ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2017
Adenosine effectively restores endotoxin-induced inhibition of human neutrophil chemotaxis via A1 receptor-p38 pathway.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- The Role and Mechanistic Effects of Methotrexate in the Treatment of Rheumatoid Arthritis.European journal of rheumatology · 2025Article
- The role of adenosine AInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- A novel definition and treatment of hyperinflammation in COVID-19 based on purinergic signalling.Purinergic signalling · 2022Review
- Reperfusion Cardiac Injury: Receptors and the Signaling Mechanisms.Current cardiology reviews · 2022Review
- Pannexin Channel Regulation of Cell Migration: Focus on Immune Cells.Frontiers in immunology · 2021Review
- Porcine CXCR1/2 antagonist CXCL8Scientific reports · 2020Article
- Extracellular AMP Suppresses Endotoxemia-Induced Inflammation by Alleviating Neutrophil Activation.Frontiers in immunology · 2020Article
- Mesenchymal Stem Cells Ameliorate Hepatic Ischemia/Reperfusion Injury via Inhibition of Neutrophil Recruitment.Journal of immunology research · 2018Article
- Purinergic Regulation of Neutrophil Function.Frontiers in immunology · 2018Review
- Purinergic signalling links mechanical breath profile and alveolar mechanics with the pro-inflammatory innate immune response causing ventilation-induced lung injury.Purinergic signalling · 2017Review
- Gabapentin Attenuates Ocular Inflammation:Frontiers in pharmacology · 2017Article
- Purinergic Signalling: Therapeutic Developments.Frontiers in pharmacology · 2017Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophil chemotaxis plays an essential role in recruiting neutrophils to sites of inflammation. Neutrophil chemotaxis is suppressed both after exposure to lipopolysaccharide (LPS) in vitro and during clinical and experimental endotoxemia, leading to serious consequences. Adenosine (ADO) is a potent anti-inflammatory agent that acts on a variety of neutrophil functions. However, its effects on human neutrophil chemotaxis during infection have been less well characterized. In the present study, we investigated the effect of ADO and its receptor-specific antagonist and agonist on neutrophil chemotaxis in an in vitro LPS-stimulated model. The results showed that increasing the concentration of ADO effectively restored the LPS-inhibited neutrophil chemotaxis to IL-8. A similar phenomenon occurred after intervention with a selective A1 receptor agonist but not with a selective antagonist. Pre-treatment with cAMP antagonist failed to restore LPS-inhibited chemotaxis. Furthermore, protein array and western blot analysis showed that the activation of A1 receptor significantly decreased LPS-induced p38 MAPK phosphorylation. However, the surface expression of the A1 receptor in LPS-stimulated neutrophils was not significantly changed. Taken together, these data indicated that ADO restored the LPS-inhibited chemotaxis via the A1 receptor, which downregulated the phosphorylation level of p38 MAPK, making this a promising new therapeutic strategy for infectious diseases.
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