ArticleThe American journal of pathology1998
Bradykinin stimulates type II alveolar cells to release neutrophil and monocyte chemotactic activity and inflammatory cytokines.
Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 56 citations in OpenAlex.
- Review
- SARS-CoV-2 and ACE2: The biology and clinical data settling the ARB and ACEI controversy.EBioMedicine · 2020Review
- The Effect of Perioperative Ischemia and Reperfusion on Multiorgan Dysfunction following Abdominal Aortic Aneurysm Repair.BioMed research international · 2015Review
- Article
- Novel effects mediated by bradykinin and pharmacological characterization of bradykinin B2 receptor antagonism in human synovial fibroblasts.British journal of pharmacology · 2009Article
- Regulation of COX-2 expression and IL-6 release by particulate matter in airway epithelial cells.American journal of respiratory cell and molecular biology · 2009Article
- Kinin B2 receptor regulates chemokines CCL2 and CCL5 expression and modulates leukocyte recruitment and pathology in experimental autoimmune encephalomyelitis (EAE) in mice.Journal of neuroinflammation · 2008Article
- Pulmonary epithelium, cigarette smoke, and chronic obstructive pulmonary disease.International journal of chronic obstructive pulmonary disease · 2007Review
- Effects of transforming growth factor-beta in the development of inflammatory pseudotumour-like lesions in a murine model.International journal of experimental pathology · 2006Article
- Effects of sivelestat, a new elastase inhibitor, on IL-8 and MCP-1 production from stimulated human alveolar epithelial type II cells.Journal of anesthesia · 2006Article
- Carbon black nanoparticles induce type II epithelial cells to release chemotaxins for alveolar macrophages.Particle and fibre toxicology · 2005Article
- Effect of a kinin B2 receptor antagonist on LPS- and cytokine-induced neutrophil migration in rats.British journal of pharmacology · 2003Article
- Role of the bradykinin B2 receptor for the local and systemic inflammatory response that follows severe reperfusion injury.British journal of pharmacology · 2003Article
- Implication of the bradykinin receptors in antigen-induced pulmonary inflammation in mice.British journal of pharmacology · 2003Article
- Primary human alveolar epithelial cells can elicit the transendothelial migration of CD14+ monocytes and CD3+ lymphocytes.Immunology · 2001Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study, we evaluated the potential of bradykinin (BK) to induce the release of neutrophil and monocyte chemotactic activity (NCA and MCA) and cytokines from an alveolar type II epithelial cell line, A549 cells. BK stimulated A549 cells to release NCA and MCA in a dose- and time-dependent manner (P < 0.001). Checkerboard analysis revealed that both NCA and MCA involved chemotactic and chemokinetic activity. Molecular sieve column chromatography showed three molecular weight masses (near 19 kd, 8 kd, and 400 d) for NCA and several molecular weight peaks (near 66 kd, 25 kd, 19 kd, 16 kd, and 400 d) for MCA. The release of NCA and MCA was inhibited by cycloheximide and lipoxygenase inhibitors (P < 0.01). The NCA and MCA were inhibited by leukotriene B4 (LTB4) receptor antagonist (P < 0.01), and the concentration of LTB4 was high enough for NCA and MCA. Antibodies to interleukin (IL)-8 and granulocyte colony-stimulating factor (G-CSF) attenuated NCA (P < 0.01), and antibodies to monocyte chemotactic protein-1 (MCP-1), G-CSF, and transforming growth factor (TGF)-beta attenuated MCA (P < 0.01). The levels of IL-8, G-CSF, MCP-1, and TGF-beta increased time dependently (P < 0.01). BK also stimulated the release of ILeukin-6 from A549 cells (P < 0.001). The receptors responsible for the release of NCA, MCA, and individual chemokines involved both BKB1 and BKB2 receptors. These data suggest that BK may stimulate alveolar type II pneumocytes to release inflammatory cytokines, which then may modulate the lung inflammation.
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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.