Vasoactive intestinal peptide suppresses macrophage‐mediated inflammation by downregulating interleukin‐17A expression via PKA‐ and PKC‐dependent pathways

Summary
Interleukin (IL)‐17A is a pro‐inflammatory cytokine that markedly enhances inflammatory responses in the lungs by recruiting neutrophils and interacting with other pro‐inflammatory mediators. Reducing the expression of IL‐17A could attenuate inflammation in the lungs. However, whether VIP exerts its anti‐inflammatory effects by regulating the expression of IL‐17A has remained unclear. Here, we show that there is a remarkable increase of IL‐17A in bronchoalveolar lavage fluid (BALF) and lung tissue of mice with acute lung injury (ALI). Moreover, lipopolysaccharides (LPS) stimulated elevated expression of IL‐17A, which was evident by the enhanced levels of mRNA and protein observed. Furthermore, we also found that VIP inhibited LPS‐mediated IL‐17A expression in a time‐ and dose‐dependent manner in an in vitro model of ALI and that this process might be mediated via the phosphokinase A (PKA) and phosphokinase C (PKC) pathways. Taken together, our results demonstrated that VIP might be an effective protector during ALI by suppressing IL‐17A expression.

Source: International Journal of Experimental Pathology - February 1, 2015 Category: Pathology Authors: Wen‐Zhuo Ran, Liang Dong, Chun‐Yan Tang, Yong Zhou, Guo‐Ying Sun, Tian Liu, Yong‐Ping Liu, Cha‐Xiang Guan Tags: Original Article Source Type: research