Moyar Qing Ge, Kokalari, Blerina, Flayer, Cameron H., Killingbeck, Sarah S., Redai, Imre G., MacFarlane, IV, Alexander W., Hwang, Jin W., Kolupoti, Anisha, Kemeny, Michael D., Campbell, Kerry S., and Haczku, Angela
The roles of NK cells, surfactant protein D (SP-D), and IFNγ, as well as the effect of ozone (O3) inhalation, were studied on recirculation of pulmonary dendritic cells (DC) to the mediastinal lymph nodes.O3 exposure and lack of SP-D reduced NK cell IFNγ and lung tissue CCL21 mRNA expression and impaired DC homing to the mediastinal lymph nodes. Notably, addition of recombinant SP-D to naive mononuclear cells stimulated IFNγ release in vitro. Because NKp46, a glycosylated membrane receptor, was necessary for dosedependent SP-D binding to NK cells in vitro and DC migration in vivo, we speculate that SP-D may constitutively stimulate IFNγ production by NK cells, possibly via NKp46. This mechanism could then initiate the IFN-7/IL-I2 feedback circuit, a key amplifier of DC lymph node homing. Inhibition of this process during an acute inflammatory response causes DC retention in the peripheral lung tissue and contributes to injury. [ABSTRACT FROM AUTHOR]