Abstract:
:Persistent exposure to ambient fine particulate matter (PM2.5) can exacerbate allergic diseases in humans. Mast cells play an important role in allergic inflammation in peripheral tissues, such as skin, mucosa, and lung. Engagement of the high-affinity Fc receptor leads to mast cell degranulation, releasing a variety of highly active mediators including histamine, leukotrienes, and inflammatory cytokines. How PM2.5 exposure affects mast cell activation and function remains largely unknown. To characterize the effect of PM2.5 on mast cells, we used bone marrow-derived mast cells (BMMCs) to examine whether PM2.5 affected FcεRI-mediated signaling, cytokine production, and degranulation. Exposure to high doses of PM2.5 caused pronounced apoptosis and death of BMMCs. In contrast, exposure to low doses of PM2.5 enhanced mast cell degranulation and FcεRI-mediated cytokine production. Further analysis showed that PM2.5 treatment increased Syk activation and subsequently phosphorylation of its substrates including LAT, PLC-γ1, and SLP-76. Moreover, PM2.5 treatment led to activation of the PI3K and MAPK pathways. Intriguingly, water-soluble fraction of PM2.5 were found responsible for the enhancement of FcεRI-mediated signaling, mast cell degranulation, and cytokine production. Our data suggest that PM2.5, mainly water-soluble fraction of PM2.5, could affect mast cell activation through enhancing FcεRI-mediated signaling.
journal_name
Cell Signaljournal_title
Cellular signallingauthors
Jin Y,Zhu M,Guo Y,Foreman D,Feng F,Duan G,Wu W,Zhang Wdoi
10.1016/j.cellsig.2019.01.010subject
Has Abstractpub_date
2019-05-01 00:00:00pages
102-109eissn
0898-6568issn
1873-3913pii
S0898-6568(19)30019-1journal_volume
57pub_type
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