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Purinergic 2X7Receptor is Involved in the Podocyte Damage of Obesity-Related Glomerulopathy via Activating nucleotide-binding and Oligomerization Domain-Like Receptor Protein 3 Inflammasome

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Chinese Medical Journal 2018年第22期131卷 2713-2725页

作者： Xiao-Xia Hou Hong-Rui Dong Li-Jun Sun Min Yang Hong Cheng Yi-Pu Chen Division of Nephrology Beijing Anzhen HospitalCapital Medical UniversityBeijing 100029China

Background:The nucleotide-binding and oligomerization domain-like receptor protein 3 (NLRP3) inflammasome composed of NLRP3,apoptosis-associated speck-like protein containing CARD (ASC),and caspase-1 is engaged in the inflammatory response of many kidney diseases and can be activated by purinergic 2X7 receptor (P2X7R).This study was conducted to explore whether P2X7R plays a pathogenic role in the podocyte damage of obesity-related glomerulopathy (ORG) and whether this role is mediated by the activation ofNLRP3 ***:A mouse model of ORG was established by high-fat diet *** conditionally immortalized mouse podocytes were cultured with leptin or with leptin and P2X7R antagonist (KN-62 or A438079).The mRNA and protein expression of the P2X7R and NLRP3 inflammasome components including NLRP3,ASC,and caspase-1,as well as the podocyte-associated molecules including nephrin,podocin,and desmin in mouse renal cortex or cultured mouse podocytes were tested by real-time-polymerase chain reaction and Westem blot analysis,***:The significantly upregulated expression of P2X7R and NLRP3 inflammasome components and the NLRP3 inflammasome activation were observed in the renal cortex (in fact their location in podocytes was proved by confocal microscopy) of ORG mice in vivo,which were accompanied with the morphological changes of podocyte damage and the expression changes of podocyte-associated *** changes in the expression of P2X7R and NLRP3 inflammasome components as well as in the expression ofpodocyte-associated molecules were also observed in the cultured podocyte studies treated by leptin in vitro,and all of the above changes were significantly attenuated by the P2X7R antagonist KN-62 or ***:P2X7R could trigger the activation ofNLRP3 inflammasome,and the activated P2X7R/NLRP3 inflammasome in podocytes might be involved in the podocyte damage of ORG.

关键词： Desmin nucleotide-binding and Oligomerization Domain-Like Receptor Protein 3 Inflammasome Obesity-Related Glomerulopathy Podocytes Purinergic 2X7Receptor

Transcomplementation, but not Physical Association of the CC-NB-ARC and LRR Domains of Tomato R Protein Mi-1.2 is Altered by Mutations in the ARC2 Subdomain

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Molecular Plant 2008年第3期1卷 401-410页

作者： Gerben van Ooijen Gabriele Mayr Mario Albrecht Ben J. C. Cornelissen Frank L.W. Takken Plant Pathology Swammerdam Institute for Life Sciences University of Amsterdam PO Box 94062 1090 GB Amsterdam the Netherlands Max Planck Institute for Informatics Stuhlsatzenhausweg 85 66123 Saarbrücken Germany

Race-specific disease resistance in plants is mediated by Resistance （R） proteins that recognize pathogen at- tack and initiate defence responses. Most R proteins contain a central NB-ARC domain and a C-terminal leucine-rich repeat （LRR） domain. We analyzed the intramolecular interaction of the LRR domain of tomato R protein Mi-1.2 with its N- terminus. We expressed the CC-NB-ARC and LRR parts in trans and analyzed functional transcomplementation and physical interactions. We show that these domains functionally transcomplement when expressed in trans. Known autoactivating LRR domain swaps were found to induce a hypersensitive response （HR） upon co-expression. Likewise, autoactivating mutants in the NB subdomain transcomplemented to induce HR. Point mutations in the ARC2 subdomain that induce strong autoactivation in the full-length Mi-1.2 protein, however, fail to induce HR in the transcomplementation assay, These data indicate distinct functions for the NB-ARC subdomains in induction of HR signalling. Furthermore, dissociation of the LRR is not required to release its negative regulation, as in all combinations of CC-NB-ARC and LRR domains tested, a physical interaction was observed.

关键词： RESISTANCE PROTEIN DISEASE RESISTANCE nucleotide-binding CELL-DEATH HYPERSENSITIVE RESPONSE

酒精性肝病患者肝组织NLRP3炎症复合体基因水平检测及其意义

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实用肝脏病杂志 2016年第6期19卷 678-682页

作者：张龙玉孙颖黄昂郝书理李保森张纪元邹正升北京大学医学部教学医院/解放军第302医院非感染性肝病诊疗中心北京市100039 北京大学医学部教学医院/解放军第302医院肝病生物治疗研究中心北京市100039

目的探讨核苷酸结合性寡聚区蛋白样受体(NLR)P3炎症复合体在酒精性肝病(ALD)发病中的作用。方法本研究获得酒精性肝炎(AH)12例、酒精性肝硬化(ALC)4例和健康人(HC)12例肝组织,采用RT-PCR法检测肝组织NLRP3、Caspase-1和IL-1βm RNA水平... 详细信息

目的探讨核苷酸结合性寡聚区蛋白样受体(NLR)P3炎症复合体在酒精性肝病(ALD)发病中的作用。方法本研究获得酒精性肝炎(AH)12例、酒精性肝硬化(ALC)4例和健康人(HC)12例肝组织,采用RT-PCR法检测肝组织NLRP3、Caspase-1和IL-1βm RNA水平。采集ALD患者84例【AH20例、ALC48例(Child-Pugh A级19例、B级22例和C级7例)和重症酒精性肝炎(SAH)16例】和健康人40例血浆,采用ELISA法检测血浆IL-1β水平,采用Spearman秩相关分析血浆IL-1β水平与临床检验指标的相关性。结果 AH和ALC患者肝组织NLRP3 m RNA水平分别为(28.1±2.8)和(28.4±3.1),均显著高于HC组【(8.8±1.8),P0.05);ALD患者血浆IL-1β水平与ALT和AST/ALT比值呈正相关。结论 NLRP3炎症复合体主要组分及促炎细胞因子IL-1β在ALD患者肝组织和血浆水平升高,可能参与了ALD发病的炎症反应过程。

关键词：酒精性肝病核苷酸结合性寡聚区蛋白样受体P3炎症复合体 Caspase-1 白介素-1β nucleotide-binding and oligomerization domain-like receptors P3 Caspase-1 Interleukin-1β

Spontaneous bacterial peritonitis: The clinical challenge of a leaky gut and a cirrhotic liver

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World Journal of Hepatology 2015年第3期7卷 304-314页

作者： Philipp Lutz Hans Dieter Nischalke Christian P Strassburg Ulrich Spengler Department of Internal Medicine I University of Bonn German Center for Infection Research

Spontaneous bacterial peritonitis(SBP) is a frequent, life-threatening bacterial infection in patients with liver cirrhosis and ascites. Portal hypertension leads to increased bacterial translocation from the intestine. Failure to eliminate invading pathogens due to immune defects associated with advanced liver disease on the background of genetic predisposition may result in SBP. The efficacy of antibiotic treatment and prophylaxis has declined due to the spread of multi-resistant bacteria. Patients with nosocomial SBP and with prior antibiotictreatment are at a particularly high risk for infection with resistant bacteria. Therefore, it is important to adapt empirical treatment to these risk factors and to the local resistance profile. Rifaximin, an oral, nonabsorbable antibiotic, has been proposed to prevent SBP, but may be useful only in a subset of patients. Since novel antibiotic classes are lacking, we have to develop prophylactic strategies which do not induce bacterial resistance. Farnesoid X receptor agonists may be a candidate, but so far, clinical studies are not available. New diagnostic tests which can be carried out quickly at the patient's site and provide additional prognostic information would be helpful. Furthermore, we need tools to predict antibiotic resistance in order to tailor first-line antibiotic treatment of spontaneous bacterial peritonitis to the individual patient and to reduce mortality.

关键词： Ascites Cirrhosis Farnesoid X receptor Liver nucleotide-binding oligomerization domaincontaining 2 Rifaximin Prophylaxis Spontaneousbacterial peritonitis Toll-like receptor 2

NOD2 mutations and colorectal cancer - Where do we stand?

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World Journal of Gastrointestinal Surgery 2016年第4期8卷 284-293页

作者： Diogo Branquinho Paulo Freire Carlos Sofia Servico de Gastrenterologia Centro Hospitalar e Universitário de Coimbra3000-075 Coimbra Portugal Faculdade de Medicina da Universidade de Coimbra 3004-504 CoimbraPortugal

Due to the overwhelming burden of colorectal cancer(CRC), great effort has been placed on identifying genetic mutations that contribute to disease development and progression. One of the most studied polymorphisms that could potentially increase susceptibility to CRC involves the nucleotide-binding and oligomerization-domain containing 2(NOD2) gene. There is growing evidence that the biological activity of NOD2 is far greater than previously thought and a link with intestinal microbiota and mucosal immunity is increasingly sought after. In fact, microbial composition may be an important contributor not only to inflammatory bowel diseases(IBD) but also to CRC. Recent studies have showed that deficient NOD2 function confers a communicable risk of colitis and CRC. Despite the evidence from experimental models, population-based studies that tried to link certain NOD2 polymorphisms and an increase in CRC risk have been described as conflicting. Significant geographic discrepancies in the frequency of such polymorphisms and different interpretations of the results may have limited the conclusions of those studies. Since being first associated to IBD and CRC, our understanding of the role of this gene has come a long way, and it is tempting to postulate that it may contribute to identify individuals with susceptible genetic background that may benefit from early CRC screening programs or in predicting response to current therapeutic tools. The aim of this review is to clarify the status quo of NOD2 mutations as genetic risk factors to chronic inflammation and ultimately to CRC. The use of NOD2 as a predictor of certain phenotypic characteristics of the disease will be analyzed as well.

关键词： Colorectal cancer Fecal microbiota Cancer susceptibility Intestinal inflammation nucleotide-binding and oligomerization-domain containing 2 mutations