FEMS immunology and medical microbiology最新文献

{"title":"Mutational analysis of the Helicobacter pylori carbonic anhydrases","authors":"Frank Nils Stähler ,&nbsp;Lynn Ganter ,&nbsp;Kathrin Lederer ,&nbsp;Manfred Kist ,&nbsp;Stefan Bereswill","doi":"10.1016/j.femsim.2004.10.021","DOIUrl":"10.1016/j.femsim.2004.10.021","url":null,"abstract":"<div><p><span>In the gastric microenvironment, </span><span><span>Helicobacter pylori</span></span><span> is exposed to bicarbonate, urea and acid. Here it is demonstrated that both </span><em>H. pylori</em><span><span> carbonic anhydrases (CAs) are required for maintaining </span>urease activity and therefore influence </span><em>H. pylori</em> urea resistance at neutral pH. Furthermore, the β-CA is required for acid resistance as indicated by a growth defect of the corresponding mutant at low pH. The α- and β-CA mutants as well as the double mutant were more resistant to bicarbonate, indicating that both enzymes are involved in bicarbonate metabolism. These phenotypes support important CA-functions in <em>H. pylori</em> urea and bicarbonate metabolism and acid resistance. Thus, both CA enzymes might be required for survival in the gastric niche.</p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.10.021","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25087288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of Helicobacter spp. in the pathogenesis of primary biliary cirrhosis and primary sclerosing cholangitis","authors":"Sacha Y. Boomkens ,&nbsp;Sjoerd de Rave ,&nbsp;Raymond G.J. Pot ,&nbsp;Herman F. Egberink ,&nbsp;Louis C. Penning ,&nbsp;Jan Rothuizen ,&nbsp;Pieter E. Zondervan ,&nbsp;Johannes G. Kusters","doi":"10.1016/j.femsim.2004.11.002","DOIUrl":"10.1016/j.femsim.2004.11.002","url":null,"abstract":"<div><p>\u0000<span><em>Helicobacter</em></span><span> species DNA has been detected in liver tissue of patients affected by primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC). To investigate a potential causative relation between </span><em>Helicobacter</em> species and PBC/PSC, we compared the presence of <em>Helicobacter</em> species-specific DNA in liver tissue of patients with PBC/PSC (<em>n</em>\u0000<!--> <!-->=<!--> <!-->18/<em>n</em>\u0000<!--> <!-->=<!--> <!-->13) with those of a control group of patients with various liver diseases with known cause (<em>n</em>\u0000<!--> <!-->=<!--> <!-->29). A PCR with <em>Helicobacter</em><span> genus-specific 16S rRNA primers was performed on DNA isolated from paraffin embedded liver tissue. Control patients had hepatitis-B (</span><em>n</em>\u0000<!--> <!-->=<!--> <span>9), alcoholic cirrhosis (</span><em>n</em>\u0000<!--> <!-->=<!--> <span>14), or non-cirrhotic metabolic liver disease (</span><em>n</em>\u0000<!--> <!-->=<!--> <!-->6). There was no significant difference between the incidence of <em>Helicobacter</em> spp.-specific DNA in PBC/PSC (9/31; 29%) and the control group (10/29; 34%). Sequence analysis confirmed <em>Helicobacter</em> spp. DNA. Because <em>Helicobacter</em> spp. DNA can be found in approximately one-third of all samples tested, it is unlikely that PSC and PBC are caused by <em>Helicobacter</em> infection.</p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.11.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25087293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of matrix metalloprotease-2, -7 and -9 on human colon, liver and bile duct cell lines by enteric and gastric Helicobacter species","authors":"Naoko Yanagisawa,&nbsp;Linda Geironson,&nbsp;Waleed Abu Al-Soud,&nbsp;Åsa Ljungh","doi":"10.1016/j.femsim.2004.11.009","DOIUrl":"10.1016/j.femsim.2004.11.009","url":null,"abstract":"<div><p>Gastric and enteric <span><em>Helicobacter</em></span><span><span><span> species have been associated with malignant and inflammatory diseases of the stomach, liver, gall </span>bladder and intestine. </span>Matrix metalloproteinases<span><span> (MMPs) participate in degradation of extracellular matrix, which allows bacteria to come in contact with and interact with the cells. Enhanced level of MMPs facilitates </span>metastasis and cell invasion of tumor cells by removal of physical barriers, as well as modulation of biologic activities of the proteins residing in the extracellular matrix. The aim of this study was to evaluate the effect of gastric and enteric </span></span><em>Helicobacter</em> on induction of MMPs in hepatocytes and epithelial cells of gall bladder and colon. Human hepatocytes HepG2, gall bladder epithelial cells TFK-1, and colon epithelial cells HT29 were infected with strains of <span><em>H. </em><em>pylori</em><em> cagA</em></span>+, <em>cagE</em>+, <em>H. pylori cagA</em>-, <em>cagE</em>−, <em>H. pullorum</em>, <em>H. cholecystus</em>, <em>H. bilis</em> and <em>H. hepaticus</em>. Protein levels of MMPs were analyzed by enzyme-linked immunosorbent assay and immunohistochemistry. Reverse transcription-quantitative polymerase chain reaction was used to study mRNA levels. Increased expression of MMP-2 and MMP-9 was observed on HepG2, TFK-1 and HT29 infected with <em>H. pylori cagA</em>+, <em>cagE</em>+ and <em>H. cholecystus</em> strains. <em>H. pylori cagA</em>+, <em>cagE</em>+, <em>H. cholecystus</em>, <em>H. pullorum</em>, <em>H. bilis</em> and <em>H. hepaticus</em> strains increased expression of MMP-7 on HT29, compared to uninfected control cells. The effect of MMP upregulation on HepG2, TFK-1 and HT29 was bacterial dose dependent. <em>H. pylori cagA</em>−, <em>cagE</em><span>− strain did not increase expression of MMPs. Inducible MMPs on colon and bile duct epithelial cells as well as hepatocytes may play an important role in facilitating invasion and progression of cancer by </span><em>Helicobacter</em> species colonizing the hepatobiliary and gastrointestinal tract.</p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.11.009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25087290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Helicobacter pylori VacA cytotoxin interacts with fibronectin and alters HeLa cell adhesion and cytoskeletal organization in vitro","authors":"Ewa E. Hennig ,&nbsp;Michał M. Godlewski ,&nbsp;Eugeniusz Butruk ,&nbsp;Jerzy Ostrowski","doi":"10.1016/j.femsim.2004.10.020","DOIUrl":"10.1016/j.femsim.2004.10.020","url":null,"abstract":"<div><p><span><em>Helicobacter pylori</em></span><span> vacuolating cytotoxin<span><span><span> VacA causes multiple effects on epithelial cell function and morphology, but the effects of VacA on signal transduction pathways and the </span>cytoskeleton<span> have not been investigated in detail. In this study, we analyzed the effects of native VacA on HeLa and AGS cell adhesion to </span></span>fibronectin<span><span> and laminin under serum-free conditions. Confocal microscopic examination revealed increased number of cells with rounded morphology and inhibition of actin fiber formation, in the presence of VacA. VacA binds to fibronectin in vitro in a dose-dependent manner. This interaction was partly inhibited by a peptide containing an arginine-glycine-aspartic acid motif. The adhesion of HeLa cells to fibronectin, but not to laminin, was decreased in the presence of VacA. Thus, VacA may interact with fibronectin and influence </span>integrin receptor-induced cell signaling and cytoskeleton-dependent cell functions.</span></span></span></p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.10.020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25089014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Helicobacter pylori, T cells and cytokines: the “dangerous liaisons”","authors":"Mario Milco D’Elios,&nbsp;Amedeo Amedei,&nbsp;Marisa Benagiano,&nbsp;Annalisa Azzurri,&nbsp;Gianfranco Del Prete","doi":"10.1016/j.femsim.2004.10.013","DOIUrl":"10.1016/j.femsim.2004.10.013","url":null,"abstract":"<div><p><span><em>Helicobacter </em><em>pylori</em></span><span><span> infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop chronic and life threatening diseases, as peptic ulcer, gastric cancer, B-cell lymphoma, or autoimmune </span>gastritis<span>. The type of host immune response against </span></span><em>H. pylori</em> is crucial for the outcome of the infection. A predominant <em>H. pylori</em><span>-specific Th1 response, characterized by high IFN-γ, TNF-α, and IL-12 production associates with peptic ulcer, whereas combined secretion of both Th1 and Th2 cytokines are present in uncomplicated gastritis. Gastric T cells from MALT lymphoma exhibit abnormal help for autologous B-cell proliferation and reduced perforin- and Fas–Fas ligand-mediated killing of B cells. In </span><em>H. pylori</em><span>-infected patients with autoimmune gastritis cytolytic T cells infiltrating the gastric mucosa cross-recognize different epitopes of </span><em>H. pylori</em> proteins and H⁺K⁺<span> ATPase autoantigen. These data suggest that peptic ulcer can be regarded as a Th1-driven immunopathological response to some </span><em>H. pylori</em> antigens, whereas deregulated and exhaustive <em>H. pylori</em>-induced T cell-dependent B-cell activation can support the onset of low-grade B-cell lymphoma. Alternatively, <em>H. pylori</em> infection may lead in some individuals to gastric autoimmunity via molecular mimicry.</p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.10.013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25260792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD4+CD25+ suppressor T cells regulate pathogen induced inflammation and disease","authors":"Sukanya Raghavan,&nbsp;Jan Holmgren","doi":"10.1016/j.femsim.2004.10.017","DOIUrl":"10.1016/j.femsim.2004.10.017","url":null,"abstract":"<div><p>A key suppressor role has recently been ascribed to the natural CD4⁺<span>CD25</span>⁺<span><span><span><span> regulatory T cells (Treg), the removal of which leads to the development of autoimmune disease and aggravated pathogen-induced inflammation in otherwise normal hosts. The repertoire of </span>antigen specificities of Treg is as broad as that of </span>naïve T cells<span><span>, recognizing both self and non-self antigens, enabling Treg to control a broad range of immune responses. Although widely acknowledged to play a role in the maintenance of self-tolerance, recent studies indicate that Treg can be activated and expanded against bacterial, viral and parasite antigens in vivo. Such pathogen-specific Treg can prevent infection-induced immunopathology but may also increase the load of infection and prolong pathogen persistence by suppressing protective immune responses. This review discusses the role of Treg in the prevention of exaggerated inflammation favoring </span>chronicity in bacterial or </span></span>fungal infections and latency in viral infections. Special attention is given to the role of Treg in the modulation of gastric inflammation induced by </span><span><span>Helicobacter pylori</span></span> infection. Findings in both experimentally infected mice and humans with natural infection indicate that Treg are important in protecting the <em>H. pylori</em><span>-infected host against excessive gastric inflammation and disease symptoms but on the negative side promote bacterial colonization at the gastric and duodenal mucosa which may increase the risk in </span><em>H. pylori</em><span>-infected individuals to develop duodenal ulcers.</span></p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.10.017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25260793","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"cagA gene variants in Malaysian Helicobacter pylori strains isolated from patients of different ethnic groups","authors":"Mohamed Ramelah ,&nbsp;Ahmad Aminuddin ,&nbsp;Hanafiah Alfizah ,&nbsp;Mohd Rose Isa ,&nbsp;Ali Yaakob Jasmi ,&nbsp;Huck Joo Tan ,&nbsp;A. Jamal A. Rahman ,&nbsp;Abdul Manap Rizal ,&nbsp;M. Zawawi Mazlam","doi":"10.1016/j.femsim.2005.02.001","DOIUrl":"10.1016/j.femsim.2005.02.001","url":null,"abstract":"<div><p><span><em>Helicobacter </em><em>pylori</em></span> infection of a distinct subtype of <span><em>cagA</em></span> may lead to different pathological manifestation. The aim of this study is to determine the presence of <em>cagA</em> gene and its variants in <em>H. pylori</em> infection among different ethnic groups and its effect on gastroduodenal diseases. Overall detection of <em>cagA</em> among the 205 clinical isolates of <em>H. pylori</em> was 94%. Variations in size of the 3′ region of <em>cagA</em> gene were examined among 192 Malaysian <em>H. pylori cagA</em>-positive strains. Results showed that three <em>cagA</em> variants differing in fragment length of PCR products were detected and designated as type A (621–651<!--> <!-->bp), type B (732–735<!--> <!-->bp) and type C (525 bp). Although there was no association between any of the <em>cagA</em><span> subtypes with peptic ulcer disease (</span><em>p</em> <!-->&gt;<!--> <!-->0.05), an association between <em>cagA</em> subtypes with a specific ethnic group was observed. Specific-<em>cagA</em> subtype A strains were predominantly isolated from Chinese compared to Malays and Indians (<em>p</em> <!-->&lt;<!--> <!-->0.0005), and <em>cagA</em> subtype B strains were predominantly isolated from Malays and Indians compared to Chinese (<em>p</em> <!-->&lt;<!--> <!-->0.05). The <em>cagA</em> type A strains of <em>H. pylori</em> is commonly found in the Chinese patients who have a higher risk of peptic ulcer disease, thus indicating that it could be used as an important clinical biomarker for a more severe infection.</p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2005.02.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25088331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel plasmids for gene expression analysis and for genetic manipulation in the gastric pathogen Helicobacter pylori","authors":"Stefan Bereswill ,&nbsp;Ruth Schönenberger ,&nbsp;Arnoud H.M. van Vliet ,&nbsp;Johannes G. Kusters ,&nbsp;Manfred Kist","doi":"10.1016/j.femsim.2004.10.016","DOIUrl":"10.1016/j.femsim.2004.10.016","url":null,"abstract":"<div><p>To facilitate gene expression analysis in the human gastric pathogen <span><em>Helicobacter </em><em>pylori</em></span>, we constructed the plasmids pHPLAC-KAN and pHPLAC-CAT containing a promoterless <em>Escherichia coli lacZ</em> gene located upstream from the antibiotic resistance genes <em>aphA-3</em> or <em>cat</em>, respectively. The suitability of the plasmids for <em>H. pylori</em><span> mutagenesis and gene expression analysis was evaluated by plasmid integration into the genome of </span><em>H. pylori</em><span> strain 1061 by single homologous recombination, using the </span><em>rpl9</em><span> gene encoding ribosomal protein L9 as target. By monitoring β-galactosidase production from the resulting </span><em>rpl9::lacZ</em> fusion, it was demonstrated that <em>H. pylori rpl9</em><span><span> displays the classical growth phase-dependent regulation of components of the protein synthesis machinery, as β-galactosidase production dropped fivefold in the stationary growth phase. The plasmids described in this study extend our methodological repertoire for </span>genetic modification and molecular analysis of </span><em>H. pylori</em>, and may also be of use for other bacteria, as the resistance cassettes and the <em>lacZ</em> gene are active in the related <em>Campylobacter</em> species.</p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.10.016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25089016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Helicobacter pylori antibodies and gastric cancer: a gender-related difference","authors":"Daiva Janulaityte-Günther ,&nbsp;Limas Kupcinskas ,&nbsp;Alvydas Pavilonis ,&nbsp;Konstantinas Valuckas ,&nbsp;Leif Percival Andersen ,&nbsp;Torkel Wadström","doi":"10.1016/j.femsim.2004.11.011","DOIUrl":"10.1016/j.femsim.2004.11.011","url":null,"abstract":"<div><p><span><span>Helicobacter pylori</span></span><span> has been proposed as a causative agent of gastric cancer. The aim of this study was to define serum antibodies response against different </span><em>H. pylori</em><span><span> antigens in patients with gastric cancer. Serum samples were collected from 115 Lithuanian patients with non-cardia gastric cancer and 110 age- and sex-matched controls without cancer. Heat-stable, low-molecular-mass, and outer membrane proteins were used as antigens to analyze serum </span>IgG antibody response against </span><em>H. pylori</em><span> by enzyme-linked immunosorbent assay. Seroprevalence of </span><em>H. pylori</em> using low-molecular-mass antigen was significantly higher in gastric cancer patients, compared to controls (77% versus 57%, <em>p</em> <!-->&lt;<!--> <!-->0.05). Significant differences in the prevalence of <em>H. pylori</em> infection between gastric cancer patients and controls were found in females using all three studied antigens: heat-stable (98% versus 84%, <em>p</em> <!-->&lt;<!--> <!-->0.05), low-molecular-mass (88% versus 48%, <em>p</em> <!-->&lt;<!--> <!-->0.05) and outer membrane proteins (78% versus 57%, <em>p</em> <!-->&lt;<!--> <!-->0.05). In males, no significant differences were revealed between gastric cancer patients and controls. There may be other cofactors in addition to <em>H. pylori</em> that are important for the development of gastric cancer. <em>H. pylori</em> seems, however, to be a more important for development of gastric cancer in females than in males or males may have more confounding risk factors for gastric cancer than females.</p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.11.011","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25087289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrolide-affected Toll-like receptor 4 expression from Helicobacter pylori-infected monocytes does not modify interleukin-8 production","authors":"Joon Yong Park ,&nbsp;Hak Yang Kim ,&nbsp;Ja Young Lee ,&nbsp;Kyung Ho Kim ,&nbsp;Myung Kook Jang ,&nbsp;Jin Heon Lee ,&nbsp;Jae Young Yoo ,&nbsp;Dong Soo Han ,&nbsp;Joon Soo Hahm","doi":"10.1016/j.femsim.2005.01.007","DOIUrl":"10.1016/j.femsim.2005.01.007","url":null,"abstract":"<div><p><span>Macrolide antibiotics<span> have an anti-inflammatory effect by suppressing lipopolysaccharide-induced IL-8 production. IL-8 secretion from monocytes is observed in </span></span><span><em>Helicobacter </em><em>pylori</em></span> infection. Although <em>cag</em><span> gene products are known to induce IL-8 secretion, whether other bacterial substances can initiate the reaction is not determined. In this study, we show that clarithromycin induced down-regulation of Toll-like receptor 4 expression and did not lead to a decrease in IL-8 production and </span><em>H. pylori</em><span> lipopolysaccharide. However, Toll-like receptor 4 activation was possibly not the main cause in the induction of inflammation during </span><em>H. pylori</em> infection.</p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2005.01.007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25089018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}