Nanostring analysis of macrophage subsets following zymosan-induced peritonitis
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ABSTRACT:
PROVIDER: PRJNA693010 | ENA |
REPOSITORIES: ENA
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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: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:Card9 protects zymosan-induced peritonitis through regulating autophagy in macrophage
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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:Impact of mPGES-1 on the resolution of zymosan-induced peritonitis in mice
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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: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:Here we demonstrate for the first time evidence of lineage switch from B-1 B lymphocyte to a macrophage , or so-called transdifferentiation, occurring in mature cells in vivo. Specifically, using transgenic B6.Mb1-iCre/Rosa26-YFP mice, in which YFP expression is restricted exclusively to B cell lineage, we discovered that a significant portion of tissue-resident macrophages in peritoneum, pleural cavity and intestine in steady state are positive for YFP. B cell origin of YFP+ macrophages was confirmed by next-generation sequencing of genomic DNA locus encoding immunoglobulin heavy chain genes. Eliciting a self-resolving zymosan peritonitis showed that during inflammation a subset of B-1 B cells gives rise to inflammation-induced macrophages. The aim of this study was to perform transcriptome analysis of B-1 B cell-derived macrophages (B-1/macrophages) from the naM-ove and inflamed murine peritoneum and compare them to already established populations of naM-ove tissue-resident macrophages, inflammation-experienced resident (yolk-sac-derived) macrophages and inflammation-induced (monocyte-derived) macrophages.
2018-09-01 | E-MTAB-1878 | biostudies-arrayexpress
Project description:TLRs are considered important for innate immune responses that combat bacterial infections. Here, the role of TLRs in severe septic peritonitis using the colon ascendens stent peritonitis (CASP) model was examined. We demonstrate that mice deficient for MyD88 and TRIF had markedly reduced bacterial numbers both in peritoneal cavity and peripheral blood, indicating that bacterial clearance in this model is inhibited by TLR signals. Moreover, survival of Myd88-/-;TrifLps2/Lps2 mice was significantly improved. The lack of TLR signals prevented the excessive induction of inflammatory cytokines and of IL 10. Notably, the expression of IFN-gamma, which has an essential protective role in septic peritonitis, and of IFN-regulated genes including several p47 and p65 GTPases as well as IP 10 was independent of TLR signaling. These results provide evidence that, in severe septic peritonitis, TLR deficiency balances the innate immune response in a favorable manner by attenuating deleterious responses such as excessive cytokine release, while leaving intact protective IFN-gamma production. In this dataset, expression data of genes induced by septic peritonitis in spleens from TLR-deficient and wildtype mice are included. 3 groups (septic TLR-deficient mice, septic wildtype mice, and untreated wildtype mice) with 4 replicates each.
2011-06-27 | E-GEOD-24327 | biostudies-arrayexpress
Project description:TLRs are considered important for innate immune responses that combat bacterial infections. Here, the role of TLRs in severe septic peritonitis using the colon ascendens stent peritonitis (CASP) model was examined. We demonstrate that mice deficient for MyD88 and TRIF had markedly reduced bacterial numbers both in peritoneal cavity and peripheral blood, indicating that bacterial clearance in this model is inhibited by TLR signals. Moreover, survival of Myd88-/-;TrifLps2/Lps2 mice was significantly improved. The lack of TLR signals prevented the excessive induction of inflammatory cytokines and of IL 10. Notably, the expression of IFN-gamma, which has an essential protective role in septic peritonitis, and of IFN-regulated genes including several p47 and p65 GTPases as well as IP 10 was independent of TLR signaling. These results provide evidence that, in severe septic peritonitis, TLR deficiency balances the innate immune response in a favorable manner by attenuating deleterious responses such as excessive cytokine release, while leaving intact protective IFN-gamma production.
2011-06-28 | GSE24327 | GEO