ArticlePloS one2012
Augmented TLR2 expression on monocytes in both human Kawasaki disease and a mouse model of coronary arteritis.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
- Combination of S100A12/TLR2 signaling molecules and clinical indicators in a new predictive model for IVIG-resistant Kawasaki disease.Scientific reports · 2024Article
- Involvement of IL-17 A/IL-17 Receptor A with Neutrophil Recruitment and the Severity of Coronary Arteritis in Kawasaki Disease.Journal of clinical immunology · 2024Article
- CD14 down-modulation as a real-time biomarker in Kawasaki disease.Clinical & translational immunology · 2024Article
- A machine learning model for distinguishing Kawasaki disease from sepsis.Scientific reports · 2023Article
- From Co-Infections to Autoimmune Disease via Hyperactivated Innate Immunity: COVID-19 Autoimmune Coagulopathies, Autoimmune Myocarditis and Multisystem Inflammatory Syndrome in Children.International journal of molecular sciences · 2023Review
- G0S2 regulates innate immunity in Kawasaki disease via lncRNA HSD11B1-AS1.Pediatric research · 2022Article
- Prenatal and early life exposure to air pollution and the incidence of Kawasaki disease.Scientific reports · 2022Article
- Exploration of Potential Biomarker Genes and Pathways in Kawasaki Disease: An IntegratedFrontiers in genetics · 2022Article
- CD36 is Associated With the Development of Coronary Artery Lesions in Patients With Kawasaki Disease.Frontiers in immunology · 2022Article
- Profile of Urinary Cytokines in Kawasaki Disease: Non-Invasive Markers.Diagnostics (Basel, Switzerland) · 2021Article
- Higher senescence associated secretory phenotype and lower defense mediator in urinary extracellular vesicles of elders with and without Parkinson disease.Scientific reports · 2021Article
- Inhibition of IL-6 in the LCWE Mouse Model of Kawasaki Disease Inhibits Acute Phase Reactant Serum Amyloid A but Fails to Attenuate Vasculitis.Frontiers in immunology · 2021Article
- Epigenetics in Kawasaki Disease.Frontiers in pediatrics · 2021Review
- Increased Risk of Kawasaki Disease in Infants Born of Mothers With Immune Disorders.Frontiers in pediatrics · 2021Article
- A novel score system of blood tests for differentiating Kawasaki disease from febrile children.PloS one · 2021Article
- Epigenetic Regulation of Macrophage Marker Expression Profiles in Kawasaki Disease.Frontiers in pediatrics · 2020Article
- How toll-like receptors reveal monocyte plasticity: the cutting edge of antiinflammatory therapy.Cellular and molecular life sciences : CMLS · 2019Review
- Association of Toll-like receptor 2-positive monocytes with coronary artery lesions and treatment nonresponse in Kawasaki disease.Korean journal of pediatrics · 2017Article
- Tocilizumab reverses cerebral vasculopathy in a patient with homozygous SAMHD1 mutation.Clinical rheumatology · 2017Review
- Identifying genetic hypomethylation and upregulation of Toll-like receptors in Kawasaki disease.Oncotarget · 2017Article
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKawasaki disease (KD) of unknown immunopathogenesis is an acute febrile systemic vasculitis and the leading cause of acquired heart diseases in childhood. To search for a better strategy for the prevention and treatment of KD, this study compared and validated human KD immunopathogenesis in a mouse model of Lactobacillus casei cell wall extract (LCWE)-induced coronary arteritis.
methodsRecruited subjects fulfilled the criteria of KD and were admitted for intravenous gamma globulin (IVIG) treatment at the Kaohsiung Chang Gung Memorial Hospital from 2001 to 2009. Blood samples from KD patients were collected before and after IVIG treatment, and cardiovascular abnormalities were examined by transthoracic echocardiography. Wild-type male BALB/c mice (4-week-old) were intraperitoneally injected with LCWE (1 mg/mL) to induce coronary arteritis. The induced immune response in mice was examined on days 1, 3, 7, and 14 post injections, and histopathology studies were performed on days 7 and 14.
resultsBoth human KD patients and LCWE-treated mice developed coronary arteritis, myocarditis, valvulitis, and pericarditis, as well as elevated plasma levels of interleukin (IL)-2, IL-6, IL-10, monocyte chemoattractant protein (MCP)-1, and tumor necrosis factor (TNF)-α in acute phase. Most of these proinflammatory cytokines declined to normal levels in mice, whereas normal levels were achieved in patients only after IVIG treatment, with a few exceptions. Toll-like receptor (TLR)-2, but not TLR4 surface enhancement on circulating CD14+ monocytes, was augmented in KD patients before IVIG treatment and in LCWE-treated mice, which declined in patients after IVIG treatment.
conclusionThis result suggests that that not only TLR2 augmentation on CD14+ monocytes might be an inflammatory marker for both human KD patients and LCWE-induced CAL mouse model but also this model is feasible for studying therapeutic strategies of coronary arteritis in human KD by modulating TLR2-mediated immune activation on CD14+ monocytes.
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