DataSheet_1_Bacterial and Fungal Toll-Like Receptor Activation Elicits Type I IFN Responses in Mast Cells.pdf (1.34 MB)
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DataSheet_1_Bacterial and Fungal Toll-Like Receptor Activation Elicits Type I IFN Responses in Mast Cells.pdf

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posted on 12.02.2021, 05:01 authored by Lisa Kornstädt, Sandra Pierre, Andreas Weigert, Stefanie Ebersberger, Tim J. Schäufele, Anja Kolbinger, Tobias Schmid, Jennifer Cohnen, Dominique Thomas, Nerea Ferreirós, Bernhard Brüne, Ingo Ebersberger, Klaus Scholich

Next to their role in IgE-mediated allergic diseases and in promoting inflammation, mast cells also have antiinflammatory functions. They release pro- as well as antiinflammatory mediators, depending on the biological setting. Here we aimed to better understand the role of mast cells during the resolution phase of a local inflammation induced with the Toll-like receptor (TLR)-2 agonist zymosan. Multiple sequential immunohistology combined with a statistical neighborhood analysis showed that mast cells are located in a predominantly antiinflammatory microenvironment during resolution of inflammation and that mast cell-deficiency causes decreased efferocytosis in the resolution phase. Accordingly, FACS analysis showed decreased phagocytosis of zymosan and neutrophils by macrophages in mast cell-deficient mice. mRNA sequencing using zymosan-induced bone marrow-derived mast cells (BMMC) revealed a strong type I interferon (IFN) response, which is known to enhance phagocytosis by macrophages. Both, zymosan and lipopolysaccharides (LPS) induced IFN-β synthesis in BMMCs in similar amounts as in bone marrow derived macrophages. IFN-β was expressed by mast cells in paws from naïve mice and during zymosan-induced inflammation. As described for macrophages the release of type I IFNs from mast cells depended on TLR internalization and endosome acidification. In conclusion, mast cells are able to produce several mediators including IFN-β, which are alone or in combination with each other able to regulate the phagocytotic activity of macrophages during resolution of inflammation.

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