| Literature DB >> 33668084 |
Anne-Kathrin Knuth1, Arnaud Huard2, Zumer Naeem3, Peter Rappl2, Rebekka Bauer2, Ana Carolina Mota2, Tobias Schmid2, Ingrid Fleming3, Bernhard Brüne2, Simone Fulda1, Andreas Weigert2.
Abstract
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 in order to allow efficient clearance and resolution of inflammation.Entities:
Keywords: RNA sequencing; Zymosan-induced peritonitis; apoptosis; peritoneal macrophages; proliferation
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Year: 2021 PMID: 33668084 PMCID: PMC7956251 DOI: 10.3390/ijms22052230
Source DB: PubMed Journal: Int J Mol Sci ISSN: 1422-0067 Impact factor: 5.923