Skip to main content
. 2023 Feb 13;19(4):1163–1177. doi: 10.7150/ijbs.79915

Figure 3.

Figure 3

Pretreatment with rLCN2 promotes acute lung inflammation in LPS-treated WT and LCN2 KO mice. (A) Percent survival following intratracheal instillation with 20 mg/kg LPS after rLCN2 pretreatment. (n = 10). (B) Experimental schematic of rLCN2 pretreatment in LPS-treated mice. (C-D) ELISA analyses of LCN2 concentrations in serum (C) and BALF (D). (n = 4-8). (E) Representative images of Ly6G and F4/80 immunoreactivity in lung sections of rLCN2+LPS-treated WT and LCN2 KO mice. Scale bar, 20 μm. (F) Ly6G- and F4/80-positive cells were counted and analyzed in two fields (300x300 μm2) for each slide (n = 6). (G) Western blot and quantification of LCN2, F4/80, and IL-6 proteins in lung tissues (n = 5-7). β-actin served as a loading control. Differences between two groups were evaluated using unpaired Student's t-tests. *P < 0.05 versus LPS-treated WT. †P < 0.05 versus rLCN2+LPS-treated WT. All data are presented as mean ± SEM.