Journal
INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY
Volume 96, Issue 4, Pages 269-275Publisher
WILEY
DOI: 10.1111/iep.12130
Keywords
interleukin-17A; lipopolysaccharides; macrophages; vasoactive intestinal peptide
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Funding
- National Natural Science Foundation of China [81170059]
- Hunan Provincial Natural Science Foundation of China [14JJ2040]
- Hunan Provincial Innovation Foundation for Postgraduate [CX2013B094]
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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 inbronchoalveolar 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 invitro 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.
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