Dectin-1/Syk signaling is involved in Lactobacillus casei cell wall extract-induced mouse model of Kawasaki disease

Lin, I-Chun; Suen, Jau‐Ling; Huang, Shau‐Ku; Huang, Shun‐Chen; Huang, Hsin‐Chun; Kuo, Ho‐Chang; Wei, Chi-Chen; Wang, Feng-Shen; Yu, Hong‐Ren; Yang, Kuender D.

doi:10.1016/j.imbio.2012.04.004

Cited by 22 publications

(21 citation statements)

References 44 publications

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“…In Lactobacillus casei cell wall extract-induced coronary arteritis, toll-like receptor-2 and Dectin-1 are reported to trigger the pathogenesis. 30,31 Dectin-2 might be responsible for Candida albicans watersoluble fraction-induced KD, as Dectin-2 mediates the production of proinflammatory cytokines in response to Candida albicans water-soluble fraction. 32 It will be intriguing to investigate whether cardiac CD11c + macrophages also contribute to pathogenesis in other KD models that are triggered through these pattern recognition receptors.…”

Section: Discussionmentioning

confidence: 99%

Identification of Pathogenic Cardiac CD11c ⁺ Macrophages in Nod1-Mediated Acute Coronary Arteritis

Motomura

Kanno

Asano

et al. 2015

ATVB

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Objective— Nod1 is an intracellular pattern recognition receptor for bacterial peptidoglycan fragments. We previously reported that a synthetic Nod1 ligand, FK565, induced acute coronary arteritis in mice similar to that of Kawasaki disease. However, the molecular mechanisms underlying this characteristic inflammation have remained elusive. Approach and Results— We found that CD11c + MHC class II + cells accumulated in the heart of FK565-treated mice before arteritis development. Morphological features and gene expression signatures of the cardiac CD11c + MHC class II + cells suggested that this population is closely related to macrophages, and thus, we designated them cardiac CD11c + macrophages. Nod1 in nonhematopoietic cells, rather than hematopoietic cells, was required for the increase of cardiac CD11c + macrophages and arteritis development. Among nonhematopoietic cells, cardiac endothelial cells produced a large amount of chemokines in response to FK565. Endothelial cell–specific blockade of Nod1 signaling suppressed FK565-induced expression of these chemokines, accumulation of cardiac CD11c + macrophages, and subsequent coronary arteritis development. We also found that CCR2 + Ly6C hi inflammatory monocytes in peripheral blood supplied precursors of cardiac CD11c + macrophages. CCR2-deficient mice or pertussis toxin–treated mice exhibited decreased numbers of cardiac CD11c + macrophages and reduced arteritis. Conclusions— These results suggest that Ly6C hi monocytes are recruited to FK565-activated endothelial cells to generate cardiac CD11c + macrophages, which play a pivotal role in the pathogenesis of acute coronary arteritis.

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Section: Discussionmentioning

confidence: 99%

Identification of Pathogenic Cardiac CD11c ⁺ Macrophages in Nod1-Mediated Acute Coronary Arteritis

Motomura

Kanno

Asano

et al. 2015

ATVB

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“…Additionally, we demonstrated that LCWE-treated mice had continuing increases in aortic IL-6 mRNA expression from days 3 to 14, reflecting pathologic disease progression from no obvious infiltrates to massive inflammatory infiltrates; furthermore, their aortic TNF-α mRNA reached maximum levels on the seventh day after LCWE injection. 25 Aortic VEGF-A mRNA levels showed an early positive and a late negative relationship with the IL-6 mRNA level; this finding might be attributable to the differential involvement of VEGF-A in different stage of CALs. IL-6 is a pro-fibrotic regulatory factor, mediating cardiac fibrosis in response to angiotensin II infusion.…”

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confidence: 85%

“…32 For in vivo arteritis-ameliorated experiments, BAY 61-3606 hydrochloride hydrate (BAY, a specific Syk inhibitor; SigmaAldrich) was administrated as previously prescribed. 25 In the BAY-treated (BAY+LCWE) group, the severity of the arteritis was significantly reduced. 25 Several organs, including the aortic roots and ventricular myocardial, as well as the liver, kidneys, lungs, spleen, and peripheral blood leukocytes (PBLs), were extracted from mice at indicated time-points post-injection for further experiments.…”

Section: Mice and A Mouse Model Of Coronary Arteritismentioning

confidence: 99%

“…25 LPS was reported to cause no induction of CALs in mice. 32 For in vivo arteritis-ameliorated experiments, BAY 61-3606 hydrochloride hydrate (BAY, a specific Syk inhibitor; SigmaAldrich) was administrated as previously prescribed.…”

Section: Mice and A Mouse Model Of Coronary Arteritismentioning

confidence: 99%

“…25 All blots were incubated overnight at 4°C with each of the following Abs: a mouse monoclonal Ab for VEGF-A (Santa Cruz Biotechnology, Inc, San Diego, CA, USA) and for endothelial nitric oxide synthase (eNOS) (Transduction Laboratories, Lexington, KY, USA), the rat anti-mouse Abs for tumor necrosis factor (TNF)-α and IL-6 (BioLegend, Inc, San Diego, CA, USA), and a goat polyclonal Ab for dimethylarginine dimethylaminohydrolase (DDAH)-1 (Santa Cruz Biotechnology) and for DDAH-2 (Santa Cruz Biotechnology). Next, the blots were washed with tris-buffered saline with tween 20, incubated with horseradish peroxidase-coupled goat anti-mouse IgG for VEGF-A and eNOS, goat anti-rat IgG for TNF-α and IL-6, and donkey anti-goat IgG for DDAH-1 and DDAH-2, at room temperature for 1 h, then developed using enhanced chemiluminescent detection (Amersham Pharmacia Biotech, Uppsala, Sweden), and finally exposed to film.…”

Section: Western Blot Analysismentioning

confidence: 99%

See 2 more Smart Citations

Vascular Endothelial Growth Factor-A in <i>Lactobacillus Casei </i>Cell Wall Extract-Induced Coronary Arteritis of a Murine Model

Lin

Sheen

Tain

et al. 2014

Circ J

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Cardiac involvement in primary systemic vasculitis and potential drug therapies to reduce cardiovascular risk

Misra

Shenoy

2016

Rheumatol Int

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Cardiac involvement is common in primary systemic vasculitides and may be due to direct effect of the disease on the heart or due to therapy. We shall review involvement of the heart in the various forms of primary systemic vasculitis. Among anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV), eosinophilic granulomatosis with polyangiitis most commonly involves the heart. Involvement of the heart confers poorer prognosis in AAV, which is also complicated by increased risk of cardiovascular events. Kawasaki's disease (KD) is the most common form of medium-vessel vasculitis to affect the heart, with coronary artery aneurysms being the most common manifestation. These predispose patients with KD to develop premature ischemic heart disease. Takayasu's arteritis is the most common large-vessel vasculitis to involve the heart and can result in aortic incompetence, myocarditis, or coronary heart disease. Involvement of the heart in Behcet's disease is usually in the form of intracardiac mass lesions, thrombosis, or endomyocardial fibrosis. Drugs used in the treatment of systemic vasculitis influence the risk of developing cardiovascular events. Corticosteroid therapy has been shown to increase the risk of myocardial infarction, whereas methotrexate, azathioprine, mycophenolate mofetil, rituximab, and anti-tumor necrosis alpha agents favorably modulate the risk of cardiovascular events, predominantly by dampening systemic inflammation. Awareness of cardiac involvement in vasculitis and accelerated cardiovascular risk in these patients should help clinicians to maximize the modulation of modifiable risk factors for heart disease in these individuals.

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Dectin-1/Syk signaling is involved in Lactobacillus casei cell wall extract-induced mouse model of Kawasaki disease

Cited by 22 publications

References 44 publications

Identification of Pathogenic Cardiac CD11c ⁺ Macrophages in Nod1-Mediated Acute Coronary Arteritis

Identification of Pathogenic Cardiac CD11c ⁺ Macrophages in Nod1-Mediated Acute Coronary Arteritis

Vascular Endothelial Growth Factor-A in <i>Lactobacillus Casei </i>Cell Wall Extract-Induced Coronary Arteritis of a Murine Model

Cardiac involvement in primary systemic vasculitis and potential drug therapies to reduce cardiovascular risk

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Dectin-1/Syk signaling is involved in Lactobacillus casei cell wall extract-induced mouse model of Kawasaki disease

Cited by 22 publications

References 44 publications

Identification of Pathogenic Cardiac CD11c + Macrophages in Nod1-Mediated Acute Coronary Arteritis

Identification of Pathogenic Cardiac CD11c + Macrophages in Nod1-Mediated Acute Coronary Arteritis

Vascular Endothelial Growth Factor-A in <i>Lactobacillus Casei </i>Cell Wall Extract-Induced Coronary Arteritis of a Murine Model

Cardiac involvement in primary systemic vasculitis and potential drug therapies to reduce cardiovascular risk

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Product

Resources

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Identification of Pathogenic Cardiac CD11c ⁺ Macrophages in Nod1-Mediated Acute Coronary Arteritis

Identification of Pathogenic Cardiac CD11c ⁺ Macrophages in Nod1-Mediated Acute Coronary Arteritis