Apoptotic cells induce proliferation of peritoneal macrophages
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ABSTRACT:
PROVIDER: PRJNA691612 | ENA |
REPOSITORIES: ENA
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Project description:The interaction of macrophages with apoptotic cells is required for efficient resolution of inflammation. While apoptotic cell removal prevents inflammation due to secondary necrosis, it also alters the macrophage phenotype to hinder further inflammatory reactions. The interaction between apoptotic cells and macrophages is often studied by chemical or biological induction of apoptosis, which may introduce artifacts by affecting the macrophages as well and/or triggering unrelated signaling pathways. Here, we set up a pure cell death system in which NIH 3T3 cells expressing dimerizable Caspase-8 were co-cultured with peritoneal macrophages in a transwell system. Phenotype changes in macrophages induced by apoptotic cells were evaluated by RNA sequencing, which revealed an unexpectedly dominant impact on macrophage proliferation. This was confirmed in functional assays with primary peritoneal macrophages and IC-21 macrophages. Moreover, inhibition of apoptosis during Zymosan-induced peritonitis in mice decreased mRNA levels of cell cycle mediators in peritoneal macrophages. Proliferation of macrophages in response to apoptotic cells may be important to increase macrophage numbers to allow efficient clearance and resolution of inflammation.
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Project description:Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the production of autoantibodies, immune complex deposition, and tissue damage. Several studies have demonstrated the contribution of innate immune cells, including macrophages, in promoting SLE. Macrophages, one of the most abundant cell populations in the peritoneal cavity, are considered multifunctional and phenotypically diverse. Moreover, they can change their phenotype and function in response to environmental signals. However, macrophages' tissue-specific properties in the peritoneal cavity in steady-state and during the progression of SLE remain poorly defined. Using the BWF1 murine model of SLE, we analyzed the phenotype and function of peritoneal macrophages during the disease’s onset. We found a higher frequency of peritoneal macrophages in diseased mice than age-matched controls. Additionally, macrophages from diseased animals expressed lower levels of CD206, MHC-II, and Sirpa. RNAseq analysis identified 286 differentially expressed genes in peritoneal macrophages from diseased-BWF1 mice compared to control mice. Functional experiments demonstrate that peritoneal macrophages from diseased-BWF1 mice secrete higher levels of cytokines when activated with R848 or CpG compared to control cells. Additionally, we observed that peritoneal macrophages from both diseased and control mice could inhibit the activation and proliferation of peritoneal LPS-activated B cells. Advancing awareness of the role and phenotype of peritoneal macrophages in SLE may contribute to a better understanding of these types of diseases and the development of novel therapies.
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Project description:Purpose: Characterize the gene expression profile of of peritoneal mouse macrophages in Endotoxic shock and Tolerance through RNA sequencing Methods: RNA sequencing of RNA from peritoneal macrophages in Endotoxic shock and Tolerance isolated by peritoneal lavage and FACS sorting (F4/80+ CD11b+) Results: Endotoxic shock and Tolerance peritoneal mouse macrophages display differential gene expression. Conclusions: Endotoxic shock and Tolerance peritoneal mouse macrophages display differential gene expression.
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