ArticleInflammation2018
Neutrophils as a Potential Source of Chitinase-3-like Protein 1 in Cystic Fibrosis.
Article in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed.
- Structural optimization of CHI3L1 inhibitors with improved pharmacokinetics and functional activity in 3D glioblastoma models.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Human YKL-40 antibody alleviates atopic dermatitis-like skin inflammation by inhibiting exosome secretion via the JAK3/STAT6 pathway.Archives of pharmacal research · 2025Article
- Article
- Review
- Inflammatory Effects and Regulatory Mechanisms of Chitinase-3-like-1 in Multiple Human Body Systems: A Comprehensive Review.International journal of molecular sciences · 2024Review
- Chitin-mediated blockade of chitinase-like proteins reduces tumor immunosuppression, inhibits lymphatic metastasis and enhances anti-PD-1 efficacy in complementary TNBC models.Breast cancer research : BCR · 2024Article
- Chitinase 3-like-1 Expression in the Microenvironment Is Associated with Neutrophil Infiltration in Bladder Cancer.International journal of molecular sciences · 2023Article
- Increased Plasma YKL-40 Level and Chitotriosidase Activity in Cystic Fibrosis Patients.Inflammation · 2022Article
- Targeting protumor factor chitinase-3-like-1 secreted by Rab37 vesicles for cancer immunotherapy.Theranostics · 2022Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The chitinase-3-like protein 1, also known as YKL-40, is an inflammatory marker increased in blood of patients with cystic fibrosis (CF). Systemic levels of YKL-40 are increased in dysglycemic patients with CF. Our objective is to determine if YKL-40 is expressed and released by CF neutrophils. We also assessed if specific stimulus, such as glucose and lipopolysaccharide (LPS), can induce the secretion of YKL-40. Neutrophil cells of healthy adults and patients with CF were isolated. Immunostaining of whole blood and neutrophils was done. CF and healthy neutrophils were cultured with either LPS or varying concentrations of glucose. YKL-40 protein was measured using specific immunoassay ELISA. Isolated neutrophil cells from 11 patients with CF (32.3 ± 8.0 years) were compared to five age-matched healthy individuals (28.3 ± 5.5 years). Although there is a significant increase in the concentration of YKL-40 in CF neutrophils compared to healthy neutrophils (P = 0.027), the spontaneous release of YKL-40 into the media is similar in CF and healthy neutrophils. CF neutrophils stimulated with LPS or glucose do not stimulate the release of YKL-40 (P = 0.995 for glucose and P = 0.624 for LPS). CF neutrophils have higher intracellular level of YKL-40 than neutrophils from healthy volunteers, but they do not release more YKL-40 when stimulated with exogenous stimulus. These results suggest that the increased levels of circulating YKL-40 in CF patients might originate from another cellular source.
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Registered trials
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