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Background Antimicrobial resistance of Helicobacter pylori reduces the eradication rate. This study aimed to investigate changes in antimicrobial susceptibility of H pylori isolated from children in Taiwan in the past two decades. Methods This study enrolled children receiving esophagogastroduodenoscopy for upper gastrointestinal diseases in a national tertiary referring hospital from 1998 to 2018. H pylori infection was diagnosed by culture. The minimal inhibitory concentrations (MICs) of antibiotics were tested using the E test. The antibiotic resistance rates and MICs of amoxicillin, clarithromycin, metronidazole, levofloxacin, and tetracycline were compared between 1998-2008 and 2009-2018. Results A total of 70 Helicobacter pylori isolates (29 from 1998 to 2008 and 41 from 2009 to 2018) were identified. The esophagogastroduodenoscopy findings included duodenal ulcers (n = 31), gastric ulcers (n = 9), and gastritis (n = 30). The overall antimicrobial resistance rates of clarithromycin and metronidazole were 22.9% and 21.4%, respectively. The dual resistance rate of clarithromycin and metronidazole was 10%. Resistance rates of levofloxacin and amoxicillin were 8.3% and 2.9%, respectively. None of the isolates were resistant to tetracycline. Compared with the isolates from 1998 to 2008, those from 2009 to 2018 had higher MICs and resistance rates of clarithromycin (26.8% vs 17.2%, P = 0.35) and metronidazole (26.8% vs 13.8%, P = 0.19), but not levofloxacin (9.8% vs 5.3%, P = 1.0) or coresistance to clarithromycin and metronidazole (12.2% vs 6.9%, P = 0.69). Conclusions The antimicrobial resistance rates of pediatric H pylori isolates to clarithromycin and metronidazole increased during the past decade. The selection of antimicrobial agents other than clarithromycin and metronidazole is crucial to increase pediatric H pylori eradication rates.

A consensus on the management of Helicobacter pylori has been developed. We aimed to assess whether dissemination through continuing medical education (CME) could enhance the adoption of this consensus among clinicians and to explore potential barriers to acceptance.Four CME courses were held to disseminate the consensus. Adoption surveys were performed to evaluate participants' behavior in the past and their commitment to adopt the consensus in future clinical practice after CME. The gaps and barriers to adoption were also surveyed.A total of 240 physicians had attended the CME courses and received surveys with the 22 statements/substatements of the consensus. Before CME, adoption was good in six, fair in ten, and poor in six. After CME, 21 statements had either an initial90% adoption or improvement to good or fair (P 0.001), but one still had poor even though it showed improvement (P = 0.02). Although commitment was good or fair after CME, there was a20% gap between "commitment" and "no barrier" to adoption for 11 statements, ten of which had a main barrier of financial incentives. Among the statements with fair or poor commitment after CME, less commitment to adoption and more barriers related to financial incentives were pronounced in clinicians serving in regional/district hospitals or clinics compared to those serving in medical centers.Continuing medical education may improve the adoption of the H. pylori consensus. The financial incentives were shown to be a main barrier to adoption of the consensus and should be improved.

Background Helicobacter pylori infection increases the risk of gastric cancer. The study aimed to compare cost-effectiveness ratios of H. pylori test-and-treat programs to prevent gastric cancer in Taiwan, referring to the nationwide reimbursement database and expected years of life lost. Materials and Methods During 1998–2009, there were 12,857 females and 24,945 males with gastric adenocarcinoma in Taiwan National Cancer Registry. They were followed up to 2010 and linked to the reimbursement database of National Health Insurance and the national mortality registry to determine lifetime health expenditures and expected years of life lost. Cost-effectiveness ratios of H. pylori test-and-treat programs for prevention of gastric adenocarcinoma were compared between screenings with 13C-urea breath test and with anti-H. pylori IgG. Results The test-and-treat program with anti-H. pylori IgG to prevent gastric adenocarcinoma had lower incremental cost-effectiveness ratios than that with 13C-urea breath test in both sexes (females: 244 vs 1071 US dollars/life-year; males: 312 vs 1431 US dollars/life-year). Cost saving would be achieved in an endemic area where H. pylori prevalence was >73.5%, or by selecting subpopulations with high absolute risk reduction rates of cancer after eradication. Moreover, expected years of life lost of gastric adenocarcinoma were higher and the incremental cost-effectiveness ratios of test-and-treat programs were more cost-effective in young adults (30–69 y/o) than in elders (≥70 y/o). Conclusions The test-and-treat program with anti-H. pylori IgG shall be cost-effective to prevent gastric adenocarcinoma in a high endemic area, especially beginning at 30 years of age when H. pylori prevalence rates become stabilized.

Background Flagellar motility of Helicobacter pylori has been shown to be important for the bacteria to establish initial colonization. The ferric uptake regulator (Fur) is a global regulator that has been identified in H. pylori which is involved in the processes of iron uptake and establishing colonization. However, the role of Fur in H. pylori motility is still unclear. Materials and Methods Motility of the wild-type, fur mutant, and fur revertant J99 were determined by a soft-agar motility assay and direct video observation. The bacterial shape and flagellar structure were evaluated by transmission electron microscopy. Single bacterial motility and flagellar switching were observed by phase-contrast microscopy. Autoinducer-2 (AI-2) production in bacterial culture supernatant was analyzed by a bioluminescence assay. Results The fur mutant showed impaired motility in the soft-agar assay compared with the wild-type J99 and fur revertant. The numbers and lengths of flagellar filaments on the fur mutant cells were similar to those of the wild-type and revertant cells. Phenotypic characterization showed similar swimming speed but reduction in switching rate in the fur mutant. The AI-2 production of the fur mutant was dramatically reduced compared with wild-type J99 in log-phase culture medium. Conclusions These results indicate that Fur positively modulates H. pylori J99 motility through interfering with bacterial flagellar switching.

Background Corpus-predominant gastritis index (CGI) is an early histological marker to identify Helicobacter pylori-infected gastric cancer relatives at risk of cancer. This study validated whether CGI is more prevalent in H. pylori-infected nonulcer dyspepsia (NUD) subjects than in duodenal ulcer (DU) controls and whether it is reversible after H. pylori eradication or is correlated with noninvasive biomarkers. Materials and Methods In this longitudinal cohort study, 573 H. pylori-infected subjects were enrolled, including 349 NUD and 224 DU. Gastric specimens were provided to assess CGI, spasmolyic polypeptide-expressing metaplasia (SPEM), and Operative Link on Gastric Intestinal Metaplasia assessment (OLGIM). Serum pepsinogen I and II levels were assessed using enzyme-linked immunosorbent assay. CGI subjected were followed up at least 1 year after H. pylori eradication. Results NUD subjects had higher prevalence rates of CGI (47.0% vs 29.9%, P

BACKGROUND AND AIMS Spasmolytic polypeptide-expressing metaplasia (SPEM) is a preneoplastic gastric cancer lesion related to epigenetic microRNA (miRNA) expression. This study elucidated whether Helicobacter pylori-infected first-degree relatives of patients with gastric cancer (GCF) are susceptible to have SPEM and correlated with miR-21, 155, and 223 expressions. We also validated whether SPEM and these miRNAs can be regressed after H pylori eradication. METHODS We prospectively enrolled 148 GCF and 148 nonulcer dyspepsia (NUD) subjects without gastric cancer familial history as controls. Each case had received a panendoscopy to determine H pylori status and gastric histology, including SPEM. The cases with SPEM were followed after H pylori eradication to determine SPEM regression. The total RNA was extracted to analyze tissues miR-21, 155, and 223 before and after eradication. RESULTS GCF subjects had a higher prevalence of H pylori infection (73% vs 32%) and SPEM (42% vs 14%, P

Background Previous international consensus statements provided general policies for the management of Helicobacter pylori infection. However, there are geographic differences in the prevalence and antimicrobial resistance of H. pylori, and in the availability of medications and endoscopy. Thus, nationwide or regional consensus statements are needed to improve control of H. pylori infection and gastric cancer. Materials and Methods This consensus statement for management of H. pylori in Taiwan has three major sections: (1) optimal diagnosis and indications; (2) current treatment strategies; and (3) screening-to-treat and surveillance for control of gastric cancer. The literature review emphasized recent data for development of draft statements and determination of levels of evidence. Twenty-five Taiwan experts conducted a consensus conference, by a modified Delphi process, to modify the draft statements. Consensus, defined as an agreement of least 80% of the experts, and recommendation grade were determined by anonymous voting. Results There were 24 consensus statements. Section 1 has seven statements on recommendations for the diagnosis and indications for treatment of H. pylori infection. Section 2 has 10 statements that provide an updated treatment algorithm for first-line, second-line, and third-line regimens. Section 3 has seven statements regarding H. pylori eradication for reducing the risk of gastric cancer, with a cost-benefit analysis. After H. pylori eradication, the consensus highlights the use of endoscopic surveillance and/or chemoprevention to further reduce the burden of gastric cancer. Conclusions This consensus statement has updated recommendations for improving the clinical management of H. pylori infection in areas such as Taiwan, which have high prevalence of H. pylori infection and gastric cancer.

Background & aims Gastric cancer has familial clustering in incidence, and the familial relatives of gastric cancer sufferers are prone to have spasmolytic polypeptide-expressing metaplasia (SPEM), and intestinal metaplasia (IM) after H. pylori infection. This study tested whether serum pepsinogen I/II and trefoil factor family (TFF) proteins can predict SPEM or IM in the H. pylori-infected relatives of patients with gastric cancer. Methods We prospectively enrolled 119 H. pylori-infected relatives of gastric cancer patients of noncardiac gastric cancer patients, who then received panendoscopy to obtain gastric biopsy to define the presence of corpus gastritis index (CGI), SPEM, and IM. The advanced SPEM in histology was defined by TFF2 immunohistochemistry. Each patient also had checkups of serum TFF2, TFF3, and pepsinogen I/II by enzyme-linked immunosorbent assay (ELISA). Results The 119 H. pylori-infected relatives included 61 with SPEM, and 34 with IM. The presence of either IM or SPEM was not related to the serum TFF2, TFF3, and pepsinogen I/II levels (p > .05). Serum TFF2 levels were higher in relatives with CGI who also had advanced SPEM (p = .032). For relatives without CGI, the elevated serum TFF2 levels correlated with higher H. pylori density and more severe gastritis in antrum (p = .001). Conclusion The serum TFF2 level cannot predict SPEM or IM in H. pylori-infected relatives of patients with gastric cancer. For H. pylori-infected relatives with CGI, serum TFF2 levels may predict the advanced severity of SPEM. Elevated serum TFF2 levels may indicate severe H. pylori-related inflammation, at risk of development or progression of SPEM in relatives without CGI.

Background and Aim Intestinal metaplasia (IM) has overexpressions of COX-2. Short-term 8-week celecoxib, a selective COX-2 inhibitor, exerts a preliminary hint to improve regression in part for persistent IM after Helicobacter pylori eradication. This study further validated whether or not a prolonged duration of celecoxib of up to 1 year can be safe and effective. Methods One hundred and forty patients, with persistent IM after H. pylori eradication for 1 year, were included with half of them receiving celecoxib 200 mg/day for 12 months and the other half serving as controls. Each patient received serial checkups of blood creatinine levels every 4 months. After the 1-year follow-up, panendoscopy was repeated to assess the IM regression. The serial gastric specimens, taken before and after celecoxib therapy, were immunochemically stained for COX-2. Results The intention-to-treat (ITT) and per-protocol (PP) analyses to the rates of IM regression were higher in the celecoxib group than in the controls (ITT: 44.3% [31/70] vs 14.3% [10/70], p

Backgrounds: The levofloxacin resistance caused by gyrA gene mutation is rising rapidly to limit wide application for Helicobacter pylori eradication. We investigated whether gemifloxacin has a superior antimicrobial activity to levofloxacin against H. pylori. Materials and Methods: Forty-four consecutive clinical H. pylori isolates with levofloxacin resistance and 80 randomly selected levofloxacin-sensitive controls were tested for gemifloxacin sensitivity by E-test. The resistance to levofloxacin or gemifloxacin was defined as minimal inhibitory concentration (MIC) >1 mg/L. The clinical features and GyrA mutation patterns checked by direct sequencing were also analyzed to assess its association with the H. pylori gemifloxacin resistance. Results: All levofloxacin-sensitive H. pylori isolates were sensitive to gemifloxacin. Eight strains (18.2%) resistant to levofloxacin could be still sensitive to gemifloxacin. Gemifloxacin achieved a 5-time lower in MIC levels against levofloxacin-resistant isolates. Nearly all levofloxacin-resistant isolates (97.7%, 43/44) had GyrA mutation at amino acid position 87 or 91. Double mutation sites may play dual roles in quinolone resistance, as N87K plus H57Y or D91N plus V77A mutations showed high-level resistance to both quinolones; whereas D91Y plus A97V or D91N plus A97V mutations showed low level levofloxacin resistance to become sensitive to gemifloxacin. In H. pylori isolates with single N87K, D91Y or D91N mutation, near 20% was gemifloxacin-sensitive and levofloxacin-resistant. The gemifloxacin-resistant rate of H. pylori was higher in patients with gastric ulcer than in those without (p

Background: The benefits of probiotics to the pediatric Helicobacter pylori infection remain uncertain. We tested whether the H. pylori-infected children have an altered gut microflora, and whether probiotics-containing yogurt can restore such change and improve their H. pylori-related immune cascades. Methods: We prospectively included 38 children with H. pylori infection confirmed by a positive 13 C-urea breath test (UBT) and 38 age- and sexmatched noninfected controls. All of them have provided the serum and stool samples before and after 4-week ingestion of probiotics-containing yogurt. The serum samples were tested for the TNF-a, IL-10, IL-6, immunoglobulin (Ig) A, G, E, pepsinogens I and II levels. The stool samples were tested for the colony counts of Bifidobacterium spp. and Escherichia coli. The follow-up UBT indirectly assessed the H. pylori loads after yogurt usage. Results: The H. pylori-infected children had lower fecal Bifidobacterium spp. count (p = .009), Bifidobacterium spp. ⁄E. coli ratio (p = .04), serum IgA titer (p = .04), and pepsinogens I ⁄II ratio (p < .001) than in controls. In the H. pylori-infected children, 4-week yogurt ingestion reduced the IL-6 level (p < .01) and H. pylori loads (p = .046), but elevated the serum IgA and pepsinogen II levels (p < .001). Moreover, yogurt ingestion can improve the childhood fecal Bifidobacterium spp. ⁄E. coli ratio (p = .03). Conclusions: The H. pylori-infected children have a lower Bifidobacterium microflora in gut. The probiotics-containing yogurt can offer benefits to restore Bifidobacterium spp. ⁄E. coli ratio in children and suppress the H. pylori load with increment of serum IgA but with reduction in IL-6 in H. pylori-infected children.

Background: Helicobacter pylori uses SabA to interact with sialyl-Lewis x on the gastric mucosal surface to establish persistent colonization. The number of CT repeats in sabA is variable and thus influences SabA translation, but the expression of SabA determined by Western blotting does not fully match with a CT sequence-based prediction. Furthermore, a homopolymeric thymidine (polyT) tract located upstream of sabA has been observed, but its role in regulating sabA expression is still unknown. Methods: The transcriptional start site (TSS) of sabA in strains J99 and Hp258 was determined by 5′ RACE. One hundred and fifteen clinical isolates were sequenced to analyze the distribution of the polyT tract length and promoter sequence. Finally, RT-PCR and an E. coli-lux reporter system were used to determine the sabA promoter activity with different lengths of the polyT tract. Results: The TSS of sabA was located at 66 or 64 bp upstream of the translational start codon in J99 and Hp258, respectively. The polyT tract close to the −35 element varied from T10 to T28 in 115 clinical isolates, and 70% of the isolates contained a stretch of 14–19 Ts. The sabA gene displayed slipped strand mispairing (SSM) of the polyT tract, generating varying genotypes in J99 (16–18 Ts) and Hp258 (14–15 Ts). Furthermore, J99 with lengths of T16 and T30, had higher sabA promoter activity than the common length of T18. Conclusion: Our findings indicate that the sabA promoter region modulates its transcriptional activity through a variable polyT tract, and SSM generates mixed genotypes in the population.

Background: Osteopontin (OPN) is involved in the gastric cancer progression. The study validated whether OPN expressions correlate with Helicobacter pylori-related chronic gastric inflammation and the precancerous change as intestinal metaplasia (IM). Methods: This study included 105 H. pylori-infected patients (63 without and 42 with IM) and 29 H. pylori-negative controls. In each subject, the gastric OPN expression intensity was evaluated by immunohistochemistry, and graded from 0 to 4 for the epithelium, lamina propria, and areas with IM, respectively. For the H. pylori-infected subjects, the gastric inflammation was assessed by the Updated Sydney System. Forty-nine patients received follow-up endoscopy to assess OPN change on gastric mucosa after H. pylori eradication. The in vitro cell-H. pylori coculture were performed to test the cell origin of OPN. Results: The H. pylori-infected patients had higher gastric OPN expression than the noninfected controls (p

Background: Both ghrelin and leptin are important appetite hormones secreted from the stomach. We examined whether demographic background, Helicobacter pylori infection, or its related gastritis severity could be associated with circulating ghrelin and leptin levels. Methods: This study prospectively enrolled 341 dyspeptic patients (196 females, 145 males), who had received endoscopy to provide the gastric specimens over both antrum and corpus for histology reviewed by the updated Sydney's system. The fasting blood sample of each patient was obtained for total ghrelin and leptin analysis. Results: Without H. pylori infection, there were similar ghrelin levels between female and male patients. In the H. pylori-infected patients, the males had lower plasma ghrelin levels than females (1053 vs. 1419 pg/mL, p

Background: Fluoroquinolone-containing therapy is effective in eradicating Helicobacter pylori. However, the resistance rate of H. pylori to fluoroquinolones in Taiwan has not yet been reported. In this study, we aimed to investigate the susceptibility to antibiotics commonly used in eradication schedules and fluoroquinolones in H. pylori. Methods: A total of 210 clinical isolates of H. pylori were collected from April 1998 to September 2007 from patients in southern Taiwan. The in vitro activities of six antimicrobial agents were determined by the agar dilution method and Etest. The mutations in quinolone resistance-determining regions of gyrA and gyrB were investigated by direct sequencing. Results: Overall, 5.7% of the isolates were resistant to ciprofloxacin and levofloxacin. The resistance rate to amoxicillin, clarithromycin, metronidazole, and tetracycline was 1.0% (two of 210), 9.5% (20 of 210), 27.6% (58 of 210), and 0.5% (one of 210), respectively. The resistance rate to either ciprofloxacin or to levofloxacin increased from 2.8% (1998–2003) to 11.8% (2004–2007). The mutations in gyrA at N87 or D91 had an impact on primary fluoroquinolone resistance in H. pylori. Garenoxacin, but not moxifloxacin, had a good in vitro inhibitory effect against ciprofloxacin/levofloxacin-resistant strains compared with objective minimal inhibitory concentration values. Conclusions: Drug resistance to ciprofloxacin and levofloxacin in H. pylori collected from 2004 to 2007 increased significantly compared with resistance level observed during 1998–2003. The continuous surveillance of quinolone resistance among H. pylori is important in this area.

Objective: To identify the optimal dosage of levofloxacin to eradicate persistent Helicobacter pylori when triple therapy with amoxicillin, clarithromycin, and omeprazole fails. Methods: We investigated 124 patients whose triple therapy including clarithromycin had failed. Clarithromycin resistance was indirectly assessed by the 13C-urea breath test, with a post-treatment value cut-off point at 15. All patients were randomly divided into two groups, to receive 1-week amoxicillin 1 g and lansoprazole 30 mg twice daily, plus either levofloxacin 500 mg once (ALL-500 group) or twice daily (ALL-1000 group). Six weeks later, the 13C-urea breath test was repeated to assess whether H. pylori was eradicated. Results: Intention-to-treat (ITT) and per-protocol (PP) analysis showed no difference in H. pylori eradication rates in both the ALL-500 and ALL-1000 groups (ITT: 79% vs. 80.6%, p > .05; PP: 86% vs. 87.5%, p > .05). For both groups, the per-protocol H. pylori eradication rates were also similarly high between patients with a post-treatment value of 13C-urea breath test ≤ 15 and those with a value > 15 (ALL-500: 85% vs. 86.5%, p > .05; ALL-1000: 88.9% vs. 86.8%, p > .05). Conclusion: One-week levofloxacin 500 mg daily-based triple therapy is effective for eradicating the persistent H. pylori after a failed triple therapy with amoxicillin, clarithromycin, and omeprazole.

Background Osteopontin, an important immune modulator and oncogenic promoter, is upregulated in H. pylori-infected gastric mucosa. However, the underlying mechanisms and biological significance are poorly understood. We investigated whether osteopontin was upregulated in gastric epithelial cells by H. pylori and the virulence factors involved. Moreover, cellular component changes caused by osteopontin were also investigated. Materials and Methods The gastric epithelial cell line MKN45 was cocultured with wild-type and mutant H. pylori to analyze osteopontin expression. Beta-catenin levels in cell lysate and interleukin-8 levels in supernatant were analyzed. The difference in osteopontin expression levels in both gastric epithelium and plasma was compared between H. pylori-infected patients and uninfected controls. Results H. pylori induced intracellular, but not secretory, osteopontin expression in MKN45 cells. Accordingly, osteopontin expression intensity in gastric epithelium was higher in H. pylori-infected patients than in controls, but osteopontin levels in plasma were similar between both patient groups. H. pylori virulence factor CagA delivered via the type IV secretion system was essential for intracellular osteopontin upregulation. H. pylori induced β-catenin accumulation and interleukin-8 secretion, whereas osteopontin knockdown completely abrogated these effects, in MKN45 cells. TLR2 antagonist abolished iOPN expression induced by H. pylori gastritis strain, but not by H. pylori cancer strain. Conclusions H. pylori is dependent on CagA translocation via the type IV secretion system to induce intracellular osteopontin expression in gastric epithelial cells. Upregulated intracellular osteopontin may promote gastric carcinogenesis via increased β-catenin accumulation and interleukin-8 secretion.

Background. We tested whether Helicobacter pylori-infected dyspeptic mothers had a higher rate of H. pylori infection in their children, and whether such H. pylori-infected children were predisposed to iron deficiency or growth retardation. Materials and methods. A total of 163 children from 106 dyspeptic mothers (58 with and 48 without H. pylori infection) were enrolled to evaluate body weight, height, hemoglobin, serum ferritin, and H. pylori infection using the 13C-urea breath test. A questionnaire was used to evaluate demographic factors of each child. Results. The rate of H. pylori infection in children with H. pylori-infected dyspeptic mothers was higher than that of children with noninfected mothers (20.5% vs. 5.3%; p

Purpose. We tested whether the serological response to Flavodoxin-A (FldA) protein and anti-Helicobacter pylori immunoblots correlated to the degree of mucosa-associated lymphoid tissue (MALT) in the stomach. Methods. Eighty H. pylori-infected patients with different degrees of MALT in the stomach were investigated with serum sampling and endoscopy on enrolment, the 2nd and the 12th months after anti-H. pylori therapy. All sera were tested for the anti-FldA protein and anti-H. pylori immunoblots, including 19.5, 26.5, 30, 35, 89, and 116 KDa (CagA). Regression of follicular gastritis was assessed by histology. Results. Patients with dense lymphoid follicles had higher prevalence rates of anti-FldA protein, 19.5, 26.5, and 30 KDa antibodies of H. pylori (p

Background. Even after partial gastrectomy, Helicobacter pylori may persist in the residual stomach but be less abundant in the bacterial load. H. pylori stool antigen is a reliable noninvasive tool to detect H. pylori infection in patients without gastrectomy. We thus test whether [1] the course of H. pylori eradication therapy could be diminished [2]; stool antigen can effectively detect H. pylori infection for the patients with gastrectomy. Methods. One hundred and eight patients who had undergone partial gastrectomy were enrolled to receive panendoscopy and provided stool samples for H. pylori stool antigen within 3 days after endoscopy. The H. pylori-infected patients were then randomized to receive either a 3- or 7-day triple therapy for H. pylori eradication. Six weeks later, to evaluate the success of H. pylori eradication, patients received a follow-up endoscopy and again provided stool samples for H. pylori stool antigen. Results. Seventy out of 108 patients, proven to have H. pylori infection, were evenly randomized into 3-day and 7-day therapy groups. The H. pylori eradication rates were similar between the 3-day and 7-day triple therapy (90.9 vs. 93.8%, p > .05). Before therapy, the H. pylori stool antigen was 93% sensitive and 100% specific to detect H. pylori. After therapy, H. pylori stool antigen remain 100% sensitive and 88.3% specific to detect the failure of eradication therapy. Conclusion.H. pylori stool antigen is a highly reliable tool to screen H. pylori infection before therapy and to assess the success of eradication therapy in partial gastrectomy patients. To eradicate H. pylori infection for patients with partial gastrectomy, the duration of triple therapy can be shortened.

Background Motility mediated by the flagella of Helicobacter pylori has been shown to be required for normal colonization and is thought to be important for the bacteria to move toward the gastric mucus in niches adjacent to the epithelium. Barnard et al. showed that CsrA appears to be necessary for full motility and the ability to infect mice, but its mechanism of regulation is still unclear. Methods Motility and cell adhesion ability were determined in wild-type, csrA mutant, and revertant J99 strains. The bacterial shape and flagellar structure were evaluated by transmission electron microscopy. The expression of two major flagellins, flaA/flaB, and the alternative sigma factor rpoN (σ54) were determined by real-time quantitative RT-PCR and Western blot. Results The csrA mutant showed loss of motility and lower adhesion ability compared with the wild-type and revertant J99 strains. The csrA mutant was not flagellated. Transcription of flaA and flaB mRNA decreased to only 40% and 16%, respectively, in the csrA mutant compared with the wild-type J99 (p = .006 and

Background Motility mediated by the flagella of Helicobacter pylori is important for the cells to move toward the gastric mucus in niches adjacent to the epithelium; then, H. pylori uses the adhesin SabA to interact with sialyl-Lex on inflammatory host cells for persistent infection. Here, we reveal the clinical association of bacterial motility, SabA expression, and pathological outcomes. Methods Ninety-six clinical isolates were screened for bacterial motility, and the expression of SabA of each isolate was confirmed by Western blotting. H. pylori-infected patients were assessed for their bacterial density, sialyl-Lex expression, inflammatory scores, and clinical diseases. Results The mean diameter in the motility assay was 17 mm, and eight (8.3%) of the strains had impaired motility, with a diameter

Osteopontin (OPN) is involved in the gastric cancer progression. The study validated whether OPN expressions correlate with Helicobacter pylori-related chronic gastric inflammation and the precancerous change as intestinal metaplasia (IM).This study included 105 H. pylori-infected patients (63 without and 42 with IM) and 29 H. pylori-negative controls. In each subject, the gastric OPN expression intensity was evaluated by immunohistochemistry, and graded from 0 to 4 for the epithelium, lamina propria, and areas with IM, respectively. For the H. pylori-infected subjects, the gastric inflammation was assessed by the Updated Sydney System. Forty-nine patients received follow-up endoscopy to assess OPN change on gastric mucosa after H. pylori eradication. The in vitro cell-H. pylori coculture were performed to test the cell origin of OPN.The H. pylori-infected patients had higher gastric OPN expression than the noninfected controls (p.001). For the H. pylori-infected patients, an increased OPN expression correlated with more severe chronic gastric inflammation (p.001) and the presence of IM (OR: 2.6, 95% CI: 1.15-5.94, p = .02). Within the same gastric bits, lamina propria expressed OPN stronger than epithelium (p.001), suggesting OPN predominantly originates from inflammatory cells. The in vitro assay confirmed H. pylori stimulate OPN expression in the monocytes, but not in the gastric epithelial cells. After H. pylori eradication, the gastric OPN expression could be decreased only in areas without IM (p.05).Increased gastric OPN expression by H. pylori infection can correlate with a more severe gastric inflammation and the presence of IM.

Background: Helicobacter pylori infection causes chronic gastric inflammation and intestinal metaplasia (IM), related with deregulation of Wnt pathway and over-expressions of COX-2, matrix metalloproteinase (MMP), and tissue inhibitors of matrix metalloproteinase (TIMP). We thus test the host genomic predispositions related to the risk of IM after H. pylori infection. Methods: We enrolled 296 H. pylori-infected patients to provide gastric biopsies for histology and genomic DNA for genotypes of single nucleotide polymorphisms (SNPs), including APC, COX-2, IL-1B, IL-1RN, IL-10, MMP-2, MMP-9, TIMP-1, and TIMP-2 determined by sequence specific oligonucleotide probe, sequence specific primers, restriction fragment length polymorphism, or real-time polymerase chain reaction. Results: There was no association between the presence of IM and SNPs in APC, COX-2, IL-1B, IL-1RN, IL-10, MMP-2, and TIMP-2. The risk of IM was increased up to 2.29-folds in males with TIMP-1 372 C, and 3.03-fold in females with T carrier (p

To identify the optimal dosage of levofloxacin to eradicate persistent Helicobacter pylori when triple therapy with amoxicillin, clarithromycin, and omeprazole fails.We investigated 124 patients whose triple therapy including clarithromycin had failed. Clarithromycin resistance was indirectly assessed by the (13)C-urea breath test, with a post-treatment value cut-off point at 15. All patients were randomly divided into two groups, to receive 1-week amoxicillin 1 g and lansoprazole 30 mg twice daily, plus either levofloxacin 500 mg once (ALL-500 group) or twice daily (ALL-1000 group). Six weeks later, the (13)C-urea breath test was repeated to assess whether H. pylori was eradicated.Intention-to-treat (ITT) and per-protocol (PP) analysis showed no difference in H. pylori eradication rates in both the ALL-500 and ALL-1000 groups (ITT: 79% vs. 80.6%, p.05; PP: 86% vs. 87.5%, p.05). For both groups, the per-protocol H. pylori eradication rates were also similarly high between patients with a post-treatment value of (13)C-urea breath testor = 15 and those with a value15 (ALL-500: 85% vs. 86.5%, p.05; ALL-1000: 88.9% vs. 86.8%, p.05).One-week levofloxacin 500 mg daily-based triple therapy is effective for eradicating the persistent H. pylori after a failed triple therapy with amoxicillin, clarithromycin, and omeprazole.

Background. Metronidazole-resistant H. pylori associating with mutations of rdxA or frxA is still a debated topic. This study investigates whether rdxA and frxA mutations of H. pylori accounted for the high MIC value (≥ 64 µg/ml) of metronidazole (Mtz). Material and Methods. From 126 clinical H. pylori isolates, we examined 14 Mtz-sensitive, 18 Mtz-resistant H. pylori, and eight pairs of Mtz-sensitive and Mtz-resistant colonies simultaneously present within a single gastric biopsy. The paired strains from one single biopsy were proven identical by PCR-RFLP. MICs of Mtz were checked by the E-test and agar dilution method. The mutations of rdxA and frxA sequencing were matched with the Mtz-susceptible ATCC 26695 and J99. Results. There were 89% (16/18) of Mtz-resistant isolates with mutation of RdxA. Half of the 14 Mtz-sensitive strains, all without mutation of RdxA, still contained truncation of FrxA. Within the paired isolates from a single biopsy, rdxA mutation (86%) was more common than frxA mutation (43%) in those isolates with high-level Mtz-resistant H. pylori. RdxA truncation was more prevalent in Mtz-resistant strains with high MICs than in those with low to moderate MICs (75% vs. 20%, p = .01, OR: 12, 95% CI: 1.8–81.7). Conclusion. Mutations in the rdxA gene rather than the frxA gene generally determine a high MIC level of Mtz-resistant H. pylori in Taiwan.

Aim. To test whether vitamin C and E supplements to triple therapy can improve the Helicobacter pylori eradication rate and gastric inflammation. Methods. A total of 104 H. pylori-infected patients were randomized to receive: either lansoprazole, amoxicillin, and metronidazole twice daily for 1 week (triple-only group) or lansoprazole, amoxicillin, metronidazole plus vitamin C (250 mg) and vitamin E (200 mg) twice daily for 1 week, followed immediately by vitamin C and E once daily for 6 consecutive weeks (triple-plus-vitamin group). Eight weeks after the completion of triple therapy, patients were assessed for the effectiveness of H. pylori eradication. The severity of gastric inflammation in histology was assessed for the acute and chronic inflammation scores. Results. Intention-to-treat and per-protocol eradication rates were 59.1% and 64.4% in the triple-only group, and 40% and 44% in the triple-plus-vitamin group. In the patients infected with metronidazole susceptible isolates, the triple-only group had a higher intention-to-treat eradication rate than those in the triple-plus-vitamin group (80% vs. 53.1%, p