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| Status |
Public on Jan 27, 2021 |
| Title |
RNA Sequencing Shows Activation of Type I Interferon Pathway in Zymosan-Induced Mast Cells |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
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 Tolllike 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-b synthesis in BMMCs in similar amounts as in bone marrow derived macrophages. IFN-b 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-b, 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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| Overall design |
mRNA sequencing of bone marrow-derived mast cells treated with 10 μg/ml zymosan for 24 h or 48 h or left untreated (control, 0 h), 4 samples per condition.
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| Contributor(s) |
Kornstädt L, Schmid T, Ebersberger S, Ebersberger I, Scholich K |
| Citation(s) |
33643293 |
| Submission date |
Jan 26, 2021 |
| Last update date |
Apr 20, 2021 |
| Contact name |
Klaus Scholich |
| E-mail(s) |
scholich@em.uni-frankfurt.de
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| Organization name |
University Hospital Goethe-University Frankfurt
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| Department |
Institute of Clinical Pharmacology
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| Street address |
Theodor Stern Kai 7
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| City |
Frankfurt am Main |
| ZIP/Postal code |
60590 |
| Country |
Germany |
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| Platforms (1) |
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| Samples (12)
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| Relations |
| BioProject |
PRJNA694864 |
| SRA |
SRP303305 |
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