Progranulin Improves Acute Lung Injury through Regulating the Differentiation of Regulatory T Cells and Interleukin-10 Immunomodulation to Promote Macrophage Polarization

Figure 2

PGRN ameliorated LPS-induced ALI through antiapoptosis, inflammatory infiltration, and neutrophil aggregation. C57BL/6 mice were randomly divided into WT, WT+LPS, WT+LPS+PGRN, and PGRN-deficient (PGRN^-/-) mice with a C57/BL6 background which were randomly divided into the PGRN^-/-+LPS and PGRN^-/-+LPS+PGRN groups (/group). (a) PGRN had an antiapoptotic effect on the lungs in the LPS-induced ALI mouse model. Apoptosis was detected by TUNEL staining, and strongly positive apoptosis appeared in the lungs of the WT+LPS and PGRN^-/-+LPS groups compared with the WT group. Apoptosis was reduced in mice treated with PGRN. (b) PGRN exerted a protective effect on the LPS-induced ALI mouse model, at least in part by IL-10 immune modulation. The expression of IL-10 in the lung tissues increased significantly in the WT+LPS and PGRN^-/-+LPS groups compared to the WT group. After the intervention of PGRN, IL-10 expression declined significantly. (c) PGRN reduced the level of MPO-producing neutrophils and played a protective role in the LPS-induced ALI mouse model. (d) PGRN reduced the total number of PMNs in BALF in the LPS-induced mouse models. ns: not significant; and by one-way ANOVA followed by the Tukey Post Hoc test comparing the WT, WT+LPS, WT+LPS+PGRN, PGRN^-/-+LPS, and PGRN^-/-+LPS+PGRN groups. Representative data are shown.

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