WordNet

a process in which individuals (or small groups) penetrate an area (especially the military penetration of enemy positions without detection)
the chief phagocytic leukocyte; stains with either basic or acid dyes (同)neutrophile

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浸透 / 侵入,潜入

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1. 好中球機能異常症の検査での評価 laboratory evaluation of neutrophil disorders
2. 顆粒球輸血 granulocyte transfusions
3. 好中球二次顆粒欠損症 neutrophil specific granule deficiency
4. 貧血を有する成人患者に対するアプローチ approach to the adult patient with anemia
5. アルコール性肝疾患の病因 pathogenesis of alcoholic liver disease

English Journal

Altered leukotriene B4 metabolism in CYP4F18-deficient mice does not impact inflammation following renal ischemia.

Winslow V1, Vaivoda R1, Vasilyev A1, Dombkowski D2, Douaidy K1, Stark C1, Drake J3, Guilliams E3, Choudhary D4, Preffer F2, Stoilov I4, Christmas P5.Author information 1Nephrology Division, Department of Medicine, Massachusetts General Hospital, Charlestown, MA 02129, USA.2Department of Pathology, Massachusetts General Hospital, Boston, MA 02114, USA.3Biology Department, Radford University, Radford, VA 24142, USA.4Department of Surgery, University of Connecticut Health Center, Farmington, CT 06030, USA.5Nephrology Division, Department of Medicine, Massachusetts General Hospital, Charlestown, MA 02129, USA; Biology Department, Radford University, Radford, VA 24142, USA. Electronic address: pchristma2@radford.edu.AbstractInflammatory responses to infection and injury must be restrained and negatively regulated to minimize damage to host tissue. One proposed mechanism involves enzymatic inactivation of the pro-inflammatory mediator leukotriene B4, but it is difficult to dissect the roles of various metabolic enzymes and pathways. A primary candidate for a regulatory pathway is omega oxidation of leukotriene B4 in neutrophils, presumptively by CYP4F3A in humans and CYP4F18 in mice. This pathway generates ω, ω-1, and ω-2 hydroxylated products of leukotriene B4, depending on species. We created mouse models targeting exons 8 and 9 of the Cyp4f18 allele that allows both conventional and conditional knockouts of Cyp4f18. Neutrophils from wild-type mice convert leukotriene B4 to 19-hydroxy leukotriene B4, and to a lesser extent 18-hydroxy leukotriene B4, whereas these products were not detected in neutrophils from conventional Cyp4f18 knockouts. A mouse model of renal ischemia-reperfusion injury was used to investigate the consequences of loss of CYP4F18 in vivo. There were no significant changes in infiltration of neutrophils and other leukocytes into kidney tissue as determined by flow cytometry and immunohistochemistry, or renal injury as assessed by histological scoring and measurement of blood urea nitrogen. It is concluded that CYP4F18 is necessary for omega oxidation of leukotriene B4 in neutrophils, and is not compensated by other CYP enzymes, but loss of this metabolic pathway is not sufficient to impact inflammation and injury following renal ischemia-reperfusion in mice.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 Jun;1841(6):868-79. doi: 10.1016/j.bbalip.2014.03.002. Epub 2014 Mar 14.
Inflammatory responses to infection and injury must be restrained and negatively regulated to minimize damage to host tissue. One proposed mechanism involves enzymatic inactivation of the pro-inflammatory mediator leukotriene B4, but it is difficult to dissect the roles of various metabolic enzymes
PMID 24632148

Interleukin-37 ameliorates myocardial ischaemia/reperfusion injury in mice.

Wu B1, Meng K, Ji Q, Cheng M, Yu K, Zhao X, Tony H, Liu Y, Zhou Y, Chang C, Zhong Y, Zhu Z, Zhang W, Mao X, Zeng Q.Author information 1The Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.AbstractInnate immune and inflammatory responses are involved in myocardial ischaemia/reperfusion (I/R) injury. Interleukin (IL)-37 is a newly identified member of the IL-1 family, and functions as a fundamental inhibitor of innate immunity and inflammation. However, its role in myocardial I/R injury remains unknown. I/R or sham operations were performed on male C57BL/6J mice. I/R mice received an injection of recombinant human IL-37 or vehicle, immediately before reperfusion. Compared with vehicle treatment, mice treated with IL-37 showed an obvious amelioration of the I/R injury, as demonstrated by reduced infarct size, decreased cardiac troponin T level and improved cardiac function. This protective effect was associated with the ability of IL-37 to suppress production of proinflammatory cytokines, chemokines and neutrophil infiltration, which together contributed to a decrease in cardiomyocyte apoptosis and reactive oxygen species (ROS) generation. In addition, we found that IL-37 inhibited the up-regulation of Toll-like receptor (TLR)-4 expression and nuclear factor kappa B (NF-kB) activation after I/R, while increasing the anti-inflammatory IL-10 level. Moreover, the administration of anti-IL-10R antibody abolished the protective effects of IL-37 in I/R injury. In-vitro experiments further demonstrated that IL-37 protected cardiomyocytes from apoptosis under I/R condition, and suppressed the migration ability of neutrophils towards the chemokine LIX. In conclusion, IL-37 plays a protective role against mouse myocardial I/R injury, offering a promising therapeutic medium for myocardial I/R injury.
Clinical and experimental immunology.Clin Exp Immunol.2014 Jun;176(3):438-51. doi: 10.1111/cei.12284.
Innate immune and inflammatory responses are involved in myocardial ischaemia/reperfusion (I/R) injury. Interleukin (IL)-37 is a newly identified member of the IL-1 family, and functions as a fundamental inhibitor of innate immunity and inflammation. However, its role in myocardial I/R injury remain
PMID 24527881

Obese mice are resistant to eosinophilic airway inflammation induced by diesel exhaust particles.

Yanagisawa R1, Koike E, Ichinose T, Takano H.Author information 1Center for Environmental Health Sciences, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, 305-8506, Japan.AbstractParticulate matter can exacerbate respiratory diseases such as asthma. Diesel exhaust particles are the substantial portion of ambient particulate matter with a <2.5 µm diameter in urban areas. Epidemiological data indicate increased respiratory health effects of particulate matter in obese individuals; however, the association between obesity and diesel exhaust particle-induced airway inflammation remains unclear. We aimed to investigate the differences in susceptibility to airway inflammation induced by exposure to diesel exhaust particles between obese mice (db/db) and lean mice (db/+m). Female db/db and db/+m mice were intratracheally administered diesel exhaust particles or vehicle every 2 weeks for a total of seven times. The cellular profile of bronchoalveolar lavage fluid and histological changes in the lungs were assessed and the lungs and serum were analyzed for the generation of cytokines, chemokines and soluble intercellular adhesion molecule 1. Diesel exhaust particle exposure-induced eosinophilic infiltration in db/+m mice accompanied by T-helper 2 cytokine, chemokine and soluble intercellular adhesion molecule 1 expression in the lungs. In contrast, it induced mild neutrophilic airway inflammation accompanied by elevated cytokines and chemokines in db/db mice. The lungs of db/db mice exhibited decreased expression of eosinophil activators/chemoattractants such as interleukin-5, interleukin-13 and eotaxin compared with those of db/+m mice. In addition, serum eotaxin and monocyte chemotactic protein-1 levels were significantly higher in db/db mice than in db/+m mice. In conclusion, obesity can affect susceptibility to diesel exhaust particle-induced airway inflammation, which is possibly due to differences in local and systemic inflammatory responses between lean and obese individuals. Copyright © 2013 John Wiley & Sons, Ltd.
Journal of applied toxicology : JAT.J Appl Toxicol.2014 Jun;34(6):688-94. doi: 10.1002/jat.2925. Epub 2013 Sep 18.
Particulate matter can exacerbate respiratory diseases such as asthma. Diesel exhaust particles are the substantial portion of ambient particulate matter with a <2.5 µm diameter in urban areas. Epidemiological data indicate increased respiratory health effects of particulate matter in obese in
PMID 24105835

Japanese Journal

Anti-Inflammatory Effects of Mannanase-Hydrolyzed Copra Meal in a Porcine Model of Colitis

IBUKI Masahisa,FUKUI Kensuke,KANATANI Hiroyuki,MINE Yoshinori
Journal of Veterinary Medical Science, 2014
… Inflammation was assessed by clinical signs, morphological and histological measurements, gut permeability, and neutrophil infiltration. …
NAID 130003391263

Long-term observations of clinicopathological characteristics and outcome of Japanese patients with pauci-immune crescentic glomerulonephritis

Kitagawa Kiyoki,Furuichi Kengo,Shinozaki Yasuyuki,Toyama Tadashi,Kitajima Shinji,Hara Akinori,Iwata Yasunori,Sakai Norihiko,Kaneko Shuichi,Wada Takashi
Clinical and Experimental Nephrology 17(6), 858-865, 2013-12
… Results: There were no significant differences in blood pressure, renal function or anti-neutrophil cytoplasmic antibody titer between groups. … On the other hand, the rate of crescent formation and degree of interstitial inflammatory cell infiltration were decreased in Group III. …
NAID 120005368212

miR-451 downregulates neutrophil chemotaxis via p38 mitogen-activated protein kinase.

Murata Koichi,Yoshitomi Hiroyuki,Furu Moritoshi,Ishikawa Masahiro,Shibuya Hideyuki,Ito Hiromu,Matsuda Shuichi
Arthritis and rheumatism, 2013-11-18
… The role of miR-451 in neutrophil chemotaxis was evaluated in vivo and in vitro using neutrophils of mice. … Systemic administration of miR-451 significantly disturbed the infiltration of neutrophils in air pouch model without affecting apoptosis of neutrophils. … These results suggest that miR-451 suppresses neutrophil chemotaxis via p38 MAPK and that miR-451 is a potential therapeutic target in the treatment of RA. …
NAID 120005353355