ArticleInflammation2020
CYTL1 Promotes the Activation of Neutrophils in a Sepsis Model.
Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- The origin, evolution, and molecular diversity of the chemokine system.Life science alliance · 2024Article
- NRP1 regulates autophagy and proliferation of gastric cancer through Wnt/β-catenin signaling pathway.Aging · 2023Article
- Bioinformatics-based analysis reveals elevated CYTL1 as a potential therapeutic target for BRAF-mutated melanoma.Frontiers in cell and developmental biology · 2023Article
- The Impact of Cytokines on Neutrophils' Phagocytosis and NET Formation during Sepsis-A Review.International journal of molecular sciences · 2022Review
- Antimicrobial and Immunomodulatory Effects of Selected Chemokine and Antimicrobial Peptide on Cytokine Profile duringAntibiotics (Basel, Switzerland) · 2022Article
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
As a novel cytokine, cytokine-like 1 (CYTL1) is a classical secretory protein, and its potential biological function remains to be determined. In this study, we found that expression of CYTL1 was upregulated in neutrophils upon inflammatory stimuli. We demonstrated that CYTL1 enhanced phagocytosis of Escherichia coli by activated neutrophils both in vivo and in vitro through phosphorylation of protein kinase B (Akt). CYTL1-induced chemotactic activity in lipopolysaccharide (LPS) stimulated neutrophils, and the mechanism may be related to CC chemokine receptor 2 (CCR2) mediated action. CYTL1 also increased the release of reactive oxygen species (ROS) in LPS-stimulated neutrophils. These data indicate that upon inflammatory stimulation, neutrophil-derived CYTL1 may play a crucial role in the activation of neutrophils during pathogenic infections.
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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.