IL35 Attenuated LPS-Induced Acute Lung Injury by Regulating Macrophage Polarization

Abstract

Interleukin 35 (IL35) has been reported to play a role in acute lung injury (ALI); however, the current results on the relationship between IL35 and ALI are inconsistent. Therefore, we will further determine the function of IL35 in mouse ALI and its potential mechanism in this paper. HE staining and Masson staining were used to evaluate lung injury in mice. Immunohistochemical staining was used to calculate the expression of IL35 p35, TLR4 and MD2 and the ratio of Bax/Bcl2 and p-P65/P65. The expression levels of IL35 EBi3, CD68, CD206 and MPO were detected by immunofluorescence staining. RT–PCR was used to examine the expression levels of IL1β and IL6. TUNEL staining was performed to detect apoptotic cells. Overexpression of IL35 alleviated LPS-induced acute lung injury in mice. IL35 overexpression decreased the expression of CD68 and increased the expression of CD206 in ALI mice. Furthermore, upregulation of IL35 expression obviously reduced the expression of MPO, IL1β and IL6 in lung tissues of mice with ALI. Mechanistically, IL35 suppressed the TLR4/NFκB-P65 pathway, leading to the promotion of M1 to M2 macrophage transition and inflammation relief in ALI in mice.