ArticleImmunity, inflammation and disease2023
Cathelicidin (LL-37) causes expression of inflammatory factors in coronary artery endothelial cells of Kawasaki disease by activating TLR4-NF-κB-NLRP3 signaling.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 14 citations in OpenAlex.
- [Mechanisms by which interleukin-18 binding protein regulates the NLRP3 inflammasome in Kawasaki disease-related coronary artery lesions].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Review
- LL-37: Biological Mechanisms and Emerging Therapeutic Applications in Intestinal Disease.Immunity, inflammation and disease · 2026Review
- NLRP3 Inflammasome Activation Mediates Coronary Artery Lesions in Kawasaki Disease by Inducing Endothelial Cells Pyroptosis and Glycocalyx Injury.Immunity, inflammation and disease · 2026Article
- [Gut-vascular axis in Kawasaki disease: short-chain fatty acid-mediated immune regulation and therapeutic targets].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Review
- LL-37 selectively targets Plasmodium-infected erythrocytes and exhibits antimalarial activity.PLoS pathogens · 2026Article
- Human pathological findings in Kawasaki disease: a narrative review of autopsy and biopsy evidence.Frontiers in immunology · 2026Review
- Role of Programmed Cell Death in the Pathogenesis of Kawasaki Disease: Mechanisms and Therapeutic Implications.Mediators of inflammation · 2026Review
- Article
- Hederasaponin C ameliorates chronic obstructive pulmonary disease pathogenesis by targeting TLR4 to inhibit NF-κB/MAPK signaling pathways.Chinese medicine · 2025Article
- Immunophenotype of Kawasaki Disease: Insights into Pathogenesis and Treatment Response.Life (Basel, Switzerland) · 2025Review
- Pyroptosis in Kawasaki disease: from mechanisms to targeted interventions.Frontiers in immunology · 2025Review
- Antimicrobial Peptide CATH-2 Attenuates Avian PathogenicInternational journal of molecular sciences · 2024Article
- [Role and mechanisms of CHI3L1 in coronary artery lesions in a mouse model of Kawasaki disease-like vasculitis].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2023Article
- Neutrophils in Inflammatory Diseases: Unraveling the Impact of Their Derived Molecules and Heterogeneity.Cells · 2023Review
- Cathelicidin (LL-37) causes expression of inflammatory factors in coronary artery endothelial cells of Kawasaki disease by activating TLR4-NF-κB-NLRP3 signaling.Immunity, inflammation and disease · 2023Article
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6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKawasaki disease (KD) is a type of vasculitis with an unidentified etiology. Cathelicidin (LL-37) may be involved in the development of the KD process; therefore, further research to investigate the molecular mechanism of LL-37 involvement in KD is warranted.
methodsEnzyme-linked immunosorbent assay (ELISA) was used to detect the levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, NLRP3, and LL-37 in the sera of healthy subjects, children with KD, and children with pneumonia. Subsequently, human recombinant LL-37 or/and toll-like receptors 4 (TLR4)-specific inhibitor TAK-242 stimulated human coronary artery endothelial cells (HCAECs), CCK-8 was used to detect cell proliferation, flow cytometry to detect apoptosis, transmission electron microscopy to observe cytoskeletal changes, Transwell to measure cell migration ability, ELISA to detect inflammatory factor levels, Western blot analysis to analyze protein levels of toll-like receptors 4 (TLR4) and NF-κB p-65, and quantitative real-time polymerase chain reaction (qRT-PCR) to determine LL-37, NLRP3 mRNA levels.
resultsIn this study, we found that the level of LL-37 was highly expressed in the serum of children with KD, and after LL-37 stimulation, apoptosis was significantly increased in HCAECs, and the expression levels of TLR4, NLRP3 and inflammatory factors in cells were significantly enhanced. Intervention with the TLR4-specific inhibitor TAK-242 significantly alleviated the LL-37 effects on cellular inflammation, TLR4, NLRP3 promotion effect.
conclusionsOur data suggest that LL-37 induces an inflammatory response in KD coronary endothelial cells via TLR4-NF-κB-NLRP3, providing a potential target for the treatment of KD.
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