scholarly journals A retrospective study assessing the acceleration effect of type I Helicobacter pylori infection on the progress of atrophic gastritis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Weidong Liu ◽  
Junjie Tian ◽  
Wenjia Hui ◽  
Wenjie Kong ◽  
Yan Feng ◽  
...  

AbstractBased on the antibody typing classification, Helicobacter pylori infection can be divided into type I H. pylori infection and type II H. pylori infection. To observe the effects of different H. pylori infection types on the distribution of histopathological characteristics and the levels of three items of serum gastric function (PG I, PG II, G-17). 1175 cases from October 2018 to February 2020 were collected with ratio 1:2. All patients were performed with 14C-Urea breath test (14C-UBT), H. pylori antibody typing classification, three items of serum gastric function detection, painless gastroscopy, pathological examination, etc. According to H. pylori antibody typing classification, patients were divided into three groups: type I H. pylori infection group, type II H. pylori infection group and control group. Significant difference existed among type I H. pylori infection group, type II H. pylori infection group and control group in inflammation and activity (χ2 = 165.43, 354.88, P all < 0.01). The proportion of three groups in OLGA staging had statistic difference (χ2 = 67.99, P all < 0.01); Compared with type II H. pylori infection group and control group, the level of pepsinogen I, pepsinogen II, gastrin17 in type I H. pylori infection group increased, and PG I/PG II ratio (PG I/PG II ratio, PGR) decreased, which was statistically significant (χ2 = 35.08, 166.24, 134.21, 141.19; P all < 0.01). Type I H. pylori infection worsened the severity of gastric mucosal inflammation and activity. H. pylori infection was prone to induce atrophy of gastric mucosa, while type I H. pylori infection played a key role in promoting the progress of atrophic gastritis and affected the level of serum gastric function. The study indicated that the eradication of H. pylori should be treated individually.

Author(s):  
Fehmida Ayub ◽  
Abida Naseer ◽  
Saeed Javed ◽  
Adnan Asghar ◽  
Abd Rahim Mohd Shariff ◽  
...  

Objective: Diabetes have a central contribution with type I or type II towards the healthy lifestyles of sportspersons. Aerobic exercise and daily walking stay them fit and control their glucose levels in their bloodstream. The aim of this study was to find out the effects of aerobic exercises and walk on the sportspersons of type I and II diabetes. Methodology: The existing research has experimental design itself wherein pre-tests and post-tests were employed to make sure the novelty of results. The data was collected from the diabetic sportspersons dividing them equally into control group (N-20) and experimental group (N-20). Both groups had type I (N-20) and type II (N-20) diabetic individuals. Aerobic exercise and walk protocol was applied for six weeks on experimental group, whereas, control group continued their routine activities. Afterwards, the data was collected through pre and post treatments and edited into SPSS (v-26). The collected data was analyzed through descriptive statistics using frequencies and percentages, whereas, T-test was applied to make the differences of pre and post treatments. Results: The findings has shown that aerobic exercises and walk decrease the higher levels of glucose in blood and enable to stable glycemic balance, weight loss maintenance, decrease insulin resistance, blood pressure decrease, and blood glucose control. Conclusion: The prominent differences were observed between control and experimental groups either type I or type II. It was concluded that the sportspersons may reduce the excessive glucose engaging in aerobic exercises and walk on daily basis rather than using medications. They should spend their happy lives and get rid of medications and insulin through spending their spare time using light exercises and maintain their glucose levels in blood as well.


2005 ◽  
Vol 390 (1) ◽  
pp. 223-230 ◽  
Author(s):  
Celia J. Webby ◽  
Mark L. Patchett ◽  
Emily J. Parker

DAH7P (3-Deoxy-D-arabino-heptulosonate 7-phosphate) synthase catalyses the condensation reaction between phosphoenolpyruvate (PEP) and D-erythrose 4-phosphate (E4P) as the first committed step in the biosynthesis of aromatic compounds in plants and micro-organisms. Previous work has identified two families of DAH7P synthases based on sequence similarity and molecular mass, with the majority of the mechanistic and structural studies being carried out on the type I paralogues from Escherichia coli. Whereas a number of organisms possess genes encoding both type I and type II DAH7P synthases, the pathogen Helicobacter pylori has only a single, type II, enzyme. Recombinant DAH7P synthase from H. pylori was partially solubilized by co-expression with chaperonins GroEL/GroES in E. coli, and purified to homogeneity. The enzyme reaction follows an ordered sequential mechanism with the following kinetic parameters: Km (PEP), 3 μM; Km (E4P), 6 μM; and kcat, 3.3 s−1. The enzyme reaction involves interaction of the si face of PEP with the re face of E4P. H. pylori DAH7P synthase is not inhibited by phenylalanine, tyrosine, tryptophan or chorismate. EDTA inactivates the enzyme, and activity is restored by a range of bivalent metal ions, including (in order of decreasing effectiveness) Co2+, Mn2+, Ca2+, Mg2+, Cu2+ and Zn2+. Analysis of type II DAH7P synthase sequences reveals several highly conserved motifs, and comparison with the type I enzymes suggests that catalysis by these two enzyme types occurs on a similar active-site scaffold and that the two DAH7P synthase families may indeed be distantly related.


2000 ◽  
Vol 191 (1) ◽  
pp. 115-128 ◽  
Author(s):  
Lee-Ann H. Allen ◽  
Larry S. Schlesinger ◽  
Byoung Kang

Helicobacter pylori colonizes the gastric epithelium of ∼50% of the world's population and plays a causative role in the development of gastric and duodenal ulcers. H. pylori is phagocytosed by mononuclear phagocytes, but the internalized bacteria are not killed and the reasons for this host defense defect are unclear. We now show using immunofluorescence and electron microscopy that H. pylori employs an unusual mechanism to avoid phagocytic killing: delayed entry followed by homotypic phagosome fusion. Unopsonized type I H. pylori bound readily to macrophages and were internalized into actin-rich phagosomes after a lag of ∼4 min. Although early (10 min) phagosomes contained single bacilli, H. pylori phagosomes coalesced over the next ∼2 h. The resulting “megasomes” contained multiple viable organisms and were stable for 24 h. Phagosome–phagosome fusion required bacterial protein synthesis and intact host microtubules, and both chloramphenicol and nocodazole increased killing of intracellular H. pylori. Type II strains of H. pylori are less virulent and lack the cag pathogenicity island. In contrast to type I strains, type II H. pylori were rapidly ingested and killed by macrophages and did not stimulate megasome formation. Collectively, our data suggest that megasome formation is an important feature of H. pylori pathogenesis.


2007 ◽  
Vol 122 (1) ◽  
pp. 61-64 ◽  
Author(s):  
İ Aladag ◽  
Y Bulut ◽  
M Guven ◽  
A Eyibilen ◽  
K Yelken

AbstractBackground and objectives:Chronic nonspecific pharyngitis is a chronic inflammation of the pharynx. It is found worldwide, and treatment is difficult. The underlying aetiopathogenesis is still controversial. The aim of this study was to investigate Helicobacter pylori seroprevalence in chronic nonspecific pharyngitis patients without other possible causative factors for chronic pharyngeal irritation and without H pylori gastric mucosal infection.Materials and methods:Forty-one patients with symptoms of chronic nonspecific pharyngitis and 30 healthy control subjects were enrolled in this prospective, controlled, clinical study. In both study and control groups, selected patients were shown to have gastric mucosa uninfected by H pylori, as demonstrated by the 14C-urea breath test. Comprehensive otorhinolaryngological examination did not elicit any factor contributing to the chronic pharyngeal complaint. Serum H pylori immunoglobulin G antibody titres were assayed using serum enzyme-linked immunosorbent assay. The difference between the study and control groups was analysed by the chi-square test (the likelihood ratio was used).Results:Thirty-two of the 41 patients (78 per cent) and 14 of the 30 control subjects (46.7 per cent) were found to be H pylori positive. Patients with chronic nonspecific pharyngitis were found to have a significantly higher rate of H pylori seropositivity than the control group (p = 0.016).Conclusion:These data may be important in developing future treatment strategies for chronic nonspecific pharyngitis.


2017 ◽  
Vol 54 (4) ◽  
pp. 300-304 ◽  
Author(s):  
Arezo JUDAKI ◽  
Siros NOROZI ◽  
Mohammad Reza Hafezi AHMADI ◽  
Samira Mis GHAVAM ◽  
Khairollah ASADOLLAHI ◽  
...  

ABSTRACT BACKGROUND: Endothelial dysfunction is one of the early stages of vascular diseases. OBJECTIVE: The aim of this study was to investigate the endothelial dysfunction markers in patients with chronic gastritis associated with Helicobacter pylori (H. pylori) infection. METHODS: By a cross sectional study, basic and clinical information of 120 participants (40 patients with positive H. pylori infection, 40 patients with negative H. pylori infection and 40 healthy people) were analyzed. Carotid intima media thickness and flow-mediated dilation levels were measured in all patients and controls. Soluble vascular cell adhesion molecule-1 (sVCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were measured with Elisa for all subjects. IgG level was assessed in chronic gastritis patients. RESULTS: The flow-mediated dilation level in patients with positive H. pylori infection (0.17%±0.09) was significantly lower than those with negative H. pylori infection (0.21% ±0.10, P<0.05) and compared to the control group (0.27% ±0.11, P<0.05). Carotid intima media thickness level in patients with positive H. pylori infection (0.58±0.13 mm) was significantly higher than those with negative H. pylori infection (0.48±0.32 mm, P<0.05) and compared to the control group (0.36±0.44mm, P<0.05). The mean level of sICAM-1 in positive H. pylori infection group (352.16±7.54 pg/mL) was higher than negative H. pylori infection group (332.64±8.75 pg/mL =0.75) and compared to the control group (236.32±12.43 pg/mL, P<0.05). A direct relationship was revealed between flow-mediated dilation and carotid intima media thickness changes and between sICAM-1 and sVCAM-1 associated with the level of H. pylori IgG in chronic gastritis. CONCLUSION: The levels of flow-mediated dilation, carotid intima media thickness and sICAM-1 were higher among patients with positive H. pylori infection. Patients with chronic gastritis associated with H. pylori infection are at risk of endothelial dysfunction due to flow-mediated dilation and carotid intima media thickness abnormalities and increased level of sICAM-1 and sVCAM-1.


2021 ◽  
Vol 11 (44) ◽  
pp. 167-173
Author(s):  
Ziya Şencan ◽  
Nuray Bayar Muluk ◽  
Mikail Inal ◽  
Selmin Perihan Kömürcü Erkmen ◽  
Ela Cömert

Abstract OBJECTIVE. We investigated the relationship between Lund-Mackay scale, olfactory bulb depth and width, and Keros classification in patients with chronic rhinosinusitis with nasal polyps (CRSwNP). MATERIAL AND METHODS. In this retrospective study, paranasal sinus computed tomography (PNSCT) images of 47 patients with CRSwNP and 47 healthy subjects (control) were evaluated. In the CRSwNP group, PNSCT scans were assessed based on Lund-Mackay scale. In both groups, olfactory fossae (OF) depth and width, and Keros classification were evaluated. RESULTS. The total Lund-Mackay score was 17.1±5.9. There were no significant differences between OF depth and width values of the nasal polyps group and control group. For both groups, Type II Keros was the most detected type; secondly, Keros type I and rarely Keros type III were detected. There was no significant correlation between Lund-Mackay score (All items and total score) and OF depth and width, and Keros type. There were negative correlations between ipsilateral OF depth and width (p<0.05), whereas there were positive correlations between contralateral OF depth and width (p>0.05). Keros type was positively correlated between ipsilateral and contralateral OF depth and Keros type (p<0.05). In older patients, left OF depth and Keros type decreased (p<0.05). CONCLUSION. As a conclusion, there was no correlation between Lund-Mackay score and olfactory fossa dimensions (depth and width). When considering age, one could notice that Keros type decreased in older patients.


2021 ◽  
Vol 12 ◽  
Author(s):  
Mariagrazia Piscione ◽  
Mariangela Mazzone ◽  
Maria Carmela Di Marcantonio ◽  
Raffaella Muraro ◽  
Gabriella Mincione

Worldwide, gastric cancer (GC) represents the fifth cancer for incidence, and the third as cause of death in developed countries. Indeed, it resulted in more than 780,000 deaths in 2018. Helicobacter pylori appears to be responsible for the majority of these cancers. On the basis of recent studies, and either alone or combined with additional etiological factors, H. pylori is considered a “type I carcinogen.” Over recent decades, new insights have been obtained into the strategies that have been adopted by H. pylori to survive the acidic conditions of the gastric environment, and to result in persistent infection, and dysregulation of host functions. The multistep processes involved in the development of GC are initiated by transition of the mucosa into chronic non-atrophic gastritis, which is primarily triggered by infection with H. pylori. This gastritis then progresses into atrophic gastritis and intestinal metaplasia, and then to dysplasia, and following Correa’s cascade, to adenocarcinoma. The use of antibiotics for eradication of H. pylori can reduce the incidence of precancerous lesions only in the early stages of gastric carcinogenesis. Here, we first survey the etiology and risk factors of GC, and then we analyze the mechanisms underlying tumorigenesis induced by H. pylori, focusing attention on virulence factor CagA, inflammation, oxidative stress, and ErbB2 receptor tyrosine kinase. Moreover, we investigate the relationships between H. pylori eradication therapy and other diseases, considering not only cardia (upper stomach) cancers and Barrett’s esophagus, but also asthma and allergies, through discussion of the “hygiene hypothesis. ” This hypothesis suggests that improved hygiene and antibiotic use in early life reduces microbial exposure, such that the immune response does not become primed, and individuals are not protected against atopic disorders, asthma, and autoimmune diseases. Finally, we overview recent advances to uncover the complex interplay between H. pylori and the gut microbiota during gastric carcinogenesis, as characterized by reduced bacterial diversity and increased microbial dysbiosis. Indeed, it is of particular importance to identify the bacterial taxa of the stomach that might predict the outcome of gastric disease through the stages of Correa’s cascade, to improve prevention and therapy of gastric carcinoma.


2003 ◽  
Vol 185 (9) ◽  
pp. 2927-2935 ◽  
Author(s):  
Asish K. Mukhopadhyay ◽  
Jin-Yong Jeong ◽  
Daiva Dailidiene ◽  
Paul S. Hoffman ◽  
Douglas E. Berg

ABSTRACT Very few examples of metabolic regulation are known in the gastric pathogen Helicobacter pylori. An unanticipated case was suggested, however, upon finding two types of metronidazole (Mtz)-susceptible strains: type I, in which frxA (which encodes a nitroreductase that contributes to Mtz susceptibility) is quiescent, and type II, in which frxA is well expressed. Here we report that inactivation of the fdxA ferredoxin gene (hp277) in type I strains resulted in high-level frxA expression (in effect, making them type II). However, fdxA null derivatives were obtained from only 6 of 32 type I strains tested that were readily transformed with an frxA::aphA marker. This suggested that fdxA is often essential. This essentiality was overcome in 4 of 20 strains by inactivating frxA, which suggested both that frxA overexpression is potentially deleterious and also that fdxA has additional, often vital roles. With type II strains, in contrast, fdxA null derivatives were obtained in 20 of 23 cases tested. Thus, fdxA is dispensable in most strains that normally exhibit (and tolerate) strong frxA expression. We propose that restraint of frxA expression helps maintain balanced metabolic networks in most type I strains, that other homeostatic mechanisms predominate in type II strains, and that these complex results constitute a phenotypic manifestation of H. pylori's great genetic diversity.


2021 ◽  
Vol 12 ◽  
Author(s):  
Jong Min Park ◽  
Young Min Han ◽  
Ki Baik Hahm

Chronic Helicobacter pylori infection causes gastric cancer via the progression of precancerous chronic atrophic gastritis (CAG). Therefore, repairing gastric atrophy could be a useful strategy in preventing H. pylori–associated gastric carcinogenesis. Although eradication of the bacterial pathogen offers one solution to this association, this study was designed to evaluate an alternative approach using mesenchymal stem cells to treat CAG and prevent carcinogenesis. Here, we used human placenta-derived mesenchymal stem cells (PD-MSCs) and their conditioned medium (CM) to treat H. pylori–associated CAG in a mice/cell model to explore their therapeutic effects and elucidate their molecular mechanisms. We compared the changes in the fecal microbiomes in response to PD-MSC treatments, and chronic H. pylori–infected mice were given ten treatments with PD-MSCs before being sacrificed for end point assays at around 36 weeks of age. These animals presented with significant reductions in the mean body weights of the control group, which were eradicated following PD-MSC treatment (p &lt; 0.01). Significant changes in various pathological parameters including inflammation, gastric atrophy, erosions/ulcers, and dysplastic changes were noted in the control group (p &lt; 0.01), but these were all significantly reduced in the PD-MSC/CM-treated groups. Lgr5+, Ki-67, H+/K+-ATPase, and Musashi-1 expressions were all significantly increased in the treated animals, while inflammatory mediators, MMP, and apoptotic executors were significantly decreased in the PD-MSC group compared to the control group (p &lt; 0.001). Our model showed that H. pylori–initiated, high-salt diet–promoted gastric atrophic gastritis resulted in significant changes in the fecal microbiome at the phylum/genus level and that PD-MSC/CM interventions facilitated a return to more normal microbial communities. In conclusion, administration of PD-MSCs or their conditioned medium may present a novel rejuvenating agent in preventing the progression of H. pylori–associated premalignant lesions.


2010 ◽  
Vol 17 (04) ◽  
pp. 543-545
Author(s):  
FARID IMANZADEH ◽  
AMIR IMANZADEH ◽  
ALI AKBAR SAYYARI ◽  
Mehrnosh Yeganeh ◽  
Hazhir Javaherizadeh ◽  
...  

Introduction: In most individuals H. Pylori is acquired early in the life (before 5 years). H. Pylori infection is more common in the third world countries, where about 90% of adults may be infected. Helicobacter pylori is one of the suspected causes of halitosis in children. Objectives: To evaluate the relationship of helicobacter pylori and halitosis. Patients and Material: 33 patients with chief complaint of halitosis included in our study. Halitosis was evaluated as a subjective symptom in this study. Careful history was obtained. All patients underwent physical examination in order to rule out sinusitis, otitis, and possible cause of halitosis. 67 patients without halitosis were selected as control group. All patients were aged 4-17 years old. Urea Breath Test was done for all patients. UBT has >95% sensitivity and specifity for diagnosis of H.pylori infection. Chi-square test and Yate’s corrected x2 was used to analyzes finding. Epi-info ver 6 were used. Results: In the case groups 7 patients had H. pylori infection and 26 patients had not. In the control group 18 patients had H.pylori infection and 49 patients had not halitosis (P=0.53). Conclusions: There is no significant differences between case and control group. In this study we did not find relationship between H.pylori infection and halitosis.


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