Lipopolysaccharide of Aggregatibacter actinomycetemcomitans up-regulates inflammatory cytokines, prostaglandin E2 synthesis and osteoclast formation in interleukin-1 receptor antagonist-deficient mice

2013 ◽  
Vol 48 (6) ◽  
pp. 748-756 ◽  
Author(s):  
H. Mizutani ◽  
Y. Ishihara ◽  
A. Izawa ◽  
Y. Fujihara ◽  
S. Kobayashi ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Receptor Antagonist ◽  
Inflammatory Cytokines ◽  
Interleukin 1 ◽  
Aggregatibacter Actinomycetemcomitans ◽  
Osteoclast Formation ◽  
Interleukin 1 Receptor Antagonist ◽  
Deficient Mice

scholarly journals Role of interleukin-25 in development of spontaneous arthritis in interleukin-1 receptor antagonist-deficient mice

2017 ◽  
Vol 12 ◽  
pp. 62-65
Author(s):  
Yasuharu Abe ◽  
Aya Nambu ◽  
Sachiko Yamaguchi ◽  
Ayako Takamori ◽  
Hajime Suto ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Interleukin 1 ◽  
Interleukin 1 Receptor Antagonist ◽  
Interleukin 25 ◽  
Deficient Mice

scholarly journals Toxoplasma gondii Infection Inhibits Th17-Mediated Spontaneous Development of Arthritis in Interleukin-1 Receptor Antagonist-Deficient Mice

2012 ◽  
Vol 80 (4) ◽  
pp. 1437-1444 ◽  
Author(s):  
Takuya Washino ◽  
Masataka Moroda ◽  
Yoichiro Iwakura ◽  
Fumie Aosai
Keyword(s):  
Toxoplasma Gondii ◽  
Receptor Antagonist ◽  
Th17 Cell ◽  
Interleukin 1 ◽  
Cell Polarization ◽  
Human Rheumatoid Arthritis ◽  
Th1 Cell ◽  
Content Type ◽  
Interleukin 1 Receptor Antagonist ◽  
Deficient Mice

ABSTRACTInterleukin 1 receptor antagonist (IL-1Ra)-deficient BALB/c mice develop spontaneous arthritis resembling human rheumatoid arthritis. We herein report that infection withToxoplasma gondii, an intracellular protozoan, is capable of ameliorating the spontaneous development of arthritis in IL-1Ra-deficient mice. The onset of arthritis development was delayed and the severity score of arthritis was significantly suppressed inT. gondii-infected mice. Expression of IL-12p40 mRNA from CD11c+cells of mesenteric lymph nodes (mLN) and spleen markedly increased at 1 week after peroral infection. While CD11c+cells also produced IL-10, IL-1β, and IL-6, CD4+T cells fromT. gondii-infected mice expressed significantly high levels of T-bet and gamma interferon (IFN-γ) mRNA in both mLN and spleen. Levels of GATA-3/IL-4 mRNA or RORγt/IL-17 mRNA decreased in the infected mice, indicating Th1 cell polarization and the reduction of Th2 and Th17 cell polarization. The severity of arthritis was related to Th1 cell polarization accompanied by Th17 cell reduction, demonstrating the protective role of theT. gondii-derived Th1 response against Th17 cell-mediated arthritis in IL-1Ra-deficient mice.

scholarly journals Lack of Interleukin-1 Receptor Antagonist Modulates Plaque Composition in Apolipoprotein E–Deficient Mice

2004 ◽  
Vol 24 (6) ◽  
pp. 1068-1073 ◽  
Author(s):  
Kikuo Isoda ◽  
Shojiro Sawada ◽  
Norio Ishigami ◽  
Taizo Matsuki ◽  
Koji Miyazaki ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Receptor Antagonist ◽  
Interleukin 1 ◽  
Plaque Composition ◽  
Interleukin 1 Receptor Antagonist ◽  
Deficient Mice

scholarly journals Inflammatory Bone Loss in Experimental Periodontitis Induced by Aggregatibacter actinomycetemcomitans in Interleukin-1 Receptor Antagonist Knockout Mice

2014 ◽  
Vol 82 (5) ◽  
pp. 1904-1913 ◽  
Author(s):  
A. Izawa ◽  
Y. Ishihara ◽  
H. Mizutani ◽  
S. Kobayashi ◽  
H. Goto ◽  
...  
Keyword(s):  
Bone Loss ◽  
Periodontal Disease ◽  
Receptor Antagonist ◽  
Mrna Expression ◽  
Interleukin 1 ◽  
Aggregatibacter Actinomycetemcomitans ◽  
Mrna Levels ◽  
Content Type ◽  
Interleukin 1 Receptor Antagonist ◽  
Experimental Periodontitis

ABSTRACTThe interleukin-1 receptor antagonist (IL-1Ra) binds to IL-1 receptors and inhibits IL-1 activity. However, it is not clear whether IL-1Ra plays a protective role in periodontal disease. This study was undertaken to compare experimental periodontitis induced byAggregatibacter actinomycetemcomitansin IL-1Ra knockout (KO) mice and wild-type (WT) mice. Computed tomography (CT) analysis and hematoxylin-and-eosin (H&E) and tartrate-resistant acid phosphatase (TRAP) staining were performed. In addition, osteoblasts were isolated; the mRNA expression of relevant genes was assessed by real-time quantitative PCR (qPCR); and calcification was detected by Alizarin Red staining. Infected IL-1Ra KO mice exhibited elevated (P, <0.05) levels of antibody againstA. actinomycetemcomitans, bone loss in furcation areas, and alveolar fenestrations. Moreover, protein for tumor necrosis factor alpha (TNF-α) and IL-6, mRNA for macrophage colony-stimulating factor (M-CSF), and receptor activator of NF-κB ligand (RANKL) in IL-1Ra KO mouse osteoblasts stimulated withA. actinomycetemcomitanswere increased (P, <0.05) compared to in WT mice. Alkaline phosphatase (ALP), bone sialoprotein (BSP), osteocalcin (OCN)/bone gla protein (BGP), and runt-related gene 2 (Runx2) mRNA levels were decreased (P, <0.05). IL-1α mRNA expression was increased, and calcification was not observed, in IL-1 Ra KO mouse osteoblasts. In brief, IL-1Ra deficiency promoted the expression of inflammatory cytokines beyond IL-1 and altered the expression of genes involved in bone resorption inA. actinomycetemcomitans-infected osteoblasts. Alterations consistent with rapid bone loss in infected IL-Ra KO mice were also observed for genes expressed in bone formation and calcification. In short, these data suggest that IL-1Ra may serve as a potential therapeutic drug for periodontal disease.

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