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

  • Wen-Zhuo Ran, Liang Dong, Chun-Yan Tang, Yong Zhou, Guo-Ying Sun, Tian Liu, Yong-Ping Liu, Cha-Xiang Guan
  • International Journal of Experimental Pathology, May 2015, Wiley
  • DOI: 10.1111/iep.12130

novel role of vasoactive intestinal peptide in macrophage

What is it about?

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.

Why is it important?

In this work, we first found the potential therapeutic role of vasoactive intestinal peptide on acute lung injury by downregulating IL-17A, given that it plays a central role in the development of inflammation in lung.

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The following have contributed to this page: Dr Chaxiang Guan