Serum IP-10 and IL-17 from Kawasaki disease patients induce calcification-related genes and proteins in human coronary artery smooth muscle cells in vitro

Chang, Shun‐Fu; Liu, Shih-Feng; Chen, Cheng‐Nan; Kuo, Ho-Chang

doi:10.1186/s13578-020-00400-8

Cited by 12 publications

(7 citation statements)

References 47 publications

(82 reference statements)

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“…HCASMCs treated with CXCL10 and IL-17 developed a phenotype that could promote vascular calcification in a path similar to the bone morphogenetic protein (BMP) 6 autocrine pathway. Furthermore, the BMP6 autocrine stimulation in CXCL10 and IL-17-treated HCASMCs could up regulate the activation of smad1/five-runx2 signaling and increase the bone matrix-related proteins including the osteopontin, osteocalcin and alkaline levels [80]. Lupieri and co-workers [81] demonstrated an unexpected cellular cross-communication in the arterial endothelial cells where a phosphatidylinositide 3-kinase (PD3K)-dependent T cell response resulted in CXCL10 production by smooth muscle cells inhibiting endothelial repairs.…”

Section: Mechanism Of the Cxcl10 Action In Cadmentioning

confidence: 99%

“…Zuojun and co-workers demonstrated that CXCL10 plays an important role in intimal hyperplasia as siRNA-mediated CXCL10 silencing inhibited aberrant VSMC hyperplasia and reduced restenosis in atherosclerotic patients [78,79]. In vitro studies of human coronary artery smooth muscle cells (HCASMCs) performed by Chang [80] showed a functional role for plasma-circulating CXCL10 and IL-17 in the development of vascular calcification and revealed its underlying mechanism in cardiovascular disease. HCASMCs treated with CXCL10 and IL-17 developed a phenotype that could promote vascular calcification in a path similar to the bone morphogenetic protein (BMP) 6 autocrine pathway.…”

Section: Mechanism Of the Cxcl10 Action In Cadmentioning

confidence: 99%

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The Involvement of CXC Motif Chemokine Ligand 10 (CXCL10) and Its Related Chemokines in the Pathogenesis of Coronary Artery Disease and in the COVID-19 Vaccination: A Narrative Review

et al. 2021

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Coronary artery disease (CAD) and coronary heart disease (CHD) constitute two of the leading causes of death in Europe, USA and the rest of the world. According to the latest reports of the Iranian National Health Ministry, CAD is the main cause of death in Iranian patients with an age over 35 years despite a significant reduction in mortality due to early interventional treatments in the context of an acute coronary syndrome (ACS). Inflammation plays a fundamental role in coronary atherogenesis, atherosclerotic plaque formation, acute coronary thrombosis and CAD establishment. Chemokines are well-recognized mediators of inflammation involved in several bio-functions such as leucocyte migration in response to inflammatory signals and oxidative vascular injury. Different chemokines serve as chemo-attractants for a wide variety of cell types including immune cells. CXC motif chemokine ligand 10 (CXCL10), also known as interferon gamma-induced protein 10 (IP-10/CXLC10), is a chemokine with inflammatory features whereas CXC chemokine receptor 3 (CXCR3) serves as a shared receptor for CXCL9, 10 and 11. These chemokines mediate immune responses through the activation and recruitment of leukocytes, eosinophils, monocytes and natural killer (NK) cells. CXCL10, interleukin (IL-15) and interferon (IFN-g) are increased after a COVID-19 vaccination with a BNT162b2 mRNA (Pfizer/BioNTech) vaccine and are enriched by tumor necrosis factor alpha (TNF-α) and IL-6 after the second vaccination. The aim of the present study is the presentation of the elucidation of the crucial role of CXCL10 in the patho-physiology and pathogenesis of CAD and in identifying markers associated with the vaccination resulting in antibody development.

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Section: Mechanism Of the Cxcl10 Action In Cadmentioning

confidence: 99%

Section: Mechanism Of the Cxcl10 Action In Cadmentioning

confidence: 99%

The Involvement of CXC Motif Chemokine Ligand 10 (CXCL10) and Its Related Chemokines in the Pathogenesis of Coronary Artery Disease and in the COVID-19 Vaccination: A Narrative Review

et al. 2021

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“…This is reminiscent of the Toxic Shock (TSS) -Kawasaki syndrome phenotype currently being considered as PMIS/MIS-C syndrome (35)(36)(37)(38)(39). Similar to TSS and Kawasaki's, our PedSep-C patients showed elevated IL-17a and IP10/CXCL10 levels (40)(41)(42).…”

Section: Discussionmentioning

confidence: 59%

Derivation of four computable 24-hour pediatric sepsis phenotypes to facilitate personalized enrollment in early precise anti-inflammatory clinical trials

Qin

Kernan

Fan

et al. 2021

Preprint

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Objective: Thrombotic microangiopathy induced Thrombocytopenia Associated Multiple Organ Failure and hyperinflammatory Macrophage Activation Syndrome are important causes of late pediatric sepsis mortality that are often missed or have delayed diagnosis. Our objective is to derive computable 24-hour sepsis phenotypes to facilitate enrollment in early precise anti-inflammatory trials targeting mortality from these conditions. Design: Machine learning analysis using consensus k-means clustering. Setting: Nine pediatric intensive care units. Patients: 404 children with severe sepsis. Interventions: 24-hour computable phenotypes derived using 25 bedside variables including C-reactive protein and ferritin. Measurements and Main Results: Four computable phenotypes (PedSep-A, B, C, and D) are derived. Compared to the overall population mean, PedSep-A has the least inflammation (median C-reactive protein 7.3 mg/dL, ferritin 125 ng/mL), younger age, less chronic illness, and respiratory failure (n = 135; 2% mortality); PedSep-B (median C-reactive protein 13.2 mg/dL, ferritin 225 ng/ mL) has multiple organ failure with intubated respiratory failure, shock, and Glasgow Coma Scale score < 7 (n = 102, 12% mortality); PedSep-C has elevated ferritin (median C-reactive protein 15.2 mg/dL, ferritin 405 ng/mL), lymphopenia, shock, and relative absence of intubation (n = 110; mortality 10%); and, PedSep D has hyperferritinemic (median C-reactive protein 13.1 mg/dL ferritin 610 ng/mL), thrombocytopenic multiple organ failure with more cardiovascular, hepatic, renal, hematologic, and central nervous system failures (n = 56, 34% mortality). PedSep-D has highest likelihood of Thrombocytopenia Associated Multiple Organ Failure (Adj OR 47.51 95% CI [18.83-136.83], p < 0.0001) and Macrophage Activation Syndrome (Adj OR 38.63 95% CI [13.26-137.75], p <0.0001), and shows a survival interaction with combined methylprednisolone and intravenous immunoglobulin therapy (p < 0.05). CONCLUSIONS AND RELEVANCE: Four machine learning computable phenotypes are identified (www.pedsepsis.pitt.edu). Membership in PedSep-D appears optimal for enrollment in early anti-inflammatory trials targeting Thrombocytopenia Associated Multiple Organ Failure and Macrophage Activation Syndrome.

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“…KD is acute, systemic, nonspeci c, self-limiting vasculitis. Its adverse effects depend mainly on the incidence of CALs, including coronary artery dilation, coronary aneurysm, thrombosis, myocardial ischemia, and even sudden death [7,8]. Intravenous immunoglobulin (IVIG) is one of the rst-line drugs used to treat KD.…”

Section: Discussionmentioning

confidence: 99%

“…It exerted a recruiting and chemotactic effect on T cells in autoimmune diseases and aggregated the corresponding T cells to target organs, causing tissue and organ damage [19]. IP-10/IL-17 secreted from the plasma of pediatric patients with KD acted on the calci cation of human coronary artery smooth muscle cells (HCASMCs); IL-17 might also interact with IFN-g to enhance the production of IP-10 [8]. Thus, it was inferred that IP-10 and IL-17A cooperatively in uenced the CALs in KD.…”

Section: Discussionmentioning

confidence: 99%

Impact factors for refractory KD and comparison of different treatment protocols

Wu¹,

Chen²,

Zhong³

et al. 2020

Preprint

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Background Intravenous immunoglobulin (IVIG) has been widely accepted as a standard treatment against Kawasaki disease (KD). About 20% of patients are nonresponsive after the first IVIG treatment.This study was performed to reveal the responsiveness, mechanism of action, and incidence rate of coronary artery lesions in the long-term follow-up visit of action of IVIG combined with glucocorticoids in the treatment of refractory KD. Method: A total of 633 pediatric patients with KD (experimental group) and 200 pediatric patients with upper respiratory infection hospitalized during the same period (control group) were retrospective selected. KD was treated with IVIG combined with aspirin.IVIG-nonresponsive group was given the second treatment.Protocol 1 group was administered 1 g/kg IVIG; Protocol 2 group was administered 2 g/kg IVIG; and Protocol 3 group was administered 1 g/kg IVIG + glucocorticoid (GC). Following the second treatment, the responsive group (Group A) and nonresponsive group (Group B) were classified based on whether the temperature was reduced to normal. Results IVIG-nonresponsive group had more coronary artery lesions, longer time of first application of IVIG, and higher WBC count, ESR, CRP, and higher serum levels of Meprin A, IL-1β, IL-6, IL-17A, and IP-10. Protocol 3 group was found with faster abatement of fever, higher response rate, and fewer CALs. The serum levels of Meprin A, IL-1β, and IL-17A in Group B were higher, and the incidence rate of CAL after treatment was up to 78.9% . Conclusions The levels of Meprin A, IL-17A, and IL-1β may serve as potentially good indexes to predict refractory KD. IVIG combined with GC to treat refractory KD is more advantageous compared with IVIG alone.

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Serum IP-10 and IL-17 from Kawasaki disease patients induce calcification-related genes and proteins in human coronary artery smooth muscle cells in vitro

Cited by 12 publications

References 47 publications

The Involvement of CXC Motif Chemokine Ligand 10 (CXCL10) and Its Related Chemokines in the Pathogenesis of Coronary Artery Disease and in the COVID-19 Vaccination: A Narrative Review

The Involvement of CXC Motif Chemokine Ligand 10 (CXCL10) and Its Related Chemokines in the Pathogenesis of Coronary Artery Disease and in the COVID-19 Vaccination: A Narrative Review

Derivation of four computable 24-hour pediatric sepsis phenotypes to facilitate personalized enrollment in early precise anti-inflammatory clinical trials

Impact factors for refractory KD and comparison of different treatment protocols

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