Background Helicobacter pylori infection produces progressive mucosal damage that may eventually result in gastric cancer. We studied the changes that occurred in the presence and severity of atrophic gastritis and the prevalence of H. pylori infection that occurred coincident with improvements in economic and hygienic conditions in Japan since World War II. Materials and Methods The prevalence of H. pylori infection and histologic grades of gastric damage were retrospectively evaluated using gastric biopsy specimens obtained over a 40-year period. Gastric atrophy and intestinal metaplasia were scored using the updated Sydney classification system. Results The prevalence of H. pylori and severity of atrophy were examined in 1381 patients including 289 patients examined in the 1970s (158 men; mean age, 44.9 years), 787 in the 1990s (430 men; 44.2 years), and 305 in the 2010s (163 men; 53.2 years). Overall, the prevalence of H. pylori infection decreased significantly from 74.7% (1970s) to 53% (1990s) and 35.1% (2010s) (p < .01). The prevalence of atrophy in the antrum and corpus was significantly lower in the 2010s (33, 19%, respectively) compared to those evaluated in either the 1970s (98, 82%) (p < .001) or 1990s (80, 67%) (p < .001). The severity of atrophy and intestinal metaplasia also declined remarkably among those with H. pylori infection. Conclusions There has been a progressive and rapid decline in the prevalence of H. pylori infection as well a fall in the rate of progression of gastric atrophy among H. pylori-infected Japanese coincident with the westernization and improvements in economic and hygienic conditions in Japan since World War II.
BackgroundHelicobacter pylori infection produces progressive mucosal damage that may eventually result in gastric cancer. We studied the changes that occurred in the presence and severity of atrophic gastritis and the prevalence of H.pylori infection that occurred coincident with improvements in economic and hygienic conditions in Japan since World War II. Materials and MethodsThe prevalence of H.pylori infection and histologic grades of gastric damage were retrospectively evaluated using gastric biopsy specimens obtained over a 40-year period. Gastric atrophy and intestinal metaplasia were scored using the updated Sydney classification system. ResultsThe prevalence of H.pylori and severity of atrophy were examined in 1381 patients including 289 patients examined in the 1970s (158 men; mean age, 44.9years), 787 in the 1990s (430 men; 44.2years), and 305 in the 2010s (163 men; 53.2years). Overall, the prevalence of H.pylori infection decreased significantly from 74.7% (1970s) to 53% (1990s) and 35.1% (2010s) (p<.01). The prevalence of atrophy in the antrum and corpus was significantly lower in the 2010s (33, 19%, respectively) compared to those evaluated in either the 1970s (98, 82%) (p<.001) or 1990s (80, 67%) (p<.001). The severity of atrophy and intestinal metaplasia also declined remarkably among those with H.pylori infection. ConclusionsThere has been a progressive and rapid decline in the prevalence of H.pylori infection as well a fall in the rate of progression of gastric atrophy among H.pylori-infected Japanese coincident with the westernization and improvements in economic and hygienic conditions in Japan since World War II.
BackgroundInfection of Helicobacter pylori mainly occurs in childhood. In Japan, incidence of gastric cancer is still high in the senior citizen population, but little is known about the current H.pylori infection status among children or their family members. MethodsAs a population-based study, the prevalence of H.pylori infection and change in infection status over a 1-year interval in children were determined. Family members of some participants were also invited to participate in the study to determine their infection status. All children of specific ages attending 16 schools in Sasayama, Hyogo Prefecture, were invited to participate. H.pylori infection was determined by the stool antigen test and diagnosis confirmed by polymerase chain reaction and the urea breath test. ResultsHelicobacter pylori prevalence was 1.9% among 689 children aged 0-8years in 2010 and 1.8% among 835 children aged 0-11 in 2011. No feco-conversion was observed in 430 children aged 0-8years (170 were aged 0-4years) who provided follow-up stool samples after 1year. The prevalence of infection was 6% (2 of 33) and 38% (6 of 16) in mothers of negative and positive probands (p=.04), respectively, and 12% (3 of 25) and 50% (8 of 16) (p=.01), respectively, in fathers. ConclusionHelicobacter pylori prevalence in Japanese children is approximately 1.8%, which is much lower than that reported in Japanese adults. New infection may be rare. Parent-to-child infection is thought to be the main infection route of the infrequent infection for children in Japan.
BackgroundHelicobacter pylori is one of the most common causes of chronic bacterial infection in humans, directly related to peptic ulcer and gastric cancer. It has been suggested that H.pylori can be acquired through different transmission routes, including water. In this study, culture and qPCR were used to detect and identify the presence of H.pylori in drinking water. Furthermore, the combined techniques PMA-qPCR and DVC-FISH were applied for detection of viable cells of H.pylori. ResultsAmong 24 drinking water samples, 16 samples were positive for the presence of H.pylori, but viable cells were only detected in six samples. Characteristic colonies, covered by a mass of bacterial unspecific growth, were observed on selective agar plates from an only sample, after enrichment. The mixed culture was submitted to DVC-FISH and qPCR analysis, followed by sequencing of the amplicons. Molecular techniques confirmed the growth of H.pylori on the agar plate. ConclusionsOur results demonstrate for the first time that H.pylori can survive and be potentially infective in drinking water, showing that water distribution systems could be a potential route for H.pylori transmission.
BackgroundHelicobacter pylori infection and metabolic syndrome have been reported to be positively associated. However, only a few studies have focused on this issue, and H.pylori serum antigen was used to diagnose infection in most of them. We aimed to investigate the association between metabolic syndrome factors and H.pylori infection, as diagnosed via a C-13-urea breath test. Materials and MethodsThis cross-sectional study consisted of 3578 subjects (18-64years old) enrolled from one health management center between 2008 and 2013. H.pylori infection was defined as a positive urea breath test. The risk of metabolic syndrome from H.pylori infection was assessed using a multiple logistic regression model. ResultsThe prevalence of the H.pylori was similar in both genders (20.6% in men and 19.7% in women). H.pylori -infected participants had significantly higher body mass index, fasting glucose, low-density lipoprotein, and triglycerides, and lower high-density lipoprotein (p<0.05), than uninfected ones (p<0.05). The prevalence of metabolic syndrome was higher in H.pylori -infected subjects than uninfected ones (men: 12.4% vs. 7.4%, p<0.001; women: 7.4% vs. 2.5%, p<0.001). Furthermore, H.pylori infection prevalence increased with metabolic score (P for trend <0.001, both sexes). Moreover, the association between metabolic syndrome and UBT positivity was significant in females (OR 1.91, 95% CI:1.03-3.53), but only borderline significant in males (OR 1.38, 95% CI: 0.97-1.95). ConclusionH.pylori infection is positively associated with metabolic syndrome, especially in females. The causal relationship between H.pylori infection and metabolic syndrome warrants further investigation.
BackgroundMyocardial infarction is a fatal cardiovascular disease and one of the most common death causes all around the world. The aim of the meta-analysis was to quantify the risk of myocardial infarction associated with Helicobacter pylori infection. MethodsA literature search was performed to identify studies published before 14 July, 2014, for relevant risk estimates. Fixed and random effect meta-analytical techniques were conducted for myocardial infarction. ResultsTwenty-six case-control studies involving 5829 myocardial infarction patients and more than 16,000 controls were included. Helicobacter pylori infection was associated with an increased risk of myocardial infarction (OR: 2.10, 95%CI: 1.75-2.53, p=.06). We also discovered a significant association between the bacteria and risk of myocardial infarction in young people (OR: 1.93, 95% CI: 1.41-2.66, p=.07), in elder people (OR: 2.02, 95% CI: 1.60-2.54, p=.29), in Caucasians (OR: 2.29, 95% CI: 1.99-2.63, p=.12), and in Asians (OR: 1.75, 95% CI: 1.12-2.73, p=.08). ConclusionOur meta-analyses suggested a possible indication of relationship between Helicobacter pylori infection and the risk of myocardial infarction. The pathogenicity might not be affected by age and race. More researches should be conducted to explore the mechanisms involved.
BackgroundHelicobacter pylori (H.pylori) infection leads to acute induction of Sonic Hedgehog (Shh) in the stomach that is associated with the initiation of gastritis. The mechanism by which H.pylori induces Shh is unknown. Shh is a target gene of transcription factor Nuclear Factor-B (NFB). We hypothesize that NFB mediates H.pylori-induced Shh. Materials and MethodsTo visualize Shh ligand expression in response to H.pylori infection in vivo, we used a mouse model that expresses Shh fused to green fluorescent protein (Shh::GFP mice) in place of wild-type Shh. In vitro, changes in Shh expression were measured in response to H.pylori infection using 3-dimensional epithelial cell cultures grown from whole dissociated gastric glands (organoids). Organoids were generated from stomachs collected from the fundic region of control and mice expressing a parietal cell-specific deletion of Shh (PC-Shh(KO) mice). ResultsWithin 2days of infection, H.pylori induced Shh expression within parietal cells of Shh::GFP mice. Organoids expressed all major gastric cell markers, including parietal cell marker H+,K+-ATPase and Shh. H.pylori infection of gastric organoids induced Shh expression; a response that was blocked by inhibiting NFB signaling and correlated with IB degradation. H.pylori infection of PC-Shh(KO) mouse-derived organoids did not result in the induction of Shh expression. ConclusionGastric organoids allow for the study of the interaction between H.pylori and the differentiated gastric epithelium independent of the host immune response. H.pylori induces Shh expression from the parietal cells, a response mediated via activation of NFB signaling.
BackgroundWe aimed to examine the relationship of current Helicobacter pylori infection with lipid profile and cardiovascular disease and its eradication effect. MethodsHealthy subjects, who underwent routine checkup between October 2003 and December 2007, were followed up until June 2009. Helicobacter pylori and lipid profiles were measured both baseline and follow-up. Multiple logistic regression models for odds ratios (ORs) and 95% confidence intervals (CIs) were used to estimate the effects of H.pylori infection and its eradication, on lipids and cardiovascular disease. ResultsCurrent infection with H.pylori with 50.5% (6759/13383) at baseline increased low-density lipoprotein (LDL) and decreased high-density lipoprotein (HDL) than H. pylori-negative group. Successful eradication of H.pylori decreased the risk of high LDL compared with the persistent infection (OR 0.76, 95% CI 0.59-96), which was comparable to that of the persistent negative group (OR 0.82, 95% CI 0.70-0.97), and decreased the risk of low HDL (OR 0.68, 95% CI 0.49-0.96). Current infection of H.pylori increased the risk of cardiovascular disease (OR 3.27, 95% CI 1.31-8.14) at baseline, but its eradication failed to decrease the risk at a 2-year follow-up. However, persistent negative infection decreased the risk (OR 0.57, 95% CI 0.35-0.94) comparing to persistent positive infection at follow-up. ConclusionsCurrent infection with H.pylori had a positive association with high LDL, low HDL, and cardiovascular disease. Successful H.pylori eradication decreased the risk of high LDL and low HDL, but did not reduce the risk of cardiovascular disease.
BackgroundEpidemiologic studies of the carcinogenic stomach bacterium Helicobacter pylori have been limited by the lack of noninvasive detection and genotyping methods. We developed a new stool-based method for detection, quantification, and partial genotyping of H. pylori using droplet digital PCR (ddPCR), which allows for increased sensitivity and absolute quantification by PCR partitioning. Materials and MethodsStool-based ddPCR assays for H. pylori 16S gene detection and cagA virulence gene typing were tested using a collection of 50 matched stool and serum samples from Costa Rican volunteers and 29 H. pylori stool antigen-tested stool samples collected at a US hospital. ResultsThe stool-based H. pylori 16S ddPCR assay had a sensitivity of 84% and 100% and a specificity of 100% and 71% compared to serology and stool antigen tests, respectively. The stool-based cagA genotyping assay detected cagA in 22 (88%) of 25 stools from CagA antibody-positive individuals and four (16%) of 25 stools from CagA antibody-negative individuals from Costa Rica. All 26 of these samples had a Western-type cagA allele. Presence of serum CagA antibodies was correlated with a significantly higher load of H. pylori in the stool. ConclusionsThe stool-based ddPCR assays are a sensitive, noninvasive method for detection, quantification, and partial genotyping of H. pylori. The quantitative nature of ddPCR-based H. pylori detection revealed significant variation in bacterial load among individuals that correlates with presence of the cagA virulence gene. These stool-based ddPCR assays will facilitate future population-based epidemiologic studies of this important human pathogen.
BackgroundMultiple studies have established the importance of the tol-pal gene cluster in bacterial cell membrane integrity and outer membrane vesicle (OMV) formation in Escherichia coli. In contrast, the functions of Tol-Pal proteins in pathogenic organisms, including those of the Epsilonproteobacteria, remain poorly if at all defined. The aim of this study was to characterize the roles of two key components of the Tol-Pal system, TolB and Pal, in OMV formation in the pathogenic bacterium, Helicobacter pylori. MethodsH.pylori tolB, pal and tolBpal mutants, as well as complemented strains, were generated and assessed for changes in morphology and OMV production by scanning electron microscopy and enzyme-linked immunoassay (ELISA), respectively. The protein content and pro-inflammatory properties of OMVs were determined by mass spectroscopy and interleukin-8 (IL-8) ELISA on culture supernatants from OMV-stimulated cells, respectively. ResultsH.pylori tolB and pal bacteria exhibited aberrant cell morphology and/or flagella biosynthesis. Importantly, the disruption of H.pylori tolB but not pal resulted in a significant increase in OMV production. The OMVs from H.pylori tolB and pal bacteria harbored many of the major outer membrane and virulence proteins observed in wild-type (WT) OMVs. Interestingly, tolB, pal and tolBpal OMVs induced significantly higher levels of IL-8 production by host cells, compared with WT OMVs. ConclusionsThis work demonstrates that TolB and Pal are important for membrane integrity in H.pylori. Moreover, it shows how H.pylori tolB-pal genes may be manipulated to develop hypervesiculating strains for vaccine purposes.
Background and AimSitafloxacin-containing Helicobacter pylori eradication therapy is a promising third-line therapeutic approach, but there is no previous studies between gyrA mutation status of H. pylori strains and the efficacy of 10-day sitafloxacin-containing regimens. Here, we assessed the efficacy of 2 different 10-day sitafloxacin-containing rescue regimens. MethodsPatients who failed first- and second-line eradication therapies were enrolled. The minimum inhibitory concentrations (MICs) of sitafloxacin, amoxicillin, and metronidazole and the gyrA mutation status of the H. pylori strains were determined before treatment. The patients were randomized to receive a 10-day triple therapy containing either esomeprazole (20 mg, b.i.d.), amoxicillin (500 mg, q.i.d.), and sitafloxacin (100 mg, b.i.d.) (EAS regimen) or esomeprazole (20 mg, b.i.d.), metronidazole (250 mg, b.i.d.), and sitafloxacin (100 mg, b.i.d.) (EMS regimen). Eradication rates were evaluated by the [13C] urea breath test or the H. pylori stool antigen test. ResultsAll patients with gyrA mutation-negative strains (24 in EAS and 16 in EMS) showed successful eradication, irrespective of the regimen they received. In patients with gyrA mutation-positive strains, we found eradication rates of 70.3% (26/37) and 66.7% (26/39) in the EAS and EMS groups in per-protocol population, respectively (p = .81). According to logistic regression analyses, the MICs of sitafloxacin, which were strongly associated with gyrA mutation status, were independently associated with successful eradication in both groups. This study was registered in the UMIN Clinical Trials Registry as UMIN000006483. ConclusionThere is no significant difference in the eradication rates between EAS and EMS, regardless of the gyrA mutation status of the H. pylori strains. GyrA mutation status was an important factor in predicting successful eradication with sitafloxacin-containing rescue therapies.
Back groundHelicobacter pylori infection is involved in several gastroduodenal diseases which can be cured by antimicrobial treatment. The aim of this study was to determine the prevalence of H.pylori infection and its bacterial resistance to clarithromycin, fluoroquinolones, and tetracycline in Brazzaville, Congo, by using molecular methods. Material and MethodsA cross- sectional study was carried out between September 2013 and April 2014. Biopsy specimens were obtained from patients scheduled for an upper gastrointestinal endoscopy and were sent to the French National Reference Center for Campylobacters and Helicobacters where they were tested by molecular methods for detection of H.pylori and clarithromycin resistance by real-time PCR using a fluorescence resonance energy transfer-melting curve analysis (FRET-MCA) protocol, for detection of tetracycline resistance by real-time PCR on 16S rRNA genes (rrnA and rrnB), for detection of point mutations in the quinolone resistance-determining regions (QRDR) of H. pylori gyrA gene, associated with resistance to quinolones, by PCR and sequencing. ResultsThis study showed a high H.pylori prevalence (89%), low rates of clarithromycin and tetracycline resistance (1.7% and 2.5%, respectively), and a high rate of quinolone resistance (50%). ConclusionTherefore, the use of standard clarithromycin-based triple therapy is still possible as an empiric first-line treatment as well as prescription of bismuth-based quadruple therapy, which includes tetracycline, but not a levofloxacin-based triple therapy because of the high rate of resistance to fluoroquinolones.
BackgroundHelicobacter pylori vacA genotypes play an important role in the pathogenesis of severe gastrointestinal disease. Materials and MethodsWe identified a novel polymorphic site in the 3'-end region of H. pylori vacA gene, denoted by c1/-c2 (c1: with deletion of 15 bp), and examined associations of this and the previous four sites as well as cagA status with gastroduodenal diseases, in a total of 217 Iranian H. pylori isolates. Histopathologic evaluations were performed and patients with gastric cancer (GC) were further classified based on the anatomic site of tumor, including cardia and noncardia GC, and the histopathologic type of tumor, including intestinal- and diffuse-type GC. ResultsThe vacA m1, i1, d1, c1, and cagA genotypes were significantly associated with an increased risk of GC, the odds ratio (95% confidence interval) was 4.29 (2.03-9.08), 6.11 (2.63-14.19), 3.18 (1.49-6.76), 15.13 (5.86-39.01), and 2.59 (1.09-6.12), respectively. The vacA c1 genotype had an increased age- and sex-adjusted risk for GC by the multiple logistic regression analysis; the OR was 38.32 (95% CI, 6.60-222.29). This association was independent of and larger than the associations of the m-, i-, and d-type of vacA or cagA status with GC. No significant correlation was found between s1, whether independently or in combination, and the risk of GC or peptic ulcer disease (PUD). The vacA i1 and cagA genotypes were linked to an increased risk of PUD; the OR (95% CI) was 2.80 (1.45-5.40) and 2.62 (1.23-5.61), respectively. The presence of both the vacA i1 and cagA genotypes further increased the risk of PUD; the OR was 5.20 (95% CI, 1.92-14.03). ConclusionThe H. pylori vacA c1 genotype might therefore be one of the strongest risk predictors of GC in male patients aged 55 in Iran.
BackgroundHelicobacter pylori is associated with gastrointestinal diseases such as gastritis, peptic ulcers, malignancy and lymphoma, and extra-gastrointestinal conditions. H. pylori infection is negatively associated with children's growth. Chronic inflammation of the stomach that results in the loss of appetite and, dysregulation of neuroendocrine hormones such as leptin, and ghrelin are the probable reasons of this negative association. The objective of this study is to determine the serum levels of leptin, ghrelin, and IGF-1 in H. pylori-infected children and their relations with growth. Materials and methodsA hundred and sixty-one school children aged between 6 and 14 years were selected randomly from five primary schools representing a cross section of population. Demographic and sociocultural characteristics, and anthropometric measurements were recorded. Serum H. pylori IgG, insulin-like growth factor-1, leptin, and ghrelin levels were measured in all children. The children were grouped according to the nutritional status and Helicobacter pylori seropositivity. Nutritional indices were compared among groups in association with serum leptin, ghrelin, and insulin-like growth factor-1 levels. ResultsH. pylori IgG positivity was found in 34.2%, and 14.9% of children were malnourished. H. pylori seropositivity was significantly higher in older ages (10.32 2.26 vs 9.53 +/- 2.36 years, p = .036), and body weight and height Z scores were significantly lower in H. pylori-seropositive children (-0.33 +/- 1.08 vs 0.04 +/- 1.26, p = .044 and 0.13 +/- 0.92 vs 0.23 +/- 0.91, p = .018 respectively). H. pylori seropositivity was found to be an independent risk factor for shorter body height (p = .01). Serum leptin, ghrelin, and IGF-1 levels were not associated with H. pylori IgG seropositivity (0.35 vs 0.55 ng/mL, p = .3; 3267.4 +/- 753.0 vs 2808.3 +/- 911.4 pg/mL, p = .06; 470 +/- 176 vs 521 +/- 179 ng/mL, p = .32, respectively). ConclusionsChildren infected with H. pylori are prone to short stature. This effect seems to be independent of neuroendocrine hormones.
Background: The infection route of Helicobacter pylori has been recognized to be mainly intrafamilial, preferentially mother-to-child, especially in developed countries. To determine the transmission route, we examined whether multilocus sequence typing (MLST) was useful for analysis of intrafamilial infection. The possibility of intraspousal infection was also evaluated. Materials and Methods: Clonal relationships between strains derived from 35 index Japanese pediatric patients, and their family members were analyzed by two genetic typing procedures, MLST and random amplified polymorphic DNA (RAPD) fingerprinting. Results: Mostly coincident results were obtained by MLST and RAPD. By MLST, the allele of loci in the isolates mostly matched between the index child and both the father and mother for 9 (25.7%) of the 35 patients, between the index child and the mother for 25 (60.0%) of the 35 patients. Conclusions: MLST is useful for analyzing the infection route of H. pylori as a highly reproducible method. Intrafamilial, especially mother-to-children and sibling, infection is the dominant transmission route. Intraspousal infection is also thought to occur in about a quarter in the Japanese families.
Background: Autophagy, a degradation pathway in which cytoplasmic content is engulfed and degraded by lysosomal hydrolases, plays a pivotal role in infection and inflammation. Given that defects in autophagy lead to increased susceptibility to infection, we investigated the role of autophagy in Helicobacter pylori-related gastric cancer (GC). Materials and Methods: Gene expression of 84 molecules was examined through quantitative real-time PCR in gastric epithelial cells (AGS) and macrophages (THP-1) upon exposure to H. pylori GC026 (GC) and 26695 (gastritis). Further, ATG16L1 rs2241880, IRGM rs13361189, and IRGM rs4958847, polymorphisms that have been investigated in relation to H. pylori infection or GC in Caucasians, were detected by MALDI-TOF mass spectrometry in 304 ethnic Chinese (86 noncardia GC cases/218 functional dyspepsia controls). Results: Gene expression analyses showed twenty-eight molecules involved in vesicle nucleation, elongation, and maturation to be significantly down-regulated in H. pylori GC026-challenged AGS cells. Further, core autophagy proteins and autophagy regulators were differentially expressed in H. pylorichallenged THP-1-derived macrophages. Analyses of the selected polymorphisms showed that ATG16L1 rs2241880 increased the risk of GC (OR: 2.38, 95% CI: 1.34-4.24) and H. pylori infection (OR: 1.49, 95% CI: 1.02-2.16) while IRGM rs4958847 decreased GC risk (OR: 0.26, 95% CI: 0.09-0.74) in ethnic Chinese, these effect sizes being especially strong in H. pylori-infected individuals (ATG16L1 rs2241880 and IRGM rs13361189). Conclusions: Our findings indicate that highly virulent H. pylori strains markedly modulate autophagy in the host cell. Further, for the first time, autophagy polymorphisms were associated with GC in Chinese, a high GC-risk population.
As a general rule, any clinical study where the result is already known or when the investigator(s) compares an assigned treatment against another assigned treatment known to be ineffective in the study population (e.g., in a population with known clarithromycin resistance) is unethical. As susceptibility‐based therapy will always be superior to empiric therapy in any population with a prevalence of antimicrobial resistance >0%, any trial that randomizes susceptibility‐based therapy with empiric therapy would be unethical. The journal Helicobacter welcomes susceptibility or culture‐guided studies, studies of new therapies, and studies of adjuvants and probiotics. However, the journal will not accept for review any study we judge to be lacking clinical equipoise or which assign subjects to a treatment known to be ineffective, such as a susceptibility‐based clinical trial with an empiric therapy comparator. To assist authors, we provide examples and suggestions regarding trial design for comparative studies, for susceptibility‐based studies, and for studies testing adjuvants or probiotics.
BackgroundThe Helicobacter heilmannii sensu lato (H.heilmannii s.l.) group consists of long, spiral-shaped bacteria naturally colonizing the stomach of animals. Moreover, bacteria belonging to this group have been observed in 0.2-6% of human gastric biopsy specimens, and associations have been made with the development of chronic gastritis, peptic ulceration, and gastric MALT lymphoma in humans. Materials and MethodsTo gain insight into the prevalence of H.heilmannii s.l. infections in patients suffering from gastric disease in China, H.heilmannii s.l. species-specific PCRs were performed on DNA extracts from rapid urease test (RUT)-positive gastric biopsies from 1517 patients followed by nucleotide sequencing. At the same time, Helicobacter pylori cultivation and specific PCR was performed to assess H.pylori infection in these patients. ResultsIn total, H.heilmannii s.l. infection was detected in 11.87% (178/1499) of H.pylori-positive patients. The prevalence of H.suis, H.felis, H.bizzozeronii, H.heilmannii sensu stricto (s.s.), and H.salomonis in the patients was 6.94%, 2.20%, 0.13%, 0.07%, and 2.54%, respectively. Results revealed that all patients with H.heilmannii s.l. infection were co-infected with H.pylori, and some patients were co-infected with more than two different Helicobacter species. ConclusionsHelicobacter heilmannii s.l. infections are fairly common in Chinese patients. This should be kept in mind when diagnosing the cause of gastric pathologies in patients. Helicobacter suis was shown to be by far the most prevalent H.heilmannii s.l.species.
Background: Previous findings have suggested that Helicobacter pylori induces autophagic processes and subsequently takes refuge in autophagosomes, thereby contributing to persistent infection. Recently, a noncanonical form of autophagy, LC3 (microtubule-associated protein 1 light chain 3)-associated phagocytosis (LAP), has been shown to be required for efficient clearance of some intracellular bacteria. Whether H. pylori infection induces LAP had not been examined previously. In this study, we determined the extent to which H. pylori infection induces canonical autophagy or LAP in macrophages, and the involvement of the H. pylori cag pathogenicity island (cagPAI) with these processes. Methods: Immunofluorescence confocal microscopy was used to analyze the formation of GFP-LC3 puncta and their colocalization with H. pylori. Transmission electron microscopy was used to detect the ultrastructure of H. pylori-containing compartments. Results: The majority of intracellular bacteria (85-95%) were found in phagosomes that were LC3-negative, with a small proportion (4-14%) appearing "free" in the cytosol. Only a very small percentage (0.5-6%) of intracellular H. pylori was sequestered in autophagosomes. Furthermore, no statistically significant difference in the relative distribution of H. pylori in the various compartments was observed between wild-type and cagPAI-mutant bacteria. Conclusions: In macrophages, H. pylori infection does not induce LAP, but can induce canonical autophagy, which entraps a very small fraction of intracellular bacteria. We propose that this subpopulation of intracellular H. pylori might have escaped from phagosomes into the cytosol before being sequestered by autophagosomes. The cagPAI of H. pylori has only minor influence, if any, on the extent of these processes.
BackgroundThe aim of this study was to determine the appropriateness of the recent recommendations for managing Helicobacter pylori infection in children in a university hospital in Southern Europe. Antimicrobial resistance and response to eradication therapy were also determined. Materials and MethodsThe presence of H.pylori was studied in 143 children: by gastric biopsy culture (GBC), C-13-urea breath test (UBT) and stool antigen immunochromatography test (SAIT) in 56 children; by GBC and UBT in 20, by GBC and SAIT in 18, and by GBC alone in 49. Antimicrobial susceptibility was determined by E-test. Infection was defined as a positive culture or positivity in both UBT and SAIT. Disease progression was studied in 118 patients. First evaluation of symptoms was carried out at 3-6months after diagnosis and/or after treatment of the infection. ResultsH.pylori was detected in 74 from the 143 children analyzed (100% GBC positive, 98.1% UBT positive, and 58.1% SAIT positive). The main symptom was chronic abdominal pain (n=121). Macroscopic antral nodularity was observed in 29.7% of infected patients and in 5.8% of uninfected patients, respectively. Resistance to clarithromycin and metronidazole was found in 34.7 and 16.7%, respectively. Eradication when susceptible antimicrobials were used occurred in 78.7% (48/61) versus 37.5% (3/8) when the treatment included a drug with resistance (p=.024). In patients with recurrent abdominal pain, symptoms resolved in 92.9% (39/42) patients with HP eradication versus 42.9% (6/14) without HP eradication (p<.001). ConclusionTreated patients often failed to meet the criteria established in the guidelines for H.pylori diagnostic screening and treatment because most of them had only recurrent abdominal pain, but remission of their symptoms was associated with H.pylori eradication.