Figure 3.

Myeloid EPOR deficiency aggravates inflammation in lung injury. (A) WT mice (n = 5) were treated with 3 mg/kg LPS (i.t.) at the indicated times (days 0, 1, 2, 3, and 5). The number of F4/80⁺EPOR⁺ macrophages in BALF was measured by FACS. (B) EPOR cKO and WT mice were challenged with 10 mg/kg LPS i.t., and survival was monitored (n = 6). (C) EPOR cKO and WT mice were treated with 3 mg/kg LPS (i.t.) at the indicated times. Change in body weight was monitored over 6 days (n = 4). (D) Lung tissue samples from mice with LPS administration for 48 h were dissected and subjected to H&E staining. Lung injury scores in each group were analyzed (n = 4). Scale bar: 150 µm. (E) EPOR cKO and WT mice were treated with 1 mg/kg eCIRP (i.t.). Lung tissue samples from mice with eCIRP administration for 48 h were dissected and subjected to H&E staining. Lung injury scores in each group were analyzed (n = 4). Scale bar: 150 µm. WT and EPOR cKO mice were treated with 3 mg/kg LPS (i.t.) at the indicated times (days 0, 1, 2, 3, and 5). (F) The MFI of CD80 and the percentage of CD206⁺ cells in BALF macrophages were measured by FACS at the indicated time (n = 3). (G) The concentrations of TNF-α, IL-6, and IL-10 in BALF at the indicated time was measured (n = 3). Data are representative of at least two independent experiments. Results were expressed as mean ± SD. *P < 0.05, **P < 0.01 compared to the WT group at indicated time. Statistics: Log-rank test (B) or unpaired two-tailed Student’s t-test (C–G). EPOR, erythropoietin receptor; LPS, lipopolysaccharide; eCIRP, extracellular cold-inducible RNA-binding protein; WT, wild type; BALF, bronchoalveolar lavage fluid; MFI, mean fluorescence intensity; FACS, fluorescence activated cell sorter.