ArticleThe Journal of experimental medicine2014
Neutrophils recruited by chemoattractants in vivo induce microvascular plasma protein leakage through secretion of TNF.
Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 97 citations in OpenAlex.
- Trial
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- A multicellular vessel-on-a-chip model reveals context-dependent roles for platelets in inflammation and inflammatory hemostasis.Blood vessels, thrombosis & hemostasis · 2024Article
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- Mechanistic Evaluation of Antiarthritic Effects of Citronellol in CFA-Induced Arthritic Rats.ACS omega · 2023Article
- Intercellular model predicts mechanisms of inflammation-fibrosis coupling after myocardial infarction.The Journal of physiology · 2023Article
- Elucidating the Ability of CGRP to Modulate Microvascular Events in Mouse Skin.International journal of molecular sciences · 2022Article
- Comparison of CD3e Antibody and CD3e-sZAP Immunotoxin Treatment in Mice Identifies sZAP as the Main Driver of Vascular Leakage.Biomedicines · 2022Article
- Neutrophils and polymorphonuclear myeloid-derived suppressor cells: an emerging battleground in cancer therapy.Oncogenesis · 2022Review
- Lessons From the Success and Failure of Targeted Drugs for Rheumatoid Arthritis: Perspectives for Effective Basic and Translational Research.Immune network · 2022Review
- Neutrophil Extracellular Traps Exacerbate Ischemic Brain Damage.Molecular neurobiology · 2022Review
- SARS-CoV-2 Spike Protein Destabilizes Microvascular Homeostasis.Microbiology spectrum · 2021Article
- Cytokine Networks in the Pathogenesis of Rheumatoid Arthritis.International journal of molecular sciences · 2021Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Microvascular plasma protein leakage is an essential component of the inflammatory response and serves an important function in local host defense and tissue repair. Mediators such as histamine and bradykinin act directly on venules to increase the permeability of endothelial cell (EC) junctions. Neutrophil chemoattractants also induce leakage, a response that is dependent on neutrophil adhesion to ECs, but the underlying mechanism has proved elusive. Through application of confocal intravital microscopy to the mouse cremaster muscle, we show that neutrophils responding to chemoattractants release TNF when in close proximity of EC junctions. In vitro, neutrophils adherent to ICAM-1 or ICAM-2 rapidly released TNF in response to LTB4, C5a, and KC. Further, in TNFR(-/-) mice, neutrophils accumulated normally in response to chemoattractants administered to the cremaster muscle or dorsal skin, but neutrophil-dependent plasma protein leakage was abolished. Similar results were obtained in chimeric mice deficient in leukocyte TNF. A locally injected TNF blocking antibody was also able to inhibit neutrophil-dependent plasma leakage, but had no effect on the response induced by bradykinin. The results suggest that TNF mediates neutrophil-dependent microvascular leakage. This mechanism may contribute to the effects of TNF inhibitors in inflammatory diseases and indicates possible applications in life-threatening acute edema.
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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.