ArticleInternational journal of molecular sciences2020
Nintedanib Reduces Neutrophil Chemotaxis via Activating GRK2 in Bleomycin-Induced Pulmonary Fibrosis.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Aggravated effects of human parvovirus B19 NS1 protein on bleomycin‑induced pulmonary fibrosis.Molecular medicine reports · 2026Article
- Regulation of G protein-coupled receptor kinase 2 and its role in tumors.Journal of translational medicine · 2026Review
- The Endothelial Cell Perspective in Pulmonary Fibrosis: From Cell Fate Decisions, Intercellular Communication, and EndoMT to Emerging Therapies.Canadian respiratory journal · 2026Review
- Disulfiram Attenuates Bleomycin-Induced Lung Inflammation and Fibrosis with Reduced Endothelial Pyroptosis and Neutrophil Adhesion.Journal of inflammation research · 2026Article
- PDE4-Selective Inhibition in Chronic Obstructive Pulmonary Disease and Pulmonary Fibrosis: Different Agents or Different Targets?Life (Basel, Switzerland) · 2025Review
- Improved Survival in Patients with Idiopathic Pulmonary Fibrosis Hospitalized for Acute Exacerbation.Journal of clinical medicine · 2025Article
- Review
- Identifying Mechanism of Resveratrol for the Treatment of COVID-19 and Idiopathic Pulmonary FibrosisCurrent medicinal chemistry · 2025Article
- Article
- Neutrophil dynamics in pulmonary fibrosis: pathophysiological and therapeutic perspectives.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Pathological mechanisms and novel drug targets in fibrotic interstitial lung disease.Inflammation and regeneration · 2024Review
- Review
- The Role of Immune Cells in the Pathogenesis of Idiopathic Pulmonary Fibrosis.Medicina (Kaunas, Lithuania) · 2023Review
- NLRP3 Inflammasome Activates Endothelial-to-Mesenchymal Transition via Focal Adhesion Kinase Pathway in Bleomycin-Induced Pulmonary Fibrosis.International journal of molecular sciences · 2023Article
- Inhibition of discoidin domain receptor 2 reveals kinase-dependent and kinase-independent functions in regulating fibroblast activity.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Impact of ILD-Specific Therapies on Perioperative Course in Patients with Progressive Interstitial Lung Disease Undergoing Lung Transplantation.Journal of clinical medicine · 2023Article
- The main e-cigarette component vegetable glycerin enhances neutrophil migration and fibrosis in endotoxin-induced lung injury via p38 MAPK activation.Respiratory research · 2023Article
- Nintedanib treatment for bleomycin-induced lung injury - First report.Respiratory medicine case reports · 2023Article
- Nintedanib Inhibits Endothelial Mesenchymal Transition in Bleomycin-Induced Pulmonary Fibrosis via Focal Adhesion Kinase Activity Reduction.International journal of molecular sciences · 2022Article
- HO‑1 knockdown upregulates the expression of VCAM‑1 to induce neutrophil recruitment during renal ischemia‑reperfusion injury.International journal of molecular medicine · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Neutrophils are involved in the alveolitis of idiopathic pulmonary fibrosis (IPF). However, their pathogenic mechanisms are still poorly understood. Nintedanib has antifibrotic and anti-inflammatory activity in IPF. This study aimed to investigate the regulatory mechanism of nintedanib on neutrophil chemotaxis in bleomycin (BLM)-induced pulmonary fibrosis. Nintedanib was administered via oral gavage to male C57BL/6 mice 24 h after a bleomycin intratracheal injection (1.5 U/kg). Lung histopathological findings, the expression of cytokines, and the regulatory signaling pathways of neutrophil chemotaxis were analyzed. The effect of nintedanib was also investigated in a mouse model with adoptive neutrophil transfer in vivo. Nintedanib significantly decreased the histopathological changes and neutrophil recruitment in BLM-induced pulmonary fibrosis. Nintedanib mediated a downregulation of chemokine (C-X-C motif) receptor 2 (CXCR2) and very late antigen 4 (VLA-4) expression, as well as an upregulation of G protein-coupled receptor kinase 2 (GRK2) activity in peripheral blood neutrophils in BLM-induced pulmonary fibrosis. Nintedanib also decreased the activation of endothelial cells by the decreased expression of vascular cell adhesion molecule 1 (VCAM-1). The effect of nintedanib on regulating neutrophil chemotaxis was also confirmed by a mouse model with adoptive neutrophil transfer in vivo. In conclusion, nintedanib reduces neutrophil chemotaxis and endothelial cell activation to regulate the severity of BLM-induced pulmonary fibrosis. These effects are associated with an enhancement of GRK2 activity and a reduction in CXCR2 and VLA-4 expression on neutrophils and a decrease in VCAM-1 expression on endothelial cells.
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