Disappearance of Helicobacter without Antibiotics in 12 Patients with Gastritis

Detection ofHelicobacter pyloriin endoscopic gastric biopsies has been associated with a variety of diseases, including ulcers and gastritis. Although the natural history ofH pyloriin the gastric mucosa is unknown, antibiotic regimens have been used for eradication. Gastric biopsies from 6050 endoscopic procedures done by a single gastroenterologist from 1981 to 1994 were evaluated. Of these, 2860 from April 1, 1991 to September 30, 1994 had silver-stained biopsies to facilitateH pyloridetection, and at least two upper endoscopic procedures were done with gastric biopsies in 188 patients. Twelve of the 188 patients with an initially positiveH pylorigastric biopsy becameH pylori-negative without antibiotic treatment forH pylorior other infection; 10 received omeprazole and two received no drug treatment. In two of the 12 patients recurrentH pyloriin the gastric mucosa was also documented. These findings indicate thatH pylorimay disappear and reappear in the gastric mucosa with no specific antibiotic eradication regimen, although omeprazole may eradicateH pyloriin vivo in some patients. The natural history ofH pyloriin gastric biopsies is poorly understood. Improved understanding, especially regarding the pathogenesis of upper gastrointestinal ulcerative and inflammatory disease processes, is essential before recommendations for specific antibiotic eradication regimens can be made.

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Tissue transglutaminase activity in human gastric mucosa according to Helicobacter pylori infection

Experimental Biology and Medicine ◽

10.1177/1535370218819423 ◽

2018 ◽

Vol 243 (15-16) ◽

pp. 1161-1164

Author(s):

Maria Pina Dore ◽

Giovanni Mario Pes ◽

Alessandra Errigo ◽

Alessandra Manca ◽

Giuseppe Realdi

Keyword(s):

Helicobacter Pylori ◽

Animal Models ◽

Gastric Mucosa ◽

Natural History ◽

Tissue Transglutaminase ◽

Helicobacter Pylori Infection ◽

Human Gastric Mucosa ◽

Antral Mucosa ◽

History Of ◽

H Pylori

Tissue transglutaminase (t-TG) is a multifunctional protein involved in the healing of gastric erosions and ulcers in animal models. The aim of this study was to measure gastric t-TG activity in patients with dyspepsia according to Helicobacter pylori infection and cytotoxin-associated gene A (cagA) and vacuolating cytotoxin (vacA) subtype status. Patients undergoing upper endoscopy not taking any medications were enrolled. Tissue-TG activity was determined in homogenates of antral specimens using a radiometric assay and was expressed in pmol/mg. The cagA and vacA genotypes were determined by PCR amplification using gene-specific oligoprimers. Data from 46 patients were available (17 of them were positive for H. pylori). Antral t-TG activity was significantly increased in H. pylori positive patients compared to H. pylori negative patients (6437 ± 3691 vs. 3773 ± 1530 pmol/mg; P = 0.001) according to Mann–Whitney U test. Patients with H. pylori negative gastritis had higher t-TG activity than patients with normal gastric mucosa. The specimens infected with cagA positive strains (72%) displayed greater t-TG activity than cagA negative samples (7358 ± 4318 vs. 4895 ± 1062 pmol/mg; P = 0.237). Similarly, t-TG activity was higher in H. pylori vacA s1/m1 strains vs. vacA s1/m2 (7429 vs. 5045 pmol/mg; P = 0.744), and vacA s1/m1 vs. s2/m2 (7429 vs. 4489 pmol/mg; P = 0.651) but the results were not significant. No differences were found between histology, endoscopy features and t-TG activity. These results show that t-TG activity is significantly greater in gastritis associated with H. pylori infection, suggesting that this enzyme is induced by inflammation and may have an important role in the natural history of human gastritis. Impact statement Tissue transglutaminase (t-TG) is unique among TG enzymes because of its additional role in several physiological and pathological activities, including inflammation, fibrosis, and wound healing. The presence of t-TG has previously been described in the intestine of human and animal models, yet studies on t-TG activity in human gastric mucosa are missing. Helicobacter pylori infection is the major cause of gastritis and peptic ulcers. For the first time, our results show that t-TG activity was significantly higher in antral specimens of patients with chronic active gastritis associated with H. pylori infection compared to H. pylori negative chronic gastritis and normal antral mucosa. These findings suggest that t-TG has a role in the natural history of human gastritis, which requires further investigation but may be an avenue for new therapeutic options.

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The Exopolysaccharide of Lactobacillus fermentum UCO-979C Is Partially Involved in Its Immunomodulatory Effect and Its Ability to Improve the Resistance against Helicobacter pylori Infection

Microorganisms ◽

10.3390/microorganisms8040479 ◽

2020 ◽

Vol 8 (4) ◽

pp. 479

Author(s):

Valeria Garcia-Castillo ◽

Guillermo Marcial ◽

Leonardo Albarracín ◽

Mikado Tomokiyo ◽

Patricia Clua ◽

...

Keyword(s):

Immune Response ◽

Helicobacter Pylori ◽

Gastric Mucosa ◽

Innate Immune Response ◽

Innate Immune ◽

Helicobacter Pylori Infection ◽

Beneficial Effects ◽

Ifn Γ ◽

H Pylori

Lactobacillus fermentum UCO-979C (Lf979C) beneficially modulates the cytokine response of gastric epithelial cells and macrophages after Helicobacter pylori infection in vitro. Nevertheless, no in vivo studies were performed with this strain to confirm its beneficial immunomodulatory effects. This work evaluated whether Lf979C improves protection against H. pylori infection in mice by modulating the innate immune response. In addition, we evaluated whether its exopolysaccharide (EPS) was involved in its beneficial effects. Lf979C significantly reduced TNF-α, IL-8, and MCP-1 and augmented IFN-γ and IL-10 in the gastric mucosa of H. pylori-infected mice. The differential cytokine profile induced by Lf979C in H. pylori-infected mice correlated with an improved reduction in the pathogen gastric colonization and protection against inflammatory damage. The purified EPS of Lf979C reduced IL-8 and enhanced IL-10 levels in the gastric mucosa of infected mice, while no effect was observed for IFN-γ. This work demonstrates for the first time the in vivo ability of Lf979C to increase resistance against H. pylori infection by modulating the gastric innate immune response. In addition, we advanced knowledge of the mechanisms involved in the beneficial effects of Lf979C by demonstrating that its EPS is partially responsible for its immunomodulatory effect.

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Prevalence of dual clarithromycin and metronidazole resistance in Helicobacter pylori estimated by molecular methods in Santiago, Chile

10.1101/236976 ◽

2017 ◽

Author(s):

Patricio Gonzalez-Hormazabal ◽

Maher Musleh ◽

Susana Escandar ◽

Hector Valladares ◽

Enrique Lanzarini ◽

...

Keyword(s):

Helicobacter Pylori ◽

Gastric Mucosa ◽

Initial Approximation ◽

Molecular Methods ◽

University Hospital ◽

Upper Gastrointestinal Endoscopy ◽

Metronidazole Resistance ◽

Two Samples ◽

H Pylori ◽

Upper Gastrointestinal

AbstractBackgroundCurrent available treatments for Helicobacter pylori eradication are chosen according to local clarithromycin and metronidazole resistance prevalence. The aim of this study was to estimate, by means of molecular methods, both clarithromycin and metronidazole resistance in gastric mucosa from patients infected with H.pylori.MethodsA total of 191 DNA samples were analyzed. DNA was purified from gastric mucosa obtained from patients who underwent an upper gastrointestinal endoscopy at an university hospital from Santiago, Chile, between 2011 and 2014. H.pylori was detected by real-time PCR. A 5’exonuclease assay was developed to detect A2142G and A2143G mutations among Hpylori-positive samples. rdxA gene was sequenced in samples harboring A2142G and A2143G mutations in order to detect mutations that potentially confer dual clarithromycin and metronidazole resistance.ResultsNinety-three (93) out of 191 DNA samples obtained from gastric mucosa were H. pylori-positive (48.7%). Clarithromycin-resistance was detected in 29 samples (31.2% [95%CI 22.0%-41.6%]). The sequencing of rdxA gene revealed that two samples harbored truncating mutations in rdxA, one sample had an in-frame deletion, and 11 had amino acid changes that likely cause metronidazole resistance.ConclusionsWe estimated a prevalence of clarithomycin-resistance of 31.8% in Santiago, Chile. The proportion of dual clarithromycin and metronidazole resistance could be, at least, 15.0%. Our results require further confirmation. Nevertheless, they are significant as an initial approximation in re-evaluating the guidelines for H.pylori eradication currently used in Chile.

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Are Histopathological Changes of H. pylori Infection in Young Dyspeptic Patients Necessitate Endoscopy?

Open Access Macedonian Journal of Medical Sciences ◽

10.3889/oamjms.2019.725 ◽

2019 ◽

Vol 7 (19) ◽

pp. 3211-3215

Author(s):

Wafaa Redha Mohammed Al-Sabbagh ◽

Alaa Qasim Yahya ◽

Rasha Abdelraouf Alsafi

Keyword(s):

Helicobacter Pylori ◽

Gastric Lymphoma ◽

Young Patients ◽

Chronic Atrophic Gastritis ◽

Gastric Biopsy ◽

P Value ◽

Histopathological Changes ◽

Gastric Biopsies ◽

Antigen Tests ◽

H Pylori

BACKGROUND: Helicobacter pylori is an important gastrointestinal infective bacteria with many serious complications including gastric erosions and ulceration, duodenal ulcer, gastric carcinoma and MALT gastric lymphoma. The gastric biopsy is commonly performed in H. pylori-positive dyspeptic individuals, and many previous researchers studied the histopathological features of infected gastric biopsies however little previous studies focused on the histopathological findings in young population in comparison to the older one. AIM: To make a focus on the histopathological effects of H. pylori infection in young patients compared with the older one and predicts the need for endoscopy in this population, also to estimates the prevalence of infection in Iraqi patients. MATERIAL AND METHODS: the sample for this study is 180 patients in total, they attended Marjan medical city in Iraq for dyspepsia of more than 3 months and prepared for OGD. Patients asked for their permission to do immunological tests for H. pylori. Both serology for H. pylori antibodies and stool for antigen tests are used, and the case is included in the study only if both tests were positive, after OGD, the gastric biopsies are processed and examined histopathologically. RESULTS: Normal gastric biopsy is the most common histopathological finding in young (< 25 years) patients (75%) while chronic atrophic gastritis is the most common one in patients > 25 years age (57%). The prevalence of Helicobacter pylori infection in dyspeptic patients was 73.3%, the correlation between infection and sex was insignificant (p-value 0.06), and no significant correlation between infection and age (p-value 0.07) was concluded. CONCLUSION: H. pylori-related histopathological changes of gastric mucosa in young (< 25 years) are commonly mild and does not necessitate endoscopy at this age unless there are alarming signs.

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Downregulation of Interleukin- (IL-) 17 through Enhanced Indoleamine 2,3-Dioxygenase (IDO) Induction by Curcumin: A Potential Mechanism of Tolerance towards Helicobacter pylori

Journal of Immunology Research ◽

10.1155/2018/3739593 ◽

2018 ◽

Vol 2018 ◽

pp. 1-7 ◽

Cited By ~ 7

Author(s):

Tiziana Larussa ◽

Serena Gervasi ◽

Rita Liparoti ◽

Evelina Suraci ◽

Raffaella Marasco ◽

...

Keyword(s):

Helicobacter Pylori ◽

Gastric Mucosa ◽

Antimicrobial Properties ◽

Human Gastric Mucosa ◽

T Cell Apoptosis ◽

Indoleamine 2,3 Dioxygenase ◽

Treated Sample ◽

Tryptophan Catabolism ◽

Gastric Biopsies ◽

H Pylori

The anti-inflammatory and antimicrobial properties of curcumin suggest its use as an anti-Helicobacter pylori (H. pylori) agent, but mechanisms underlying its helpful activity are still not clear. Indoleamine 2,3-dioxygenase (IDO) promotes the effector T cell apoptosis by catalyzing the rate-limiting first step in tryptophan catabolism, and its high expression in H. pylori-infected human gastric mucosa attenuates Th1 and Th17 immune response. The aim of this study was to investigate the role of curcumin in modulating the expression of IL-17 and IDO in H. pylori-infected human gastric mucosa. In an organ culture chamber, gastric biopsies from 35 patients were treated with and without 200 μM curcumin. In H. pylori-infected patients (n=21), IL-17 was significantly lower, both in gastric biopsies (p=0.0003) and culture supernatant (p=0.0001) while IDO significantly increased (p<0.00001) in curcumin-treated sample compared with untreated samples. In a subgroup of H. pylori-infected patients (n=15), samples treated with curcumin in addition to IDO inhibitor 1-methyl-L-tryptophan (1-MT) showed a higher expression of IL-17 compared with untreated samples and curcumin-treated alone (p<0.00001). Curcumin downregulates IL-17 production through the induction of IDO in H. pylori-infected human gastric mucosa, suggesting its role in dampening H. pylori-induced immune-mediated inflammatory changes.

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Interleukin-12 Drives the Th1 Signaling Pathway in Helicobacter pylori-Infected Human Gastric Mucosa

Infection and Immunity ◽

10.1128/iai.01446-06 ◽

2007 ◽

Vol 75 (4) ◽

pp. 1738-1744 ◽

Cited By ~ 34

Author(s):

Antonia Pellicanò ◽

Ladislava Sebkova ◽

Giovanni Monteleone ◽

Giovanni Guarnieri ◽

Maria Imeneo ◽

...

Keyword(s):

Helicobacter Pylori ◽

Transcription Factors ◽

Gastric Mucosa ◽

Enzyme Linked Immunosorbent Assay ◽

Human Gastric Mucosa ◽

Organ Cultures ◽

Gastric Biopsies ◽

Ifn Γ ◽

H Pylori ◽

Cell Commitment

ABSTRACT In this study we examined mechanisms that regulate T-helper lymphocyte 1 (Th1) commitment in Helicobacter pylori-infected human gastric mucosa. The levels of gamma interferon (IFN-γ), interleukin-4 (IL-4), and IL-12 in total extracts of gastric biopsies taken from H. pylori-infected and uninfected patients were determined by an enzyme-linked immunosorbent assay. The levels of signal transducer and activator of transcription 4 (STAT4), STAT6, and T-box expressed in T cells (T-bet) in total proteins extracted from gastric biopsies were determined by Western blotting. Finally, the effect of a neutralizing IL-12 antibody on expression of Th1 transcription factors and the levels of IFN-γ in organ cultures of H. pylori-infected biopsies was examined. Increased levels of IFN-γ and IL-12 were found in gastric biopsy samples of H. pylori-infected patients compared to the levels in uninfected patients. In addition, H. pylori-infected biopsies exhibited high levels of expression of phosphorylated STAT4 and T-bet. Higher levels of IFN-γ and expression of Th1 transcription factors were associated with greater infiltration of mononuclear cells in the gastric mucosa. By contrast, production of IL-4 and expression of phosphorylated STAT6 were not associated with the intensity of mononuclear cell infiltration. In ex vivo organ cultures of H. pylori-infected biopsies, neutralization of endogenous IL-12 down-regulated the expression of phosphorylated STAT4 and T-bet and reduced IFN-γ production. Our data indicated that IL-12 contributes to the Th1 cell commitment in H. pylori-infected human gastric mucosa.

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Variations in Helicobacter pylori Lipopolysaccharide To Evade the Innate Immune Component Surfactant Protein D

Infection and Immunity ◽

10.1128/iai.73.11.7677-7686.2005 ◽

2005 ◽

Vol 73 (11) ◽

pp. 7677-7686 ◽

Cited By ~ 38

Author(s):

Wafa Khamri ◽

Anthony P. Moran ◽

Mulugeta L. Worku ◽

Q. Najma Karim ◽

Marjorie M. Walker ◽

...

Keyword(s):

Helicobacter Pylori ◽

Gastric Mucosa ◽

Phase Variation ◽

Surfactant Protein ◽

Clinical Isolates ◽

Surfactant Protein D ◽

Human Gastric Mucosa ◽

H Pylori

ABSTRACT Helicobacter pylori is a common and persistent human pathogen of the gastric mucosa. Surfactant protein D (SP-D), a component of innate immunity, is expressed in the human gastric mucosa and is capable of aggregating H. pylori. Wide variation in the SP-D binding affinity to H. pylori has been observed in clinical isolates and laboratory-adapted strains. The aim of this study was to reveal potential mechanisms responsible for evading SP-D binding and establishing persistent infection. An escape variant, J178V, was generated in vitro, and the lipopolysaccharide (LPS) structure of the variant was compared to that of the parental strain, J178. The genetic basis for structural variation was explored by sequencing LPS biosynthesis genes. SP-D binding to clinical isolates was demonstrated by fluorescence-activated cell sorter analyses. Here, we show that H. pylori evades SP-D binding through phase variation in lipopolysaccharide. This phenomenon is linked to changes in the fucosylation of the O chain, which was concomitant with slipped-strand mispairing in a poly(C) tract of the fucosyltransferase A (fucT1) gene. SP-D binding organisms are predominant in mucus in vivo (P = 0.02), suggesting that SP-D facilitates physical elimination. Phase variation to evade SP-D contributes to the persistence of this common gastric pathogen.

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Helicobacter pylori Stores Nickel To Aid Its Host Colonization

Infection and Immunity ◽

10.1128/iai.00858-12 ◽

2012 ◽

Vol 81 (2) ◽

pp. 580-584 ◽

Cited By ~ 21

Author(s):

Stéphane L. Benoit ◽

Erica F. Miller ◽

Robert J. Maier

Keyword(s):

Helicobacter Pylori ◽

Gastric Mucosa ◽

Physiological Role ◽

Wild Type ◽

Rank Tests ◽

Content Type ◽

Host Mouse ◽

H Pylori ◽

Very High

ABSTRACTThe transition metal nickel (Ni) is critical for the pathogenicity ofHelicobacter pylori. Indeed the element is a required component of two enzymes, hydrogenase and urease, that have been shown to be important forin vivocolonization of the host gastric mucosa. Urease accounts for up to 10% of the total cellularH. pyloriprotein content, and therefore the bacterial Ni demand is very high.H. pyloripossess two small and abundant histidine-rich, Ni-binding proteins, Hpn and Hpn-like, whose physiological role in the host have not been investigated. In this study, special husbandry conditions were used to control Ni levels in the host (mouse), including the use of Ni-free versus Ni-supplemented food. The efficacy of each diet was confirmed by measuring the Ni concentrations in sera of mice fed with either diet. Colonization levels (based on rank tests) of theΔhpn Δhpn-like double mutants isolated from the mice provided Ni-deficient chow were statistically lower than those for mice given Ni in their diet. In contrast,H. pyloriwild-type colonization levels were similar in both host groups (e.g., regardless of Ni levels). Our results indicate that the gastric pathogenH. pylorican utilize stored Ni via defined histidine-rich proteins to aid colonization of the host.

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Successful isolation of Helicobacter pylori after prolonged incubation: A case report of prolonged incubation for H. pylori

Archives of Biological Sciences ◽

10.2298/abs1204297b ◽

2012 ◽

Vol 64 (4) ◽

pp. 1297-1299

Author(s):

Tatjana Babic ◽

Biljana Miljkovic-Selimovic ◽

Branislava Kocic ◽

A. Nagorni ◽

Ljiljana Ristic

Keyword(s):

Helicobacter Pylori ◽

Normal Growth ◽

Gastric Biopsy ◽

Gram Stain ◽

Ulcus Ventriculi ◽

Prolonged Incubation ◽

Primary Isolation ◽

Successful Isolation ◽

Gastric Biopsies ◽

H Pylori

The culture of Helicobacter pylori from a gastric biopsy is the ?gold standard? in the diagnosis of H. pylori infection. However, the primary isolation of H. pylori from gastric biopsies is rather demanding. The duration of incubation for the isolation of H. pylori has been recommended to be five to seven days: in the present case, we found that a prolonged incubation period allowed the successful isolation of H. pylori from a patient with ulcus ventriculi. Biopsies were placed directly into transport medium and processed for culture within two hours. On day 14, one suspected H. pylori-like colony appeared on one of the plates. The isolate was confirmed to be H. pylori based on its typical colony morphology, negative Gram stain, and positive urease, catalase and oxidase tests. The isolate, requiring 14 days recovery, later exhibited the normal growth characteristics of H. pylori strains, indicating its unusually long incubation requirement was a temporary predicament.

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Detection of CagA, VacA, IceA1 and IceA2 virulent genes in Helicobacter pylori isolated from gastric ulcer patients

LaboratoriumsMedizin ◽

10.1515/labmed-2018-0059 ◽

2018 ◽

Vol 42 (4) ◽

pp. 155-162

Author(s):

Lijuan Fan ◽

Ran Li ◽

Hongyun Li ◽

Jian Zhang ◽

Lingyun Wang

Keyword(s):

Helicobacter Pylori ◽

Gastric Ulcer ◽

Virulence Genes ◽

East Asian ◽

Virulence Gene ◽

Gastric Biopsy ◽

History Of ◽

Male Patients ◽

Polymerase Chain ◽

H Pylori

Abstract Background Virulence factors of Helicobacter pylori including cagA, vacA, iceA and their association with clinical manifestation varied widely with different subpopulations. The objective of the study was to determine the prevalence of cagA, iceA1, iceA2, vacA, vacA s1/s2, vacA m1/m2, Western type cagA and East Asian type cagA virulence genes in H. pylori isolated from gastric ulcer patients and evaluate the association of these genes with gender, age, smoking and alcohol consumption. Methods Gastric biopsy samples from 172 patients were collected. H. pylori virulence genes, cagA, vacA, iceA1, iceA2, vacA s1/s2, vacA m1/m2, Western type cagA and East Asian type cagA were detected using polymerase chain reaction (PCR). Results Of the gastric biopsy samples collected, 48.3% of samples grew H. pylori. The vacA (68.7%) was the predominant virulence gene detected and associated with male patients and patients within the age group of 31–40 years. The cagA was the second most common gene detected and significantly associated with alcoholic patients. Conclusions H. pylori infection rate was 48.3% and was associated with patients who were smokers or had a history of smoking. The majority of our isolates were positive for any one of the virulence genes tested indicating that these isolates were highly virulent in nature.

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