Coccoid form of Helicobacter pylori as a morphological manifestation of cell adaptation to the environment.
Ontology highlight
ABSTRACT:
SUBMITTER: Azevedo NF
PROVIDER: S-EPMC1907093 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:AimTo clone and sequence the cagA gene fragment of Helicobacter pylori (H pylori) with coccoid form.MethodsH pylori strain NCTC11637 were transformed to coccoid form by exposure to antibiotics in subinhibitory concentrations. The coccoid H pylori was collected. cagA gene of the coccoid H pylori strain was amplified by PCR. After purified, the target fragment was cloned into plasmid pMD-18T. The recombinant plasmid pMD-18T-cagA was transformed into E.coli JM109. Positive clones were screened and identified by PCR and digestion with restriction endonucleases. The sequence of inserted fragment was then analysed.ResultscagA gene of 3,444 bp was obtained from the coccoid H pylori genome DNA. The recombinant plasmid pMD-18T-cagA was constructed, then it was digested by BamH I+Sac I, and the product of digestion was identical with the predicted one. Sequence analysis showed that the homology of coccoid and the reported original sequence H pylori was 99.7%.ConclusionThe recombinant plasmid containing cagA gene from coccoid H pylori has been constructed successfully. The coccoid H pylori contain completed cagA gene, which may be related to pathogenicity of them.
| S-EPMC4576237 | biostudies-literature
Project description:Long-term infection of the stomach with Helicobacter pylori can cause gastric cancer. However, the mechanisms by which the bacteria adapt to the stomach environment are poorly understood. Here, we show that a small non-coding RNA of H. pylori (HPnc4160, also known as IsoB or NikS) regulates the pathogen's adaptation to the host environment as well as bacterial oncoprotein production. In a rodent model of H. pylori infection, the genomes of bacteria isolated from the stomach possess an increased number of T-repeats upstream of the HPnc4160-coding region, and this leads to reduced HPnc4160 expression. We use RNA-seq and iTRAQ analyses to identify eight targets of HPnc4160, including genes encoding outer membrane proteins and oncoprotein CagA. Mutant strains with HPnc4160 deficiency display increased colonization ability of the mouse stomach, in comparison with the wild-type strain. Furthermore, HPnc4160 expression is lower in clinical isolates from gastric cancer patients than in isolates derived from non-cancer patients, while the expression of HPnc4160's targets is higher in the isolates from gastric cancer patients. Therefore, the small RNA HPnc4160 regulates H. pylori adaptation to the host environment and, potentially, gastric carcinogenesis.
| S-EPMC8035401 | biostudies-literature
Project description:Geranylgeranylacetone (GGA) is used to treat patients suffering from peptic ulcers and gastritis. We examined the effect of GGA on Helicobacter pylori, which is a causative factor of gastrointestinal diseases. Previously, we have reported that GGA binds specifically to the molecular chaperone HSP70. In this paper, we report that GGA bounds to H. pylori HSP70 (product of the DnaK gene) with 26-times higher affinity than to human HSP70, and induced large conformational changes as observed from surface plasmon resonance and circular dichroism. Binding of GGA suppressed the activity of the H. pylori chaperone. GGA also altered several characteristics of H. pylori cells. GGA-treated cells elicited enhanced interleukin-8 production by gastric cancer cell lines and potentiated susceptibility to complement as compared to untreated cells. GGA also caused morphological alterations in H. pylori as reflected in fewer coccoid-like cells, suggesting that GGA converts H. pylori to an actively dividing, spiral state (vegetative form) from a non-growing, coccoid state. This morphological conversion by GGA resulted in accelerated growth of H. pylori. These results suggest a model in which GGA sensitizes H. pylori to antibiotic treatment by converting the cells to an actively growing state.
| S-EPMC4561889 | biostudies-literature
Project description:The primary mode of transmission of Helicobacter pylori, a human pathogen carried by more than half the population worldwide, is still unresolved. Some epidemiological data suggest water as a possible transmission route. H. pylori in the environment transforms into a nonculturable, coccoid form, which frequently results in the failure to detect this bacterium in environmental samples by conventional culture techniques. To overcome limitations associated with culturing, molecular approaches based on DNA amplification by PCR have been developed and used for the detection of H. pylori in clinical and environmental samples. Our results showed the glmM gene as the most promising target for detection of H. pylori by PCR amplification. Under optimal amplification conditions, glmM-specific primers generated PCR-amplified products that were specific for H. pylori and some other Helicobacter species. Genome sequence analysis revealed the existence of a conserved region linked to a hypervariable region upstream of the 16S rRNA gene of H. pylori. Selective PCR primer sets targeting this sequence were evaluated for the specific detection of H. pylori. One primer set, Cluster2 and B1J99, were shown to be highly specific for H. pylori strains and did not produce any PCR products when other Helicobacter species and other bacterial species were analyzed. In tests with 32 strains of H. pylori, 6 strains of other Helicobacter species, 8 strains of Campylobacter jejuni, and 21 strains belonging to different genera, the primers for glmM were selective for the Helicobacter genus and the primers containing the region flanking the 16S rRNA gene were selective for H. pylori species only. The combination of two sensitive PCR-based methods, one targeting the glmM gene and the other targeting a hypervariable flanking region upstream of the 16S rRNA gene, are complementary to each other. Whereas the glmM-specific primers provide a rapid, sensitive presumptive assay for the presence of H. pylori and closely related Helicobacter spp., the primers for sequences flanking the 16S rRNA gene can confirm the presence of H. pylori and locate the potential source of this bacterium.
| S-EPMC497564 | biostudies-literature
Project description:Helicobacter pylori (H. pylori) as a causative agent of gastric complications, is well adapted for the colonization of gastric mucosa. Although the infectious process depends on several factors, the adhesion to the gastric mucosa is the first and important step. Among several outer membrane proteins, BabA is one of the significant protein involving in many inflammatory processes in addition to its role in the attachment for the persistent colonization. We performed a PubMed search using the key words: "babA", "pylori", "gastric complications", "homologous recombination", "slipped strand mispairing"; a total of 249 articles were displayed. Of these we mainly focused on articles with the full text in English and published between 2005 and 2016. H. pylori BabA is involved in binding with receptors; however, its synthesis is regulated by phase variation. In this review we confirm that H. pylori babA can be modulated at the molecular and functional levels to adapt to the stress within the gastro-intestinal tract.
| S-EPMC5483490 | biostudies-other
Project description:The human gastric pathogen Helicobacter pylori colonizes the stomachs of half of the human population, and causes development of peptic ulcer disease and gastric adenocarcinoma. H. pylori-associated chronic atrophic gastritis (ChAG) with loss of the acid-producing parietal cells, is correlated with an increased risk for development of gastric adenocarcinoma. The majority of H. pylori isolates produce lipopolysaccharides (LPS) decorated with human-related Lewis epitopes, which have been shown to phase-vary in response to different environmental conditions. We have characterized the adaptations of H. pylori LPS and Lewis antigen expression to varying gastric conditions; in H. pylori isolates from mice with low or high gastric pH, respectively; in 482 clinical isolates from healthy individuals and from individuals with ChAG obtained at two time points with a four-year interval between endoscopies; and finally in isolates grown at different pH in vitro. Here we show that the gastric environment can contribute to a switch in Lewis phenotype in the two experimental mouse models. The clinical isolates from different human individuals showed that intra-individual isolates varied in Lewis antigen expression although the LPS diversity was relatively stable within each individual over time. Moreover, the isolates demonstrated considerable diversity in the levels of glycosylation and in the sizes of fucosylated O-antigen chains both within and between individuals. Thus our data suggest that different LPS variants exist in the colonizing H. pylori population, which can adapt to changes in the gastric environment and provide a means to regulate the inflammatory response of the host during disease progression.
| S-EPMC2690825 | biostudies-literature
Project description:The variability of Helicobacter pylori morphology and the heterogeneity of virulence factors expressed by these bacteria play a key role as a driving force for adaptation to the hostile stomach environment. The aim of the study was to determine the relationship between the presence of certain genes encoding virulence factors and H. pylori morphology. One reference and 13 clinical H. pylori strains with a known virulence profile (vacA, cagA, babA2, dupA, and iceA) were used in this study. Bacteria were cultured for 1 h and 24 h in stressogenic culture conditions, i.e., serum-free BHI broths at suboptimal conditions (room temperature and atmosphere, without shaking). H. pylori cell morphology was observed by light and scanning electron microscopy. The vacA polymorphism and the cagA and babA2 presence were positively correlated with the reduction in cell size. Exposure to short-time stressogenic conditions caused more intense transformation to coccoid forms in highly pathogenic H. pylori type I strains (35.83% and 47.5% for type I s1m2 and I s1m1, respectively) than in intermediate-pathogenic type III (8.17%) and low pathogenic type II (9.92%) strains. The inverse relationship was observed for the number of rods, which were more common in type III (46.83%) and II (48.42%) strains than in type I s1m2 (19.25%) or I s1m1 (6.58%) strains. Our results suggest that there is a close relationship between the presence of virulence genes of H. pylori strains and their adaptive morphological features.
| S-EPMC6529389 | biostudies-literature
Project description:Morphological variability is one of the phenotypic features related to adaptation of microorganisms to stressful environmental conditions and increased tolerance to antimicrobial substances. Helicobacter pylori, a gastric mucosal pathogen, is characterized by a high heterogeneity and an ability to transform from a spiral to a coccoid form. The presence of the coccoid form is associated with the capacity to avoid immune system detection and to promote therapeutic failures. For this reason, it seems that the investigation for new, alternative methods combating H. pylori should include research of coccoid forms of this pathogen. The current review aimed at collecting information about the activity of antibacterial substances against H. pylori in the context of the morphological variability of this bacterium. The collected data was discussed in terms of the type of substances used, applied research techniques, and interpretation of results. The review was extended by a polemic on the limitations in determining the viability of coccoid H. pylori forms. Finally, recommendations which can help in future research aiming to find new compounds with a potential to eradicate H. pylori have been formulated.
| S-EPMC7157236 | biostudies-literature
Project description:Ordered lipid domains (rafts) are generally considered to be features of eukaryotic cells, but ordered lipid domains formed by cholesterol lipids have been identified in bacteria from the genus Borrelia, and similar cholesterol lipids exist in the bacterium Helicobacter pylori. To determine whether H. pylori lipids could form ordered membrane domains, we investigated domain formation in aqueous dispersions of H. pylori whole lipid extracts, individual H. pylori lipids, or defined mixtures of H. pylori lipids and other membrane-forming lipids. DPH (1,6-diphenyl-1,3,5-hexatriene) anisotropy measurements were used to assay membrane order and FRET (Förster resonance energy transfer) was used to detect the presence of co-existing ordered and disordered domains. We found that H. pylori membrane lipid extracts spontaneously formed lipid domains. Domain formation was more stable when lipids were extracted from H. pylori cells grown in the presence of cholesterol. Certain isolated H. pylori lipids (by themselves or when mixed with other lipids) also had the ability to form ordered domains. To be specific, H. pylori cholesteryl-6-O-tetradecanoyl-?-D-glucopyranoside (CAG) and cholesterol-6-O-phosphatidyl-?-D-glucopyranoside (CPG) had the ability to form and/or stabilize ordered domain formation, while H. pylori phosphatidylethanolamine did not, behaving similarly to unsaturated phosphatidylethanolamines. We conclude that specific H. pylori cholesterol lipids have a marked ability to form ordered lipid domains.
| S-EPMC6814566 | biostudies-literature
Project description:Helicobacter pylori is one of the most prevalent infection worldwide. It affects individuals of different age groups. Elderly people tend to resist eradication treatment and worsening of infection can lead to several gastric and non-gastric pathologies. Aging-associated cellular and molecular alteration can increase the risk of other pathologies such as osteoporosis, Alzheimer's disease, Parkinson's disease, respiratory and renal dysfunction, and cancer in geriatric patients, more than other age groups. This review article highlights some of the most common old age diseases and the role of H. pylori infection as a risk factor to worsen the conditions, presented by the molecular evidences of these associations. These studies can help clinicians to understand the underlying pathogenesis of the disease and identify high-risk patients, aiding clearer diagnosis and treatment.
| S-EPMC7196471 | biostudies-literature