| First Author | Kornstädt L | Year | 2020 |
| Journal | Front Immunol | Volume | 11 |
| Pages | 607048 | PubMed ID | 33643293 |
| Mgi Jnum | J:314047 | Mgi Id | MGI:6805890 |
| Doi | 10.3389/fimmu.2020.607048 | Citation | Kornstadt L, et al. (2020) Bacterial and Fungal Toll-Like Receptor Activation Elicits Type I IFN Responses in Mast Cells. Front Immunol 11:607048 |
| abstractText | 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-beta synthesis in BMMCs in similar amounts as in bone marrow derived macrophages. IFN-beta was expressed by mast cells in paws from naive 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-beta, which are alone or in combination with each other able to regulate the phagocytotic activity of macrophages during resolution of inflammation. |
