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Helicobacter pylori arginase mutant colonizes arginase Ⅱ knockout mice

世界胃肠病学杂志：英文版 2011年第28期17卷 3300-3309页

作者： Songhee H Kim Melanie l langford Jean-luc Boucher traci l testerman David J McGee Department of Microbiology and Immunology Louisiana State University Health Sciences Center-Shreveport University of Nebraska-lincoln School of Biological SciencesLincoln laboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques Université Paris Descartes

AIM: To investigate the role of host and bacterial arginases in the colonization of mice by Helicobacter pylori (***).METHODS: *** produces a very powerful urease that hydrolyzes urea to carbon dioxide and ammonium,which neutralizes *** is absolutely essential to *** pathogenesis;therefore,the urea substrate must be in ample supply for urease to work *** urea substrate is most likely provided by arginase activity,which hydrolyzes l-arginine to l-ornithine and *** work has demonstrated that *** arginase is surprisingly not required for colonization of wild-type ***,another in vivo source of the critical urea substrate must *** hypothesized that the urea source was provided by host arginase Ⅱ,since this enzyme is expressed in the stomach,and *** has previously been shown to induce the expression of murine gastric arginase Ⅱ.To test this hypothesis,wild-type and arginase (rocF) mutant *** strain SS1 were inoculated into arginase Ⅱ knockout ***: Surprisingly,both the wild-type and rocF mutant bacteria still colonized arginase Ⅱ knockout ***,feeding arginase Ⅱ knockout mice the host arginase inhibitor S-(2-boronoethyl)l-cysteine (BEC),while inhibiting > 50% of the host arginase Ⅰ?activity in several tissues,did not block the ability of the rocF mutant *** to *** contrast,BEC poorly inhibited *** arginase ***: The in vivo source for the essential urea utilized by *** urease is neither bacterial arginase nor host arginase Ⅱ;instead,either residual host arginase Ⅰ?or agmatinase is probably responsible.

关键词：幽门螺杆菌精氨酸酶基因敲除小鼠突变寄生尿素酶野生型

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Beyond the stomach: An updated view of Helicobacter pylori pathogenesis, diagnosis, and treatment

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World Journal of Gastroenterology 2014年第36期20卷 12781-12808页

作者： traci l testerman James Morris Department of Microbiology and Immunology Uniformed Services University of the Health SciencesBethesda MD 20814 United States Department of Gastroenterology Louisiana State University Health Sciences Center-Shreveport Shreveport LA 71130 United States

Helicobacter pylori(H. pylori) is an extremely common, yet underappreciated, pathogen that is able to alter host physiology and subvert the host immune response, allowing it to persist for the life of the host. H. pylori is the primary cause of peptic ulcers and gastric cancer. In the United States, the annual cost associated with peptic ulcer disease is estimated to be $6 billion and gastric cancer kills over 700000 people per year globally. The prevalence of H. pylori infection remains high(> 50%) in much of the world, although the infection rates are dropping in some developed nations. The drop in H. pylori prevalence could be a double-edged sword, reducing the incidence of gastric diseases while increasing the risk of allergies and esophageal diseases. The list of diseases potentially caused by H. pylori continues to grow; however, mechanistic explanations of how H. pylori could contribute to extragastric diseases lag far behind clinical studies. A number of host factors and H. pylori virulence factors act in concert to determine which individuals are at the highest risk of disease. These include bacterial cytotoxins and polymorphisms in host genes responsible for directing the immune response. This review discusses the latest advances in H. pylori pathogenesis, diagnosis, and treatment. Up-todate information on correlations between H. pylori and extragastric diseases is also provided.

关键词： Enterohepatic Pathogenesis Diagnosis Treatment Ext

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Immune and microRNA responses to Helicobacter muridarum infection and indole-3-carbinol during colitis

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World Journal of Gastroenterology 2020年第32期26卷 4763-4785页

作者： Rasha Raheem Alkarkoushi Yvonne Hui Abbas S Tavakoli Udai Singh Prakash Nagarkatti Mitzi Nagarkatti Ioulia Chatzistamou Marpe Bam traci l testerman Department of Pathology Microbiology and ImmunologyUniversity of South Carolina School of MedicineColumbiaSC 29209United States College of Nursing University of South CarolinaUniversity of South CarolinaColumbiaSC 29208United States Department of Medicine Hematology and OncologyUniversity of Virginia School of MedicineCharlottesvilleVA 22908United States

BACKGROUND Indole-3-carbinol(I3C)and other aryl hydrocarbon receptor agonists are known to modulate the immune system and ameliorate various inflammatory and autoimmune diseases in animal models,including colitis induced by dextran sulfate sodium(DSS).MicroRNAs(miRNAs)are also gaining traction as potential therapeutic agents or diagnostic *** Helicobacter(EHH)species are associated with an increased risk of inflammatory bowel disease,but little is known about how these species affect the immune system or response to *** To determine whether infection with an EHH species alters the response to I3C and how the immune and miRNA responses of an EHH species compare with responses to DSS and inflammatory bowel *** We infected C57Bl/6 mice with Helicobacter muridarum(***),with and without DSS and I3C *** responses were evaluated by histological examination,symptom scores,and cytokine *** analysis was performed on mesenteric lymph nodes to further evaluate the regional immune *** *** infection alone caused colonic inflammation and upregulated proinflammatory,macrophage-associated cytokines in the colon similar to changes seen in DSS-treated *** upregulation occurred upon treatment with *** infection caused broad changes in mesenteric lymph node miRNA expression,but colitis-associated miRNAs were regulated similarly in ***-infected and uninfected,DSS-treated *** spite of causing colitis exacerbation,*** infection did not prevent disease amelioration by I3C.I3C normalized both macrophage-and T cell-associated *** Thus,I3C may be useful for inflammatory bowel disease patients regardless of EHH *** miRNA changes associated with I3C treatment are likely the result of,rather than the cause of immune response changes.

关键词： Helicobacter muridarum MicroRNA Immune T regulatory cell T helper 17 cell Colitis Cytokine

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<i>Helicobacter</i>infection decreases basal colon inflammation, but increases disease activity in experimental IBD

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Open Journal of Gastroenterology 2013年第3期3卷 177-189页

作者： Christopher P. Monceaux traci l. testerman Moheb Boktor Paul Jordan Patrick Adegboyega David J. McGee Merilyn H. Jennings Courtney P. Parker Shelly Gupta Ping Yi Vijay C. Ganta Haidy Galous Kenneth Manas J. Steven Alexander Department of Gastroenterology and Hepatology LSU Health Shreveport Shreveport USA Department of Microbiology and Immunology LSU Health Shreveport Shreveport USA Department of Molecular and Cellular Physiology LSU Health Shreveport Shreveport USA Department of Pathology LSU Health Shreveport Shreveport USA

Background: Helicobacter species are best known for their roles in the pathology of gastritis;however, several Helicobacter species also colonize the intestine, and less is known about effects of Helicobacter on the development of intestinal inflammation. To evaluate contributions of Helicobacter in inflammatory bowel disease, we investigated whether and how pre-existing intestinal colonization would affect disease severity and biomarkers of inflammation in experimental IBD. Materials and Methods: Mice were infected with H. muridarum 2 weeks prior to induction of colitis mediated by 3% dextran sulfate (DSS). Disease activity index, stool blood and consistency, colon length, myeloperoxidase, histopathology, blood and lymphatic vessels, and numbers of dilated mucosal crypts were measured in control, DSS-only, H. muridarum-infected, and H. muridarum-infected + DSS mice. Results: Prior to DSS challenge, H. muridarum-infected mice showed little distal gut injury by several indices of colon inflammation with decreased blood vessel density in the submucosa, and lower lymphatic density in the mucosa and submucosa. However, after DSS colitis, H. muridarum-infected mice exhibited significantly greater disease. Weight change, stool bleeding, diarrhea, and angiogenesis were all increased in H. muridarum-infected mice in DSS colitis compared to DSS controls. Conclusions: Our data show that Helicobacter colonization of the intestine, unlike that of the stomach, lowers basal gut inflammatory scores, but increases disease activity and inflammation in an acute colitis model. Intestinal Helicobacter infection may therefore represent a significant sub-clinical factor which predisposes the gut to inflammatory injury.

关键词： Helicobacter Colon lymphatics Crohn’s Disease Ulcerative Colitis

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二甲双胍单药控制不佳的2型糖尿病患者联合达格列净治疗的长期有效性

二甲双胍单药控制不佳的2型糖尿病患者联合达格列净治疗的长期有...

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中华医学会糖尿病学分会第十六次全国学术会议

作者： Clifford J.Bailey Jorge l.Gross Delphine Hennicken Nayyar Iqbal traci A.Mansfield James F.list life and Health Sciences Aston UniversityBirminghamUK Endocrine Division Universidade Federal do Rio Grande do SulPorto AlegreBrazil

目的达格列净(DAPA)是选择性2型钠-葡萄糖协同转运蛋白(SGlT2)抑制剂,通过增加肾脏的葡萄糖清除这一非胰岛素依赖方式来降低血糖。先前已报道了二甲双胍(MET)单药控制欠佳的2型糖尿病患者(n=546)加用DAPA[主要终点:第24周的糖化血红蛋白...

目的达格列净(DAPA)是选择性2型钠-葡萄糖协同转运蛋白(SGlT2)抑制剂,通过增加肾脏的葡萄糖清除这一非胰岛素依赖方式来降低血糖。先前已报道了二甲双胍(MET)单药控制欠佳的2型糖尿病患者(n=546)加用DAPA[主要终点:第24周的糖化血红蛋白(HbA1c)水平]的随机、双盲、安慰剂对照试验(MB102014)的24周的短期治疗效果;而本研究将报道扩展治疗至102周的结果。

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