The effects of wildfire smoke inhalation on the immune system are unknown. We hypothesized that wildfire smoke exposure activates an innate immune response.
Healthy subjects were recruited during the time of smoke exposure [WF; n=7] and 3-6 months post-wildfire season smoke exposure [postWF; n=16]. Peripheral blood was collected at recruitment and the recovered cells were stained for cytoplasmic and membrane markers with fluorescent conjugated antibodies. To study cellular components of the innate immune system, Innate Lymphoid Cell (ILC), Natural Killer (NK) cell, and Dendritic Cell (DC) multicolor characterization was performed using standard flow cytometric gating strategy. FACS data was analyzed by FlowJo®. Peripheral Blood was also collected for a CBC panel.
Compared to postWF, WF subjects had decreased counts of myeloid cDC2 [P=.022], but no change in myeloid cDC1, DC4, nor plasmacytoid DC. WF subjects had increased CCR4 positive cDC1s [P=.058], cDC2s [P=.004], and DC4 [P=.007]. WF subjects had increased CD8+ T cell count [P=.039] compared to postWF in the circulation. WF subjects also had increased counts of ILC that expressed cytoplasmic IL-13 [P=.02], decreased counts of ILC2 [P=.041], and an increase in ILC1:ILC2 [P=.003] compared to postWF subjects.
The decrease in the DC counts in the peripheral blood and an increase in their expression of the chemokine receptor CCR4 suggest increased migration of these cells to peripheral tissues. The increase in IL-13+ ILCs, and DC activation in subjects during wildfire season, compared to subjects post-wildfire season, suggests a pro inflammatory effect of wildfire smoke inhalation.