Bacterial and Fungal Toll-Like Receptor Activation Elicits Type I IFN Responses in Mast Cells.

Autor:	Kornstädt L; Institute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany., Pierre S; Institute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany., Weigert A; Faculty of Medicine, Institute of Biochemistry I, Goethe-University Frankfurt, Frankfurt, Germany., Ebersberger S; Institute of Molecular Biology gGmbH, Mainz, Germany., Schäufele TJ; Institute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany., Kolbinger A; Institute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany., Schmid T; Faculty of Medicine, Institute of Biochemistry I, Goethe-University Frankfurt, Frankfurt, Germany., Cohnen J; Institute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany., Thomas D; Institute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany., Ferreirós N; Institute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany., Brüne B; Faculty of Medicine, Institute of Biochemistry I, Goethe-University Frankfurt, Frankfurt, Germany.; Project Group Translational Medicine and Pharmacology, Fraunhofer Institute for Molecular Biology and Applied Ecology IME, Frankfurt am Main, Germany., Ebersberger I; Department for Applied Bioinformatics, Institute for Cell Biology and Neuroscience, Goethe-University Frankfurt, Frankfurt, Germany.; Senckenberg Biodiversity and Climate Research Centre (S-BIKF), Frankfurt am Main, Germany.; LOEWE Centre for Translational Biodiversity Genomics (TBG), Frankfurt am Main, Germany., Scholich K; Institute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany.; Project Group Translational Medicine and Pharmacology, Fraunhofer Institute for Molecular Biology and Applied Ecology IME, Frankfurt am Main, Germany.; Fraunhofer Cluster of Excellence for Immune-Mediated Diseases (CIMD), Frankfurt am Main, Germany.
Jazyk:	angličtina
Zdroj:	Frontiers in immunology [Front Immunol] 2021 Feb 12; Vol. 11, pp. 607048. Date of Electronic Publication: 2021 Feb 12 (Print Publication: 2020).
DOI:	10.3389/fimmu.2020.607048
Abstrakt:	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. Competing Interests: SE was employed by Institute of Molecular Biology GmbH. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2021 Kornstädt, Pierre, Weigert, Ebersberger, Schäufele, Kolbinger, Schmid, Cohnen, Thomas, Ferreirós, Brüne, Ebersberger and Scholich.)
Databáze:	MEDLINE
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