Fig. 8
Adoptive transfer of SOCS3-deficient BMDMs into WT recipient mouse induced more severe ALI and BMDMs emigration into the lung. 0.4×106 PKH26-labeled BMDMs from WT and KO mice were intraperitoneal (i.p.) injected into WT mice, in conjunction with i.t. treatment with 5 mg/kg LPS. The mice treated with PBS were used as negative controls. 2 days after cell adoptive transfer, BAL, lung tissue and blood were collected for analysis. a PKH26-labeled BMDMs (Left panel) were observed in the lung tissues of KO mice 2 days after adoptive cell transfer. Lung histology of recipient mice was analyzed by H&E staining after adoptive transfer of WT-BMDMs/LPS or KO-BMDMs/LPS. One representative photograph was shown (Right panel). b Total cell counts in BAL of groups WT-BMDMs/LPS and KO-BMDMs/LPS. The naive mice were used as controls. * p < 0.05 v.s. WT-BMDMs group, n = 5. c The presence of PKH26-labeled exogeneous BMDMs in lung and blood was analyzed by flow cytometry analysis. Exogenous BMDMs were CD11b(+)/PKH26(+) cells. One representative data was shown. BMDMs in lung (d) and blood (e) were quantitatively analyzed. * p < 0.05, ** p < 0.01 v.s. WT-BMDMs group, n = 5. f Lung neutrophils were analyzed by FACS and F4/80(−)Ly6G(+) cell population was considered as neutrophils. One representative data was shown. Adoptive transfer of SOCS3-deficient BMDMs into WT recipient mouse induced more neutrophil infiltrates into the lungs. g Quantitatively analysis of Ly6C(+) macrophage subtypes in BAL. * p < 0.05 v.s. WT-BMDMs group, n = 5. h Correlation analysis between Ly6C(+) subtype macrophages and PKH26-labeled BMDMs in BAL. Each point represents individual sample