Classification of histological severity of Helicobacter pylori-associated gastritis by confocal laser endomicroscopy

AIM: To classify the histological severity of Helicobacter pylori (H. pylori) infection-associated gastritis by confocal laser endomicroscopy (CLE). METHODS: Patients with upper gastrointestinal symptoms or individuals who were screened for gastric cancer were enrolled in this study. Histological severity of H. pylori infection-associated gastritis was graded according to the established CLE criteria. Diagnostic value of CLE for histo-logical gastritis was investigated and compared with that of white light endoscopy (WLE). Targeted biopsies from the sites observed by CLE were performed. RESULTS: A total of 118 consecutive patients with H. pylori infection-associated gastritis were enrolled in this study. Receiver operating characteristic curve analysis showedthat the sensitivity and specifi city of CLE were 82.9% and 90.9% for the diagnosis of H. pylori infection, 94.6% and 97.4% for predicting gastric normal mucosa, 98.5% and 94.6% for predicting histological active inflammation, 92.9% and 95.2% for predicting glan-dular atrophy, 98.6% and 100% for diagnosing intes-tinal metaplasia, respectively. Post-CLE image analysis showed that goblet cells and absorptive cells were the two most common parameters on the CLE-diagnosed intestinal metaplasia (IM) images (P < 0.001). More his-tological lesions of the stomach could be found by CLE than by WLE (P < 0.001). CONCLUSION: CLE can accurately show the histological severity of H. pylori infection-associated gastritis. Mapping IM by CLE has a rather good diagnostic accuracy.

Treatment of Helicobacter pylori-associated gastritis using traditional Chinese medicine

Helicobacter pylori is a pathogenic bacterium with strong pathogenicity, which can induce chronic gastritis and peptic ulcer in addition to causing gastric mucosal atrophy and intestinal metaplasia after longterm infection. It is even associated closely with the occurrence of gastric cancer and mucosa-associated lymphoid tissue lymphoma. Recently, the incidence of H. pylori-associated gastritis has increased rapidly worldwide, especially in China. The prevention and treatment of H. pylori infection has become an urgent issue to be resolved by the medical community. Traditional Chinese medicine and the combination of traditional Chinese medicine and Western medicine have recently shown unique advantages in the treatment of H. pylori–associated gastritis. The progress in this area is summarized in this review.

Expression of cytokeratins in Helicobacter pylori-associated chronic gastritis of adult patients infected with cagA+strains:An immunohistochemical study

AIM： To investigate the expression of different cytokeratins （CKs） in gastric epithelium of adult patients with chronic gastritis infected with Helicobacter pylori （H pylon） cagA ＋ strains. METHODS： The expression of CK 7, 8, 18, 19 and 20 was studied immunohistochemically in antral gastric biopsies of 84 patients. All the CKs were immunostained in cagA＋Hpylori gastritis （57 cases）, non-Hpylori gastritis （17 cases） and normal gastric mucosa （10 cases）. RESULTS： In cagA＋ H pylori gastritis, CK8 was expressed comparably to the normal antral mucosa from surface epithelium to deep glands. Distribution of CK18 and CK 19 was unchanged, i.e. transmucosal, but intensity of the expression was different in foveolar region in comparison to normal gastric mucosa. Cytokeratin 18 immunoreactivity was significantly higher in the foveolar epithelium of H pylori-positive gastritis compared to both Hpylori-negative gastritis and controls. On the contrary, decrease in CK19 immunoreactivity occurred in foveolar epithelium of H pylori-positive gastritis. In both normal and inflamed antral mucosa without Hpyloriinfection, CK20 was expressed stronglyl moderately and homogenously in surface epithelium and upper foveolar region, but in H pylod -induced gastritis significant decrease of expression in foveolar region was noted. Generally, in both normal antral mucosa and H pylori-negative gastritis, expression of CK7 was not observed, while in about half cagA＋ H pylori-infected patients, moderate focal CK7 immunoreactivity of the neck and coiled gland areas was registered, especially in areas with more severe inflammatory infiltrate. CONCLUSION： Alterations in expression of CK 7, 18, 19 and 20 together with normal expression of CK8 occur in antral mucosa of H pylori-associated chronic gastritis in adult patients infected with cagA＋ strains. Alterations in different cytokeratins expression might contribute to weakening of epithelial tight junctions observed in H pylori-infected gastric mucosa.

Urinary metabolic profiles during Helicobacter pylori eradication in chronic gastritis

BACKGROUND Helicobacter pylori(H.pylori)infection is a major risk factor for chronic gastritis,affecting approximately half of the global population.H.pylori eradication is a popular treatment method for H.pylori-positive chronic gastritis,but its mecha-nism remains unclear.Urinary metabolomics has been used to elucidate the mechanisms of gastric disease treatment.However,no clinical study has been conducted on urinary metabolomics of chronic gastritis.AIM To elucidate the urinary metabolic profiles during H.pylori eradication in patients with chronic gastritis.METHODS We applied LC–MS-based metabolomics and network pharmacology to in-vestigate the relationships between urinary metabolites and H.pylori-positive chronic gastritis via a clinical follow-up study.RESULTS Our study revealed the different urinary metabolic profiles of H.pylori-positive chronic gastritis before and after H.pylori eradication.The metabolites regulated by H.pylori eradication therapy include cis-aconitic acid,isocitric acid,citric acid,L-tyrosine,L-phenylalanine,L-tryptophan,and hippuric acid,which were involved in four metabolic pathways:(1)Phenylalanine metabolism;(2)phenylalanine,tyrosine,and tryptophan biosynthesis;(3)citrate cycle;and(4)glyoxylate and dicarboxylate metabolism.Integrated metabolomics and network pharmacology revealed that MPO,COMT,TPO,TH,EPX,CMA1,DDC,TPH1,and LPO were the key proteins involved in the biological progress of H.pylori eradication in chronic gastritis.CONCLUSION Our research provides a new perspective for exploring the significance of urinary metabolites in evaluating the treatment and prognosis of H.pylori-positive chronic gastritis patients.

Metabolic dynamics in chronic gastritis:Examining urinary profiles post Helicobacter pylori eradication

Chronic gastritis is the persistent and insidious inflammation of the gastric lining.Helicobacter pylori(H.pylori)has been identified as the most common cause of chronic gastritis and consequently elimination of H.pylori can lead to its cure.This editorial explores the use of urinary metabolic profiles before and after eradication to identify biomarkers that can aid in prognosis and treatment.Despite providing promising insights,there are limitations such as a small sample size(17 patients),a narrow treatment period of 2 wk,and treatment heterogeneity,which raise concerns.Nevertheless,these findings have opened a gateway to enhancing the treatment and prognosis of chronic gastritis through urinary metabolomics.

Non-improvement of atrophic gastritis in cases of gastric cancer after successful Helicobacter pylori eradication therapy

BACKGROUND Helicobacter pylori(H.pylori)infection is closely related to the development of gastric cancer(GC).However,GC can develop even after H.pylori eradication.Therefore,it would be extremely useful if GC could be predicted after eradication.The Kyoto classification score for gastritis(GA)is closely related to cancer risk.However,how the score for GC changes after eradication before onset is not well understood.AIM To investigate the characteristics of the progression of Kyoto classification scores for GC after H.pylori eradication.METHODS Eradication of H.pylori was confirmed in all patients using either the urea breath test or the stool antigen test.The Kyoto classification score of GC patients was evaluated by endoscopy at the time of event onset and three years earlier.In ad-dition,the modified atrophy score was evaluated and compared between the GC group and the control GA group.RESULTS In total,30 cases of early GC and 30 cases of chronic GA were evaluated.The pathology of the cancer cases was differentiated adenocarcinoma,except for one case of undifferentiated adenocarcinoma.The total score of the Kyoto classifi-cation was significantly higher in the GC group both at the time of cancer onset and three years earlier(4.97 vs 3.73,P=0.0034;4.2 vs 3.1,P=0.0035,respectively).The modified atrophy score was significantly higher in the GC group both at the time of cancer onset and three years earlier and was significantly improved only in the GA group(5.3 vs 5.3,P=0.5;3.73 vs 3.1,P=0.0475,respectively).CONCLUSION The course of the modified atrophy score is useful for predicting the onset of GC after eradication.Patients with severe atrophy after H.pylori eradication require careful monitoring.

Estimate the Prevalence of Helicobacter pylori Infection among Diabetes & Non-Diabetes Mellitus Patients and Its Correlation with Malignant Gastritis Patients Attending in Lower Shabelle Region (Somalia)

Background: Several conducted studies have reported a higher and more frequent Helicobacter pylori infection rate in type 2 diabetes mellitus (T2DM). The aim of this study was to estimation the prevalence of H. pylori and its association between H. pylori infection and T2DM. Materials and Methods: A sectional-cross study was conducted based on 200 patients studded with socioeconomic characteristics through a questionnaire & H. pylori was diagnosed by serum anti-H. pylori immunoglobulin G (IgG) and IgA. Furthermore, patients were investigated for fasting blood glucose (FBG) levels, glycosylated hemoglobin (HbA1c), serum cholesterol, and other biochemistry parameters. Results: The findings showed The prevalence of Hp positive infection was significantly higher in the total sample was 134 with (67%). While 66 out of 200 patients with (33%) was H. pylori negative infection. of H. pylori. Further, the mean values were statistically significant for diabetes with H. pylori infection for IgG > 300 titer and IgA > 250 titer, regarding, HbA1C (7.52 ± 0.41) (P Conclusions: The current study revealed that H. pylori prevalence infections were significantly higher in diabetic patients studied compared to non-diabetic patients. Furthermore, T2DM patients infected with H. pylori positive reported a higher prevalence rate of symptoms than H. pylori negative.

Helicobacter Pylori-induced Gastritis Model in BALB/c Mice Infected With Fresh Isolates from a Human Complex Ulcer Patient

A useful helicobacter pylori-induced gastritis model using BALB/c mice was established for mimicking of human gastritis induced by Helicobacter pylori (H. pylori). The H. pylori isolates were obtained freshly from a human complex ulcer patient. BALB/c mice were fasted for 24 h and then 0.25 mL of 0.2 mol·L -1 NaHCO 3 was administered after by gavage to each mouse and 0.5 mL of 10 9 colonies formation unit per milliliter (CFU/mL) of H. pylori was administered 15 min. On the 3 rd day and 5 th day, the H. pylori inoculations were repeated. The inoculated mice were sacrificed in batch on the 5 th day, in the 2 nd week, 3 rd week and 4 th week. The gastric mucous membrane near pyloric portion was removed, treated and then cultured under microaerobic condition for detection of H.pylori. The remainders of the gastric membrane were fixed by 10% formaldehyde solution for pathological detection. The results showed that the H. pylori could be separated from the gastric membranes of inoculated mice. Obvious invasion of inflammatory cells in the gastric membranes of inoculated mice could be observed from pathological sections. It can be concluded that the inoculating fresh human H. pylori isolates can produce mouse gastritis. This model of BALB/c mice can be used for evaluating the therapeutic agents for the treatment of gastritis induced by H. pylori.

Treatment of Helicobacter pylori infection in atrophic gastritis

Helicobacter pylori(Hp) is a major human pathogen causing chronic, progressive gastric mucosal damage and is linked to gastric atrophy and cancer. Hp-positive individuals constitute the major reservoir for transmission of infection. There is no ideal treatment for Hp. Hp infection is not cured by a single antibiotic, and sometimes, a combined treatment with three or more antibiotics is ineffective. Atrophic gastritis(AG) is a chronic disease whose main features are atrophy and/or intestinal metaplasia of the gastric glands, which arise from long-standing Hp infection. AG is reportedly linked to an increased risk for gastric cancer, particularly when extensive intestinal metaplasia is present. Active or past Hp infection may be detected by conventional methods in about two-thirds of AG patients. By immunoblotting of sera against Hp whole-cell protein lysates, a previous exposure to Hp infection is detected in all AG patients. According to guidelines, AG patients with Hp positivity should receive eradication treatment. The goals of treatment are as follows:(1) Cure of infection, resolution of inflammation and normalization of gastric functions;(2) possible reversal of atrophic and metaplastic changes of the gastric mucosa; and(3) prevention of gastric cancer. An ideal antibiotic regimen for Hp should achieve eradication rates of approximately 90%, and complex multidrug regimens are required to reach this goal. Amongst the factors associated with treatment failure are high bacterial load, high gastric acidity, Hp strain, smoking, low compliance, overweight, and increasing antibiotic resistance. AG, when involving the corporal mucosa, is linked to reduced gastric acid secretion. At a non-acidic intra-gastric p H, the efficacy of the common treatment regimens combining proton pump inhibitors with one or more antibiotics may not be the same as that observed in patients with Hp gastritis in an acid-producing stomach. Although the efficacy of these therapeutic regimens has been thoroughly tested in subjects with Hp infection, there is a paucity of evidence in the subgroupof patients with AG. Bismuth-based therapy may be an attractive treatment in the specific setting of AG, and specific studies on the efficacy of bismuth-based therapies are needed in patients with AG.

Proteomic analysis reveals molecular biological details in varioliform gastritis without Helicobacter pylori infection

AIM:To investigate and elucidate the molecular mechanism underlying varioliform gastritis for early detection,prevention and intervention of gastric cancer.METHODS:A combination of two-dimensional gel electrophoresis and mass spectrometry was used to detect the differentially expressed proteins between varioliform gastritis and matched normal mucosa.The selected proteins were confirmed by Western blotting and reverse transcription polymerase chain reaction(RT-PCR) in additional samples and the function of some proteins in varioliform gastritis was analyzed by bio-method preliminarily.RESULTS:We identified 21 differentially expressed proteins in varioliform gastritis,and compared them with matched normal mucosa.Eleven proteins were upregulated and ten downregulated in varioliform gastritis when compared with the same proteins in individualmatched normal gastric mucosa.These proteins are related to metabolism,oxidation,cytoskeleton,apoptosis,signal transduction and other aspects of cells.Two novel proteins,thioredoxin domain-containing protein 5(TXNDC5) upregulated in varioliform gastritis,and neuropolypeptide h3 [phosphatidylethanolamine-binding protein 1(PEBP1)] downregulated in varioliform gastritis,were further investigated.Their expressions were validated by Western blotting and RT-PCR in 12 cases of varioliform gastritis which was matched with normal mucosa.The expression level of PEBP1 in varioliform gastritis was significantly lower(P<0.05) while that of TXNDC5 was significantly higher than that in matched normal gastric mucosa(P<0.05).CONCLUSION:There are some changes of protein expression in varioliform gastritis.Downregulation of PEBP1 and upregulation of TXNDC5 are involved in the development of varioliform gastritis.

Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection

AIM:To study the association between Helicobacter pylori(H.pylori)infection and autoimmune type atrophic gastritis. METHODS:Twenty-three patients with different grades of atrophic gastritis were analysed using enzyme immunoassay-based serology,immunoblot-based serology,and histology to reveal a past or a present H.pylori infection.In addition,serum markers for gastric atrophy(pepsinogenⅠ,pepsinogenⅠ/Ⅱand gastrin)and autoimmunity[parietal cell antibodies(PCA), and intrinsic factor(IF),antibodies]were determined. RESULTS:Of the 14 patients with severe gastricatrophy,as demonstrated by histology and serum markers,and no evidence for an ongoing H.pylori infection,eight showed H.pylori antibodies by immunoblotting.All eight had elevated PCA and 4/8 also had IF antibodies.Of the six immunoblot-negative patients with severe corpus atrophy,PCA and IF antibodies were detected in four.Among the patients with low to moderate grade atrophic gastritis(all except one with an ongoing H.pylori infection),serum markers for gastric atrophy and autoimmunity were seldom detected.However,one H.pylori negative patient with mild atrophic gastritis had PCA and IF antibodies suggestive of a pre-atrophic autoimmune gastritis. CONCLUSION:Signs of H.pylori infection in autoimmune gastritis,and positive autoimmune serum markers in H.pylori gastritis suggest an etiological role for H.pylori in autoimmune gastritis.

Two stomach-originated lactobacillus strains improve Helicobacter pylori infected murine gastritis

AIM:To investigate the potential anti-Helicobacter pylori(H.pylori ) and anti-inflammation in vivo effects of two lactobacillus strains from human stomach.METHODS:Forty H.pylori infected Balb/c mice were randomly divided into 4 groups:proton pump inhibitor and antibiotics triple treated group,Lactobacillus fermenti(L.fermenti ) treated group,Lactobacillus acidophilus treated group and normal saline control group.Ten uninfected mice were also included as blank control group.The infection of H.pylori was detected by rapid urease tests,Giemsa staining and bacterial culture.The colonization of H.pylori was assessed in bacterial density score and gastric inflammation was assessed in histological score.The colonization of L.fermenti was performed by fluorescent probe.RESULTS:Histopathologic evaluation showed significant release of mucosal inflammation in gastric antrum and gastric body in lactobacillus treated groups and triple treated group.H.pylori eradication rate in both lactobacillus treated groups and triple treated group were higher than normal saline control group.Lactobacillus treated groups and triple treated group showed significant decrease of H.pylori bacterial density.CONCLUSION:Both lactobacillus strains have a significant anti-H.pylori activity;L.fermenti displays more efficient antagonistic activity in vivo against H.pylori infection.

Helicobacter pylori-related chronic gastritis as a risk factor for colonic neoplasms

To summarize the current views and insights on associations between Helicobacter pylori(H. pylori)-related chronic gastritis and colorectal neoplasm, we reviewed recent studies to clarify whether H. pylori infection/H. pylori-related chronic gastritis is associated with an elevated risk of colorectal neoplasm. Recent studies based on large databases with careful control for confounding variables have clearly demonstrated an increased risk of colorectal neoplasm associated with H. pylori infection. The correlation between H. pylori-related chronic atrophic gastritis(CAG) and colorectal neoplasm has only been examined in a limited number of studies. A recent large study using a national histopathological database, and our study based on the stage of H. pylori-related chronic gastritis as determined by serum levels of H. pylori antibody titer and pepsinogen, indicatedthat H. pylori-related CAG confers an increased risk of colorectal neoplasm, and more extensive atrophic gastritis will probably be associated with even higher risk of neoplasm. In addition, our study suggested that the activity of H. pylori-related chronic gastritis is correlated with colorectal neoplasm risk. H. pylori-related chronic gastritis could be involved in an increased risk of colorectal neoplasm that appears to be enhanced by the progression of gastric atrophy and the presence of active inflammation.

Helicobacter pylori infection with atrophic gastritis: An independent risk factor for colorectal adenomas

BACKGROUND The significance of Helicobacter pylori(H.pylori)infection and atrophic gastritis(AG)in the prevalence of colorectal adenomas has been examined in a limited number of studies.However,these studies reported disputed conclusions.AIM To investigate whether H.pylori infection,AG,and H.pylori-related AG increase the risk of colorectal adenomas.METHODS This retrospective cross-sectional study included 6018 health-check individuals.The relevant data for physical examination,laboratory testing,13C-urea breath testing,gastroscopy,colonoscopy and histopathological examination of gastric and colorectal biopsies were recorded.Univariate and multivariate logistic regression analyses were performed to determine the association between H.pylori-related AG and colorectal adenomas.RESULTS Overall,1012 subjects(16.8%)were diagnosed with colorectal adenomas,of whom 143(2.4%)had advanced adenomas.Among the enrolled patients,the prevalence of H.pylori infection and AG was observed as 49.5%(2981/6018)and 10.0%(602/6018),respectively.Subjects with H.pylori infection had an elevated risk of colorectal adenomas(adjusted odds ratio[OR]of 1.220,95%confidence interval(CI):1.053-1.413,P=0.008)but no increased risk of advance adenomas(adjusted OR=1.303,95%CI:0.922-1.842,P=0.134).AG was significantly correlated to an increased risk of colorectal adenomas(unadjusted OR=1.668,95%CI:1.352-2.059,P<0.001;adjusted OR=1.237,95%CI:0.988-1.549,P=0.064).H.pylori infection accompanied by AG was significantly associated with an increased risk of adenomas(adjusted OR=1.491,95%CI:1.103-2.015,P=0.009)and advanced adenomas(adjusted OR=1.910,95%CI:1.022-3.572,P=0.043).CONCLUSION H.pylori-related AG was associated with a high risk of colorectal adenomas and advanced adenomas in Chinese individuals.

Correlation between Helicobacter pylori-associated gastric diseases and colorectal neoplasia

AIM: To explore the correlation between Helicobacter pylori(H. pylori)-associated gastric diseases and colorectal neoplasia.METHODS: Patients included in this study underwent a colonoscopy and esophago-gastro-duodenoscopy(EGD) along with histopathological measurement between March 2012 and March 2015 at Qi-Lu Hospital of Shandong University, who also had results of H. pylori detection. A total of 233 cases were selected. Demographic data, H. pylori infection status(including results of rapid urease tests and gastric mucosa pathological examinations) and histopathological examination results of gastric and colorectal mucosa were gathered and analyzed. The statistical analysis focused on the prevalence of colorectal neoplasms among patients with various histopathological categories of the stomach. ORs and their 95%CI were calculated to describe the strengths of the associations.RESULTS: The incidence rates of colorectal adenoma without high-grade intraepithelial neoplasia(HGIEN)(OR = 2.400, 95%CI: 0.969-5.941), adenoma with HGIEN(5.333, 1.025-27.758) and adenocarcinoma(1.455, 0.382-5.543) were all higher for patients with H. pylori-associated gastritis than for those in the control group. The incidence rate of colorectal adenoma with HGIEN(3.218, 0.767-13.509) was higher in patients with intestinal metaplasia than in the control group, while the incidence rates of adenoma without HGIEN(0.874, 0.414-1.845) and adenocarcinoma(0.376, 0.096-1.470) were lower in the intestinal metaplasia group than in the control group. The incidence rate of colorectal adenoma without HGIEN(3.111, 1.248-7.753) was significantly higher in the gastric intraepithelial neoplasia group than in the control group, while the rates of adenoma with HGIEN(1.481, 0.138-15.941) and adenocarcinoma(2.020, 0.561-7.272) were higher in the gastric intraepithelial neoplasia group. Incidence rates of colorectal adenoma without HGIEN(1.067, 0.264-4.314), adenoma with HGIEN(2.667, 0.231-30.800) and adenocarcinoma(2.182, 0.450-10.585) were all higher in the gastric adenocarcinoma group than in the control group.CONCLUSION: H. pylori infection as well as H. pylori-associated gastric diseases are risk factors for colorectal neoplasia.

Correlation between CD4, CD8 cell infiltration in gastric mucosa, Helicobacter pylori infection and symptoms in patients with chronic gastritis

AIM: To evaluate the correlation between CD4, CD8 cell infiltration in gastric mucosa, Helicobacter pylori(H pylori)infection and symptoms or the assemblage of symptoms in cases with chronic gastritis.METHODS: Biopsy samples at the gastric antrum were obtained from 62 patients with chronic gastritis. CD4 and CD8 cell infiltration was evaluated by immunohistochemical assays on frozen sections of the biopsy samples. Fifteen symptoms referring to digestion-related activity and nondigestion related activity were observed. The correlation between lymphocyte infiltration and each symptom or symptom assemblage was analyzed by logistic regression and K-mean cluster methods.RESULTS: CD4 cell infiltrations in gastric mucosa were much more in patients with H pylori infection, while CD8 cell infiltrations were similar in patients with or without H pylori infection. Logistic regression analysis showed that the symptoms including heavy feeling in head or body (t= 2.563), and thirst (t= 2.478) were significantly related with CD4 cell infiltration in gastric mucosa (P＜0.05), and cool limbs with aversion to cold were related with CD8cell infiltration (t = 2.872, P＜0.05). Further analysis showed that non-digestive related symptom assemblage could increase the predicted percentage of CD4 and CD8cell infiltration in gastric mucosa, including lower CD4infiltration by 12.5%, higher CD8 infiltration by 33.3%,and also non-H pylori infection by 23.6%.K-means cluster analysis of all symptoms and CD4 and CD8 cell infiltration in gastric mucosa showed a similar tendency to increase the predicted percentage of CD4, CD8 cell infiltration and H pylori infection.CONCLUSION: Based on correlation between the gastric mucosa lymphocyte infiltration, H pylori infection and clinical symptoms, symptoms or symptomatic assemblages play an important role in making further classification of chronic gastritis, which might help find a more specific therapy for chronic gastritis.

Probiotic BIFICO cocktail ameliorates Helicobacter pylori induced gastritis

AIM: To determine the protective effect of triple viable probiotics on gastritis induced by Helicobacter pylori (H. pylori) and elucidate the possible mechanisms of protection. METHODS: Colonization of BIFICO strains in the mouse stomach was determined by counting colony-forming units per gram of stomach tissue. After treatment with or without BIFICO, inflammation and H. pylori colonization in the mouse stomach were analyzed by hematoxylin and eosin and Giemsa staining, respectively. Cytokine levels were determined by enzyme-linked immunosorbent assay and Milliplex. The activation of nuclear factor (NF)-kappa B and MAPK signaling in human gastric epithelial cells was evaluated by Western blot analysis. Quantitative reverse transcription-polymerase chain reaction was used to quantify TLR2, TLR4 and MyD88 mRNA expression in the mouse stomach. RESULTS: We demonstrated that BIFICO, which contains a mixture of Enterococcus faecalis, Bifido-bacterium longum and Lactobacillus acidophilus, was tolerant to the mouse stomach environment and was able to survive both the 8-h and 3-d courses of administration. Although BIFICO treatment had no effect on the colonization of H. pylori in the mouse stomach, it ameliorated H. pylori -induced gastritis by significantly inhibiting the expression of cytokines and chemokines such as TNF-alpha, IL-1 beta, IL-10, IL-6, G-CSF and MIP-2 (P < 0.05). These results led us to hypothesize that BIFICO treatment would diminish the H. pylori-induced inflammatory response in gastric mucosal epithelial cells in vitro via the NF-kappa B and MAPK signaling pathways. Indeed, we observed a decrease in the expression of the NF-kappa B subunit p65 and in the phosphorylation of I kappa B-alpha, ERK and p38. Moreover, there was a significant decrease in the production of IL-8, TNF-alpha, G-CSF and GM-CSF (P < 0.05), and the increased expression of TLR2, TLR4 and MyD88 induced by H. pylori in the stomach was also significantly reduced following BIFICO treatment (P < 0.05). CONCLUSION: Our results suggest that the probiotic cocktail BIFICO can ameliorate H. pylori-induced gastritis by inhibiting the inflammatory response in gastric epithelial cells.

Surveilling Russell body Helicobacter pylori-negative gastritis: A case report and review of literature

BACKGROUND Russell body gastritis(RBG)is very rare type of chronic inflammation of gastric mucosa.The pathologic hallmark of the disease is Russell bodies(RB)which represent accumulation of eosinophilic cytoplasmic inclusions in endoplasmic reticulum of mature plasma cells(Mott cells).Most published cases are associated with Helicobacter pylori(H.pylori)infection because of correlation between plasma cell activation and antigenic stimulation.There are insufficient data about H.pylori-negative RBG and very little is known about the natural course of the disease.CASE SUMMARY A 51-year-old male patient underwent endoscopic screening for mild iron deficiency anemia.Gastroscopy revealed diffuse hyperemia,edema and nodularity of the fundic and corpus mucosa.Due to non-specific endoscopic findings and iron-deficiency anemia our preliminary diagnosis was diffuse type of gastric carcinoma or gastric lymphoma.Biopsy specimens of gastric mucosa showed inflammatory infiltrate rich in Mott cells,consisting entirely of cytoplasmic RB.Absence of nuclear atypia and mitosis of the plasma cells,polyclonal pattern of the Mott cells and negative staining for cytokeratins favored diagnosis of RBG.The patient was treated with proton-pump inhibitor for 8 wk.Long-term clinical and endoscopic surveillance was scheduled.Albeit,there was no improvement in endoscopic features of the gastric mucosa in three consecutive gastroscopies,histopathological findings demonstrated that the chronic inflammatory infiltrate in the fundic mucosa is less pronounced,rich in plasma cells,with almost absent RB and Mott cells.CONCLUSION The prognosis of this entity is uncertain,that is why these patients are subjects of continuous follow up.

Interobserver variation in histopathological assessment of Helicobacter pylori gastritis

AIM:Because the presence or absence of H pylori infection has important implications for therapeutic decisions based on histological assessment,the reproducibility of Sydney system is important.The study was designed to test the reproducibility of features of Helicobacter pylori gastritis, using the updated Sydney classification. METHODS:Gastric biopsies of 40 randomly selected cases of H pylori gastritis were scored semiquantitatively by three pathologists.Variables analysed induded chronic inflammation, inflammatory activity,atrophy,intestinal metaplasia,H pylori, surface epithelial damage.κ values below 0.5 represented poor,those between 0.5 and 0.75 good and values over 0.75 excellent interobserver agreement. RESULTS:The best interobserver agreement(κ=0.62)was present for intestinal metaplasia.The agreement was the poorest for evaluating atrophy(κ=0.31). CONCLUSION:Although the results of this study were in accordance with some previous studies,an excellent agreement could not be reached for any features of H pylori gastritis.This low degree of concordance is assumed to be due to the personal evaluation differences in grading the features,the lack of standardized diagnostic criteria,and the ignorance to reach a consensus about the methods to be used in grading the features of H pylori gastritis before initiating the study.

Clinical applicability of gastroscopy with narrow-band imaging for the diagnosis of Helicobacter pylori gastritis, precancerous gastric lesion, and neoplasia

Premalignant gastric lesions such as atrophic gastritis and intestinal metaplasia frequently occur in subjects with long-term Helicobacter pylori(H.pylori)infection.The regular arrangement of collecting venules(RAC)is seen in the normal gastric corpus,whereas mucosal swelling and redness without RAC are observed in H.pylori-infected mucosa.Despite successful H.pylori eradication,the presence of atrophic gastritis and/or gastric intestinal metaplasia(GIM)is a risk factor for gastric cancer.With the development of advanced imaging technologies,recent studies have reported the usefulness of narrow-band imaging(NBI)for endoscopic diagnosis of atrophic gastritis and GIM.Using NBI endoscopy with magnification(M-NBI),atrophic gastritis is presented as irregular coiled microvessels and loss of gastric pits.Typical M-NBI endoscopic findings of GIM are a light blue crest and a white opaque substance.Based on the microvascular patterns,fine network,core vascular,and unclear patterns are useful for predicting gastric dysplasia in polypoid lesions.For diagnosis of early gastric cancer(EGC),a systematic classification using M-NBI endoscopy has been proposed on the basis of the presence of a demarcation line and an irregular microvascular/microsurface pattern.Furthermore,M-NBI endoscopy has been found to be more accurate for determining the horizontal margin of EGC compared to conventional endoscopy.In this review,we present up-to-date results on the clinical usefulness of gastroscopy with NBI for the diagnosis of H.pylori gastritis,precancerous gastric lesion,and neoplasia.