Abstract
Mast cells play a critical role in the innate immune response to bacterial infection. They internalize and kill a variety of bacteria and process antigen for presentation to T cells via MHC molecules. Although mast cell phagocytosis appears to play a significant role during bacterial infection, little is known about the proteins involved in its regulation. In this study, we demonstrate that the SNARE protein SNAP29 is involved in mast cell phagocytosis. SNAP29 is localized in the endocytic pathway and is transiently recruited to Escherichia coli (E. coli)-containing phagosomes. Interestingly, overexpression of SNAP29 significantly increases the internalization and killing of E. coli, while it does not affect mast cell exocytosis of inflammatory mediators. To our knowledge, these data are the first to demonstrate a novel function of SNAP29 in mast cell phagocytosis and have implications in protection against bacterial infection.
Highlights
Mast cells are well known for their key role in orchestrating the allergic response through the release of pro-inflammatory mediators following FceRI aggregation, a process called degranulation [1]
Mast Cells Express SNAP29 SNAP29 is a member of the SNAP25 family of SNARE proteins and contains two SNARE motifs separated by a linker region (Figure 1A)
Since SNAP29 is not involved in mast cell degranulation and our data, as well as previous studies, place SNAP29 in the endocytic pathway [17,18,19,20], we investigated whether SNAP29 played a role in mast cell phagocytosis
Summary
Mast cells are well known for their key role in orchestrating the allergic response through the release of pro-inflammatory mediators following FceRI aggregation, a process called degranulation [1]. Evidence has demonstrated a crucial role for mast cells in the innate immune response. Mast cells express Tolllike receptors 2 and 4, which allow them to recognize bacteria [2]. Stimulation through Toll-like receptors results in the secretion of pro-inflammatory cytokines, which participate in neutrophil and dendritic cell recruitment to the site of infection [3]. Mast cells are able to internalize bacteria, and present bacterial antigen to CD8+T cells via MHC class I molecules [4]. Mast cells are situated at the major entry points for pathogens, which makes them one of the first phagocytic cells that bacteria may encounter
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