host-microbiota interactions as they are involved in intestinal homeostasis and diseases. Caspase Recruitment Domain 9 (Card9) is an inflammatory bowel disease (IBD) susceptibility gene coding for an adapter protein for innate immunity toward many microorganisms. Card9 mediates colitis recovery via interleukin 22 pathway activation and Card9-/- mice have enhanced susceptibility to colitis. To reveal the mechanisms responsible of this defect in Card9-/-mice, we compared colon transcriptomics in WT and Card9-/- mice before and during DSS-induced colitis. Mice transcriptomes clusterized according to the genotype supporting a pattern clearly different in WT and Card9-/- mice. The number of up-regulated genes at day 7 was largely higher in Card9-/- compared to WT mice. Pathway analyses of the induced transcripts showed a dominance of immune-related pathway with a stronger signal in Card9-/- mice. Interestingly, NOD-like receptor signaling pathway, in which CARD9 is involved, was an exception with weaker activation in Card9-/- than in WT mice. During the recovery period at day 12, pathways involved in cell proliferation and replication were significantly activated in WT compared to Card9-/- mice confirming the healing defect in Card9-/- mice. For the induction of colitis, mice were given drinking water supplemented with 2% (w/v) Dextran sulphate sodium (DSS) for 7 days, then allowed to recover by drinking water alone for 5 additional days. 3 mice of each groups (WT and Card9-/-) were sacrified before DSS administration. 5 WT mice and 4 Card9-/- mice were sacrified 7 days after DSS administration and 5 mice of each group were sacrified at day 12.
2016-04-05 | E-GEOD-67577 | biostudies-arrayexpress