ArticleInternational journal of experimental pathology2015
Vasoactive intestinal peptide suppresses macrophage-mediated inflammation by downregulating interleukin-17A expression via PKA- and PKC-dependent pathways.
Article in International journal of experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- The Role of the Nervous System in Lung Disease.Current neurology and neuroscience reports · 2026Review
- Potential pharmaceuticals targeting neuroimmune interactions in treating acute lung injury.Clinical and translational medicine · 2024Review
- Article
- VIP modulates human macrophages phenotype via FPRL1 via activation of RhoA-GTPase and PLC pathways.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
- Macrophage Polarization and Alveolar Bone Healing Outcome: Despite a Significant M2 Polarizing Effect, VIP and PACAP Treatments Present a Minor Impact in Alveolar Bone Healing in Homeostatic Conditions.Frontiers in immunology · 2021Article
- Gut macrophages: key players in intestinal immunity and tissue physiology.Current opinion in immunology · 2020Review
- Crosstalk between human endometrial stromal cells and decidual NK cells promotes decidualization in vitro by upregulating IL‑25.Molecular medicine reports · 2018Article
- Role of vasoactive intestinal peptide inInternational journal of ophthalmology · 2018Article
- Interleukin-17A Plays the Same Role on Mice Acute Lung Injury Respectively Induced by Lipopolysaccharide and Paraquat.Inflammation · 2017Article
- Gastrointestinal neuroendocrine peptides/amines in inflammatory bowel disease.World journal of gastroenterology · 2017Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.