ArticleMediators of inflammation2016
Correlation of IL-18 with Tryptase in Atopic Asthma and Induction of Mast Cell Accumulation by IL-18.
Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- IL-18-associated basophil and mast cell activation in sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- A Narrative Review of the IL-18 and IL-37 Implications in the Pathogenesis of Atopic Dermatitis and Psoriasis: Prospective Treatment Targets.International journal of molecular sciences · 2024Review
- Allergens induce upregulated IL-18 and IL-18Rα expression in blood Th2 and Th17 cells of patients with allergic asthma.Clinical and experimental immunology · 2024Article
- IL-18 biology in severe asthma.Frontiers in medicine · 2024Review
- Interleukin-18 and IL-18BP in inflammatory dermatological diseases.Frontiers in immunology · 2023Review
- Mast Cell-Mediated Orchestration of the Immune Responses in Human Allergic Asthma: Current Insights.Clinical reviews in allergy & immunology · 2019Review
- Role of IL-18 in atopic asthma is determined by balance of IL-18/IL-18BP/IL-18R.Journal of cellular and molecular medicine · 2018Article
- Increased Mast Cell Activation in Mongolian Gerbils Infected by Hepatitis E Virus.Frontiers in microbiology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin- (IL-) 18 and tryptase were previously reported to relate to asthma, but the correlation between these two potent proinflammatory molecules in asthma and their roles in mast cell accumulation remain uninvestigated. Using flow cytometric analysis technique and ovalbumin- (OVA-) sensitized mouse model, it was found that IL-18 and tryptase levels in the plasma of moderate and severe asthma were elevated, and they correlated well with each other. Tryptase and agonist peptides of protease activated receptor- (PAR-) 2 induced substantial quantity of IL-18 release. IL-18 and tryptase provoked mast cell accumulation in peritoneum of OVA-sensitized mice. OVA-sensitization increased number of IL-18 receptor (R)(+) mast cells. IL-18 and tryptase induced dramatic increase in IL-18R(+) mast cells and mean fluorescence intensity (MFI) of IL-18R on mast cells. Moreover, while IL-18 induced an increase in PAR-2(+) mast cells in nonsensitized mice, IL-18 and tryptase provoked increases in IL-4 and thymic stromal lymphopoietin (TSLP) in the peritoneum of OVA-sensitized mice. In summary, the correlation between IL-18 and tryptase in plasma of patients with asthma indicates close interactions between them, which should be considered for development of anti-IL-18 and antitryptase therapies. Interactions between IL-18 and tryptase may contribute to mast cell recruitment in asthma.
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