Fig. 4: CXCL16 in dendritic cells has the ability to influence airway inflammation.

A Wild-type recipient mice were administrated with CXCL16-knockdown donor of CD11c⁺ BMDCs or CXCL16-overexpressed CD11c⁺ BMDCs every 4 days followed by Aspergillus challenge every other day for 3 weeks. B Representative lung sections stained with Alcian blue–periodic acid Schiff (×200 magnification and scale bar = 100 μm). C Lung sections stained with hematoxylin and eosin (×200 magnification and scale bar = 100 μm). D Numbers of total BALF inflammatory cells and differential counts (n = 6). E Th2 cytokine production in bronchoalveolar lavage (n = 6). F The protein expression of PPARγ was detected by western blot (n = 3). *P < 0.05, **P < 0.01 Aspergillus-challenged CXCL16-knockdown donor mouse BMDCs versus wild-type donor mice, or CXCL16-overexpressed BMDCs versus wild-type donor mice. DC^WT → WT, wild-type donor mouse BMDCs adoptively transferred to wild-type mice; DC^KD → WT, CXCL16-knockdown donor mouse BMDCs adoptively transferred to wild-type mice; DC^NC → WT, CXCL16 negative control plasmid–transferred BMDCs adoptively transferred to wild-type mice; DC^OE → WT, CXCL16-overexpressed plasmid-transferred BMDCs adoptively transferred to wild-type mice. A.f. stands for Aspergillus.