ArticleProceedings of the National Academy of Sciences of the United States of America1999
Cytokine-mediated Bax deficiency and consequent delayed neutrophil apoptosis: a general mechanism to accumulate effector cells in inflammation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04970225 (Functional and Phenotypic Characteristics of Blood Neutrophils in Cystic Fibrosis), which is not on this map. Cited by 88 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Functional and Phenotypic Characteristics of Blood Neutrophils in Cystic Fibrosis
Who cites it
88 citing papers in PubMed, 276 citations in OpenAlex.
- Flavones induce neutrophil apoptosis by down-regulation of Mcl-1 via a proteasomal-dependent pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Trial
- Leukocyte apoptosis and pro-/anti-apoptotic proteins following downhill running.European journal of applied physiology · 2011Trial
- Severe exercise and exercise training exert opposite effects on human neutrophil apoptosis via altering the redox status.PloS one · 2011Trial
- Dental infection is associated with early relapse in patients with ANCA-associated vasculitis.RMD open · 2026Article
- Neutrophil death-more than meets the eye.Experimental hematology · 2025Review
- Endometriosis as an immune-mediated disease: pathogenetic mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
- Review
- Neutrophil metalloproteinase driven spleen damage hampers infection control of trypanosomiasis.Nature communications · 2023Article
- Dysfunctions of Neutrophils in the Peripheral Blood of Children with Cystic Fibrosis.Biomedicines · 2023Article
- Microbes and the fate of neutrophils.Immunological reviews · 2023Review
- Leptin and Asthma: What Are the Interactive Correlations?Biomolecules · 2022Review
- The Impact of Cytokines on Neutrophils' Phagocytosis and NET Formation during Sepsis-A Review.International journal of molecular sciences · 2022Review
- Optimal regulation of tumour-associated neutrophils in cancer progression.Royal Society open science · 2022Article
- Dysregulation of neutrophil death in sepsis.Frontiers in immunology · 2022Review
- Ethanol Intoxication Impairs Respiratory Function and Bacterial Clearance and Is Associated With Neutrophil Accumulation in the Lung AfterFrontiers in immunology · 2022Article
- BCL-XL antagonism selectively reduces neutrophil life span within inflamed tissues without causing neutropenia.Blood advances · 2021Article
- A Bittersweet Response to Infection in Diabetes; Targeting Neutrophils to Modify Inflammation and Improve Host Immunity.Frontiers in immunology · 2021Review
- Molecular Mechanisms for Regulation of Neutrophil Apoptosis under Normal and Pathological Conditions.Journal of evolutionary biochemistry and physiology · 2021Article
- Vasculitis in Cystic Fibrosis.Frontiers in pediatrics · 2020Review
- A Putative Serine Protease is Required to Initiate the RIPK3-MLKL-Mediated Necroptotic Death Pathway in Neutrophils.Frontiers in pharmacology · 2020Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils are important effector cells in immunity to microorganisms, particularly bacteria. Here, we show that the process of neutrophil apoptosis is delayed in several inflammatory diseases, suggesting that this phenomenon may represent a general feature contributing to the development of neutrophilia, and, therefore, in many cases to host defense against infection. The delay of neutrophil apoptosis was associated with markedly reduced levels of Bax, a pro-apoptotic member of the Bcl-2 family. Such Bax-deficient cells were also observed upon stimulation of normal neutrophils with cytokines present at sites of neutrophilic inflammation, such as granulocyte and granulocyte-macrophage colony-stimulating factors, in vitro. Moreover, Bax-deficient neutrophils generated by using Bax antisense oligodeoxynucleotides demonstrated delayed apoptosis, providing direct evidence for a role of Bax as a pro-apoptotic molecule in these cells. Interestingly, the Bax gene was reexpressed in Bax-deficient neutrophils under conditions of cytokine withdrawal. Thus, both granulocyte expansion and the resolution of inflammation appear to be regulated by the expression of the Bax gene in neutrophils.
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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.