関: IL-1 beta

WordNet

any of several lymphokines that promote macrophages and killer T cells and B cells and other components of the immune system

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1. 周期性発熱症候群およびその他の自己炎症性疾患：概要 periodic fever syndromes and other autoinflammatory diseases an overview
2. 心血管疾患と同等のリスクと確立した危険因子の概要 overview of the risk equivalents and established risk factors for cardiovascular disease
3. クリオピリン関連周期性発熱症候群および関連疾患 cryopyrin associated periodic syndromes and related disorders
4. 肥満細胞：表面受容体とシグナル伝達 mast cells surface receptors and signal transduction
5. 高IgD症候群：マネージメント hyperimmunoglobulin d syndrome management

English Journal

Toxicity and bio-accumulation of inhaled cerium oxide nanoparticles in CD1 mice.

Aalapati S, Ganapathy S, Manapuram S, Anumolu G, Prakya BM.Author information Department of Toxicology, International Institute of Biotechnology and Toxicology [IIBAT] , Chennai , India.AbstractMale CD1 mice were subjected to nose-inhalation exposure of CeO2 nanoparticles (NPs) for 0, 7, 14 or 28 days with 14 or 28 days of recovery time at an aerosol concentration of 2 mg/m(3). Markers of lung injury and pro-inflammatory cytokines (interleukin-1beta, tumour necrosis factor-alpha, interleukin-6 and macrophage inflammatory protein-2) in bronchoalveolar lavage fluid (BALF), oxidative stress in lungs, bio-accumulation, and histopathology of pulmonary and extrapulmonary tissues were assessed. BALF analysis revealed the induction of pulmonary inflammation, as evident by an increase in the influx of neutrophils with a significant secretion of pro-inflammatory cytokines that lead to generation of oxidative stress and cytotoxicity, as is evident by induction of lipid peroxidation, depletion of glutathione and increased BALF lactate dehydrogenase and protein. The histopathological examination revealed that these inhaled CeO2 NPs were located all over the pulmonary parenchyma, inducing a severe, chronic, active inflammatory response characterised by necrosis, proteinosis, fibrosis and well-formed discrete granulomas in the pulmonary tissue and tubular degeneration leading to coagulative necrosis in kidneys. Inductively coupled plasma optical emission spectrometer results showed a significant bio-accumulation of these particles in the pulmonary and extrapulmonary tissues, even after one month of post-inhalation exposure. Together, these findings suggest that inhalation exposure of CeO2 NPs can induce pulmonary and extrapulmonary toxicity.
Nanotoxicology.Nanotoxicology.2014 Nov;8(7):786-98. doi: 10.3109/17435390.2013.829877. Epub 2013 Aug 22.
Male CD1 mice were subjected to nose-inhalation exposure of CeO2 nanoparticles (NPs) for 0, 7, 14 or 28 days with 14 or 28 days of recovery time at an aerosol concentration of 2 mg/m(3). Markers of lung injury and pro-inflammatory cytokines (interleukin-1beta, tumour necrosis factor-alpha, interleuk
PMID 23914771

Peptides in pepsin-pancreatin hydrolysates from commercially available soy products that inhibit lipopolysaccharide-induced inflammation in macrophages.

Dia VP1, Bringe NA2, de Mejia EG3.Author information 1University of Illinois, Urbana-Champaign, 1201 West Gregory Drive, Urbana, IL 61801, USA.2The WhiteWave Foods Company, 12002 Airport Way, Broomfield, CO 80021, USA.3University of Illinois, Urbana-Champaign, 1201 West Gregory Drive, Urbana, IL 61801, USA. Electronic address: edemejia@illinois.edu.AbstractThe potential of pepsin-pancreatin hydrolysates, from different foods, to inhibit inflammation using lipopolysaccharide (LPS)-induced RAW 264.7 macrophages as an in vitro model was evaluated. Eight different products were digested sequentially with pepsin and pancreatin and were evaluated for their anti-inflammatory properties. Hydrolysates from strawberry-banana soymilk (SBH), mixed berry soymilk (MXH) and vanilla soymilk (SVMH) inhibited the production of nitric oxide (27.9%, 16.4% and 28.6%, respectively), interleukin-1β (26.3%, 39.5% and 21.6%, respectively) and tumour necrosis factor-α (50.2%, 47.5% and 33.3%, respectively). In addition, SBH, MXH and SVMH inhibited the expression of pro-inflammatory enzymes: inducible nitric oxide synthase (66.7%, 65.1% and 88.0%, respectively) and cyclooxygenase-2 (62.0%, 69.9% and 40.6%, respectively). Bioactive peptides (RQRK and VIK) were generated. In conclusion, soymilk products can potentially be used to maintain health under inflammatory stress.
Food chemistry.Food Chem.2014 Jun 1;152:423-31. doi: 10.1016/j.foodchem.2013.11.155. Epub 2013 Dec 4.
The potential of pepsin-pancreatin hydrolysates, from different foods, to inhibit inflammation using lipopolysaccharide (LPS)-induced RAW 264.7 macrophages as an in vitro model was evaluated. Eight different products were digested sequentially with pepsin and pancreatin and were evaluated for their
PMID 24444957

Development of a mouse model mimicking key aspects of a viral asthma exacerbation.

Clarke DL, Davis NH, Majithiya JB, Piper SC, Lewis A, Sleeman MA, Corkill DJ, May RD.Author information *Department of Respiratory, Inflammation and Autoimmunity, MedImmune, Granta Park, Cambridge CB21 6GH, U.K.AbstractViral respiratory tract infections are known triggers of asthma exacerbations in both adults and children. The current standard of care, inhaled CS (corticosteroids) and LABAs (long-acting β2-adrenoceptor agonists), fails to prevent the loss of control that manifests as an exacerbation. In order to better understand the mechanisms underlying viral asthma exacerbations we established an in vivo model using the clinically relevant aeroallergen HDM (house dust mite) and the viral mimetic/TLR3 (Toll-like receptor 3) agonist poly(I:C). Poly(I:C) alone induced a similar neutrophilic inflammatory profile in the BAL (bronchoalveolar lavage) to that of HRV1b (human rhinovirus 1b) alone, accompanied by both elevated BAL KC (keratinocyte-derived chemokine) and IL-1β (interleukin-1β). When mice allergic to HDM were also challenged with poly(I:C) the neutrophilic inflammatory profile was exacerbated. Increased CD8+ T-cell numbers, increased CD4+ and CD8+ cell activation and elevated KC and IL-1β were observed. No increases in Th2 cytokines or the eosinophil chemoattractant CCL11 [chemokine (C-C motif) ligand 11], above those induced by HDM alone, were observed. The poly(I:C)-exacerbated neutrophilia did not translate into changes in AHR (airways hyper-responsiveness), indicating that in this model inflammation and AHR are two mechanistically independent events. To test the clinical relevance of this model CS sensitivity was assessed using prednisone, a synthetic oral CS used to manage exacerbations in asthmatic patients already on maximal doses of inhaled CS. The increased neutrophils, and accompanying cytokines/chemokines KC and IL-1β induced by poly(I:C) challenge of HDM-sensitized and challenged mice were insensitive to oral prednisone therapy. In summary we have described a CS-resistant mouse model mimicking the key aspects of viral asthma exacerbation using the clinically relevant aeroallergen HDM and the viral mimic poly(I:C). This model may provide better understanding of disease mechanisms underlying viral exacerbations and could be used to build early confidence in novel therapeutic axes targeting viral asthma exacerbations in Th2 asthmatics.
Clinical science (London, England : 1979).Clin Sci (Lond).2014 Apr 1;126(8):567-80. doi: 10.1042/CS20130149.
Viral respiratory tract infections are known triggers of asthma exacerbations in both adults and children. The current standard of care, inhaled CS (corticosteroids) and LABAs (long-acting β2-adrenoceptor agonists), fails to prevent the loss of control that manifests as an exacerbation. In order to
PMID 24152048

Japanese Journal

Orthodontic force, tooth movement, and interleukin-1β

北海道歯学雑誌 38(Special issue), 20-27, 2017-09
NAID 120006360105

Effects of bodybuilding and protein supplements in saliva, gingival crevicular fluid, and serum

Ｊｏｕｒｎａｌ　ｏｆ　Ｏｒａｌ　Ｓｃｉｅｎｃｅ 59(1), 121-130, 2017
NAID 130005519748

Cytokines Levels in Peri-Implant Crevicular Fluid in the Intial Stages of Dental Implant Treatments - A Preliminary Clinical Study

Journal of Oral Tissue Engineering 14(1), 2-8, 2016
NAID 130005277134

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★リンクテーブル★

リンク元	「IL-1 beta」「インターロイキン1β」
拡張検索	「interleukin-1beta converting enzyme」
関連記事	「interleukin」「interleukins」