Gastric Inflammation Research Articles

MicroRNA Modulation of Host Immune Response and Inflammation Triggered by Helicobacter pylori.

Helicobacter pylori (H. pylori) remains the most-researched etiological factor for gastric inflammation and malignancies. Its evolution towards gastric complications is dependent upon host immune response. Toll-like receptors (TLRs) recognize surface and molecular patterns of the bacterium, especially the lipopolysaccharide (LPS), and act upon pathways, which will finally lead to activation of the nuclear factor-kappa B (NF-kB), a transcription factor that stimulates release of inflammatory cytokines. MicroRNAs (MiRNAs) finely modulate TLR signaling, but their expression is also modulated by activation of NF-kB-dependent pathways. This review aims to focus upon several of the most researched miRNAs on this subject, with known implications in host immune responses caused by H. pylori, including let-7 family, miRNA-155, miRNA-146, miRNA-125, miRNA-21, and miRNA-221. TLR–LPS interactions and their afferent pathways are regulated by these miRNAs, which can be considered as a bridge, which connects gastric inflammation to pre-neoplastic and malignant lesions. Therefore, they could serve as potential non-invasive biomarkers, capable of discriminating H. pylori infection, as well as its associated complications. Given that data on this matter is limited in children, as well as for as significant number of miRNAs, future research has yet to clarify the exact involvement of these entities in the progression of H. pylori-associated gastric conditions.

Helicobacter pylori Subdues Cytokine Signaling to Alter Mucosal Inflammation via Hypermethylation of Suppressor of Cytokine Signaling 1 Gene During Gastric Carcinogenesis

Helicobacter pylori infection has been associated with the onset of gastric mucosal inflammation and is known to perturb the balance between T-regulatory (Treg) and T-helper 17 (Th17) cells which causes a spurt of interleukin 17 (IL17) and transforming growth factor-β (TGF-β) from Th17 and Treg cells within the gastric milieu. IL17 instigates a surge of interleukin 6 (IL6) from T-helper 1 (Th1) and T-helper 2 (Th2) cells. Further, H. pylori infection is known to stimulate the atypical DNA methylation in gastric mucosa. However, the precise role of cytokine signaling in induction of epigenetic modifications during gastric carcinogenesis is vaguely understood. In this study, patient samples from were examined using real-time polymerase chain reaction (qPCR), PCR, methylation-specific (MS)-PCR, and enzyme-linked immunosorbent assays. We found that H. pylori infection augments the production of interleukin 10 (IL10), IL6, and TGF-β in the gastric milieu and systemic circulation. Together with the IL6/IL10 mediated hyperactivation of the JAK/STAT pathway, H. pylori infection causes the inactivation of suppressor of cytokine signaling 1 (SOCS1) gene through the hypermethylation of the promoter region. This study signifies that H. pylori-mediated epigenetic silencing of SOCS1 in concert with inflammatory cytokines miffs hyperactivation of the JAK/STAT cascade during gastric carcinogenesis.

Tristetraprolin Prevents Gastric Metaplasia in Mice by Suppressing Pathogenic Inflammation

Background & AimsAberrant immune activation is associated with numerous inflammatory and autoimmune diseases and contributes to cancer development and progression. Within the stomach, inflammation drives a well-established sequence from gastritis to metaplasia, eventually resulting in adenocarcinoma. Unfortunately, the processes that regulate gastric inflammation and prevent carcinogenesis remain unknown. Tristetraprolin (TTP) is an RNA-binding protein that promotes the turnover of numerous proinflammatory and oncogenic messenger RNAs. Here, we assess the role of TTP in regulating gastric inflammation and spasmolytic polypeptide-expressing metaplasia (SPEM) development.MethodsWe used a TTP-overexpressing model, the TTPΔadenylate-uridylate rich element mouse, to examine whether TTP can protect the stomach from adrenalectomy (ADX)-induced gastric inflammation and SPEM.ResultsWe found that TTPΔadenylate-uridylate rich element mice were completely protected from ADX-induced gastric inflammation and SPEM. RNA sequencing 5 days after ADX showed that TTP overexpression suppressed the expression of genes associated with the innate immune response. Importantly, TTP overexpression did not protect from high-dose-tamoxifen–induced SPEM development, suggesting that protection in the ADX model is achieved primarily by suppressing inflammation. Finally, we show that protection from gastric inflammation was only partially due to the suppression of Tnf, a well-known TTP target.ConclusionsOur results show that TTP exerts broad anti-inflammatory effects in the stomach and suggest that therapies that increase TTP expression may be effective treatments of proneoplastic gastric inflammation. Transcript profiling: GSE164349.

Effect of Anti-Hp treatment on nutritional status of children with Helicobacter Pylori-Positive Gastritis and its clinical significance.

Objectives:To evaluate the outcome of anti-HP treatment on the nutritional status of children with Helicobacter pylori-positive gastritis.Methods:Sixty children with Helicobacter pylori-positive gastritis admitted to our hospital from June 2018 to June 2020 were selected as the experimental group, and 60 healthy normal people (Hp negative) were selected as the control group. The experimental group were given anti-HP treatment, and the improvement of their clinical symptoms after treatment and the changes of nutritional indexes such as hemoglobin and serum ferritin were observed one year after treatment. Gastroscopy was performed before treatment and four weeks after treatment, and the improvement of gastric inflammation and the positive rate of Hp were compared and analyzed before and after treatment.Results:The nutritional indicators of the children in experimental group were inferior compared with those in the control group (p<0.05). The clinical symptoms and signs of the experimental group were significantly alleviated after anti-Hp treatment, and the biochemical indicators were significantly improved after one Year of follow-up compared with those before treatment (p<0.05). The incidence of moderate and severe gastric mucosal inflammation in the experimental group decreased from 70% before treatment to 17% (p<0.05). The HP infection decreased from 100% before treatment to 13% (p<0.05).Conclusion:Helicobacter pylori infection has a negative impact on the nutritional status of children. Anti-HP therapy can improve the gastrointestinal symptoms and nutritional status of children, which plays an important role in the growth and development of children.

Investigations of the maintenance system of the Konik Polski horse and its effects on fecal microbiota activity during the winter and summer seasons.

Gastrointestinal microbiota play a key role in the nutrients digestion and hence maintaining animal health and welfare. The diet offered to the animals in captivity may differ considerably from that on natural pastures. In a stabled maintenance system, horses have a limited choice of habitat and feed. Time spend for feeding is relevant for equine welfare because the reduction of the time devoted for foraging may be responsible for inducing gastric inflammation and ulceration. Therefore, in the present study, it was hypothesized that fecal bacterial fermentative processes differ between free-roaming and stabled Konik Polski Horses (KPHs) with respect to microbial enzymatic activity, and thus the fecal concentration of short-chain fatty acids (SCFA), which can be further utilized for assessing the feeding behavior and welfare in free-roaming versus stabled horses. The SCFA concentration and profile, as well as the extracellular and intracellular activities of selected bacterial enzymes, were characterized in horse feces collected during the winter and summer feeding seasons. The results showed higher enzymatic activity and SCFA production in the feces excreted by free-roaming versus stabled horses, especially during summer. An increase in pasture plant diversity may be beneficial for the gastrointestinal microbiota and hence for maintaining health and welfare.

Ghrelin-cell physiology and role in the gastrointestinal tract.

Ghrelin was discovered in 1999; extensive research and clinical studies on ghrelin have been published in the last 20 years. Physiological research on ghrelin ranges from its appetite-stimulating effects to its association with energy homeostasis. The physiological effects of ghrelin in the gastrointestinal tract and its relevance in the pathological conditions of the gastrointestinal tract have gradually become clearer. The purpose of the review is to provide current information on ghrelin cell biology and physiology, particularly in the gastrointestinal tract. Ghrelin-producing cells in the stomach are characterized as X/A-like cells, but immunohistochemical analyses have revealed co-expression of several secreted proteins and hormones in ghrelin-producing cells such as nesfatin-1, somatostatin, and pancreastatin. Furthermore, the local physiological roles and/or mechanisms of ghrelin in gastrointestinal functions such as gastric motility and inflammation are discussed. Ghrelin is a brain-gut hormone with a wide range of physiological actions; hence, it is important to understand its effects on the physiological functions of the gastrointestinal tract to elucidate the biological significance of ghrelin.

Brassica oleracea Prevents HCl/Ethanol-Induced Gastric Damages in Mice

Brassica oleracea var. capitata L. (cabbage) is a popular vegetable with a wide range of pharmacological activities that help to promote human health. The present study investigated the beneficial effects of B. oleracea var. capitata L. extract (BOE) on HCl/ethanol (H/E)-induced gastric damages in mice. Pre-administration of BOE (25–100 mg/kg) for 7 consecutive days significantly decreased macroscopically visible lesion on the gastric mucosa induced by H/E. In addition, results from hematoxylin and eosin-stained gastric tissue showed that BOE inhibited invaded percentage of lesion and prevented the reduction in mucosal thickness in peri-ulcerative region. BOE significantly alleviated the H/E-mediated decreases in Alcian blue binding, total hexose, sialic acid, and collagen in the gastric tissue, suggesting BOE attenuates the gastric damage via preserving the integrity of gastric mucus. Moreover, BOE significantly decreased histamine level in the plasma and reduced mRNA levels associated with secreting gastric acid. Furthermore, BOE inhibited myeloperoxidase activity and suppressed nuclear factor-κB mRNA and its dependent inflammatory genes expression induced by H/E. BOE also strengthened antioxidant enzyme activity, with a mitigating H/E-mediated increase in malondialdehyde level of the gastric tissue. Thus, these results suggest that BOE has the potential to protect the gastric tissue via inhibiting gastric acid secretion, inflammation, and oxidative stress.

The Microbiome and Alzheimer's Disease: Potential and Limitations of Prebiotic, Synbiotic, and Probiotic Formulations.

The Microbiome has generated significant attention for its impacts not only on gastrointestinal health, but also on signaling pathways of the enteric and central nervous system via the microbiome gut–brain axis. In light of this, microbiome modulation may be an effective therapeutic strategy for treating or mitigating many somatic and neural pathologies, including neurodegenerative disorders. Alzheimer’s disease (AD) is a chronic neurodegenerative disease that interferes with cerebral function by progressively impairing memory, thinking and learning through the continuous depletion of neurons. Although its etiopathogenesis remains uncertain, recent literature endorses the hypothesis that probiotic, prebiotic and synbiotic supplementation alters AD-like symptoms and improves many of its associated disease biomarkers. Alternatively, a dysfunctional microbiota impairs the gut epithelial barrier by inducing chronic gastric inflammation, culminating in neuroinflammation and accelerating AD progression. The findings in this review suggest that probiotics, prebiotics or synbiotics have potential as novel biological prophylactics in treatment of AD, due to their anti-inflammatory and antioxidant properties, their ability to improve cognition and metabolic activity, as well as their capacity of producing essential metabolites for gut and brain barrier permeability.

Fermented-Rhus verniciflua extract ameliorate Helicobacter pylori eradication rate and gastritis.

An antibacterial effect of fermented‐Rhus verniciflua extract (FRVE), an urushiol‐free extract fermented by Fomitella fraxinea, on Helicobacter pylori was evaluated in mice. Minimal inhibitory concentration of FRVE against H. pylori eradication was checked with serial dilution method in vitro. H. pylori infection‐induced mice were utilized to determine the effect of oral administration of FRVE with/without standard triple therapy (STT: metronidazole, omeprazole, and clarithromycin) on H. pylori colonization and gastric inflammation. H. pylori was clearly eradicated by FRVE at a concentration of ≥2 mg/ml in vitro. In animal study, FRVE at a concentration of ≥6 mg/ml significantly reduced colonized H. pylori grading (0.2 vs. 2.2, p < .01) and improved gastric inflammation (0.4 vs. 1.6, p < .01) compared to control. STT with FRVE (3 mg/ml) exerted synergistic effect on both H. pylori colonization grade (STT, 0.6 ± 0.9; FRVE, 1.4 ± 0.5; STT + FRVE, 0.8 ± 0.4) and gastric inflammation (STT, 0.4 ± 0.5; FRVE, 1.4 ± 0.5; STT + FRVE,1.0 ± 0.1) compared with single therapy (p < .01). H. pylori eradication rate of FRVE (6 mg/ml) was higher than that of STT (60% vs. 20%). FRVE has potential antibacterial activity against H. pylori infection and can be used as an additional therapy on STT.

Potential of FTIR-Spectroscopy for Drugs Screening against Helicobacter pylori.

Helicobacter pylori colonizes the human stomach of half of the world’s population. The infection if not treated, persists through life, leading to chronic gastric inflammation, that may progress to severe diseases as peptic ulcer, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. The first line of treatment, based on 7 to 21 days of two antibiotics associated with a proton pump inhibitor, is, however, already failing most due to patient non-compliance that leads to antibiotic resistance. It is, therefore, urgent to screen for new and more efficient antimicrobials against this bacterium. In this work, Fourier Transform Infrared (FTIR) spectroscopy was evaluated to screen new drugs against H. pylori, in rapid (between 1 to 6 h), and high-throughput mode and based on a microliter volume processes in relation to the agar dilution method. The reference H. pylori strains 26,695 and J99, were evaluated against a peptide-based antimicrobial and the clinical antibiotic clarithromycin, respectively. After optimization of the assay conditions, as the composition of the incubation mixture, the time of incubation, and spectral pre-processing, it was possible to reproducibly observe the effect of the drug on the bacterial molecular fingerprint as pointed by the spectra principal component analysis. The spectra, obtained from both reference strains, after its incubation with drugs concentrations lower than the MIC, presented peak ratios statistically different (p < 0.05) in relation to the bacteria incubated with drugs concentrations equal or higher to the MIC. It was possible to develop a partial least square regression model, enabling to predict from spectra of both bacteria strains, the drug concentration on the assay, with a high correlation coefficient between predicted and experimental data (0.91) and root square error of 40% of the minimum inhibitory concentration. All this points to the high potential of the technique for drug screening against this fastidious growth bacterium.

Genistein attenuated gastric inflammation and apoptosis in Helicobacter pylori-induced gastropathy in rats

BackgroundHelicobacter pylori (H. pylori) infection is a major cause of chronic gastritis, peptic ulcer diseases and cancer. Genistein (4′,5,7-trihydroxyisoflavone), a tyrosine-specific-protein kinase inhibitor, has been shown to exert an anti-inflammatory property. The aim of this study was to examine the treatment effects of genistein and its mechanisms in rats with H. pylori infection.MethodsEighteen male Sprague-Dawley rats were divided into three groups (6 rats per group): (1) control group (Con); (2) H. pylori infected group (HP): the rats were inoculated with H. pylori (108− 1010 CFU/mL; 1 mL/rat.) for 3 consecutive days; and (3) HP + genistein group (HP + Gen): the rats were inoculated with H. pylori as above. Then, they were gavaged with genistein (16 mg/kg BW) for 14 days. Gastric tissue was used for the determination of nuclear factor (NF)-κB expression by immunohistochemistry (IHC), degree of apoptosis by the terminal deoxynucleotidyl transferasemediated dUTP nick-end labeling (TUNEL) reaction, and histopathology. Serum samples were used to measure the levels of tumor necrosis factor-alpha (TNF-α) and cytokine-induced neutrophil chemoattractant-1 (CINC-1).ResultsRats in the HP group had significantly higher levels of pro-inflammatory mediators, NF-κB expression and apoptotic cells when compared with the Con group, and these markers significantly decreased in HP + Gen group when compared with the HP group. The histopathology of HP group showed moderate gastric inflammation and many HP colonization. Gastric pathology in HP + Gen group demonstrated the attenuation of inflammatory cell infiltration and H. pylori colonization.ConclusionGenistein exerted its gastroprotective effects through the reduction of pro-inflammatory mediators, nuclear receptor NF-κB expression and gastric mucosal apoptosis in rats with H. pylori-induced gastropathy.

High prevalence of Helicobacter pylori infection, atrophic gastritis and hypochlorhydria in HIV-positive Cameroonians

Background: The human immunodeficiency virus (HIV) and Helicobacter pylori (H. pylori) are associated with significant chronic inflammation of the gastric mucosa. Gastric inflammation is a precursor to many gastrointestinal disorders including, peptic ulcer disease, atrophic gastritis (AG) and gastric cancer (GC). AG is usually accompanied by low hydrochloric acid (hypochlorhydria), low pepsinogens (PG) and high gastrin (G) levels and is the most significant risk condition for GC. Acid-free stomach is a risk factor for impaired drug absorption including anti-retroviral therapy and antibiotics. The role of H. pylori infection in HIV-infected subjects has been conflicting. We assessed the prevalence of H. pylori infection, AG and acid-free stomach (hypochlorhydria) amongst HIV/AIDS subjects in Yaounde Cameroon. Methods and materials: A total of 84 HIV/AIDS subjects were recruited in Yaounde (Cameroon) during January-May 2018. Clinical and socio-demographic data of the subjects were recorded. An aliquot of 5 ml of blood was aseptically collected for analysis by GastroPanel® (Biohit Oyj, Helsinki, Finland) biomarker test for PGI, PGII, G-17 and H.pylori IgG antibodies. GastroPanel results were interpreted using the software application GastroSoft® (Biohit). Statistical analyses were run by Epi info 7.0. The study was agreed by the Jammot Hospital of Yaounde, and ethical clearance was obtained from the National Ethics Committee. Results: Results: A total of 84 subjects were recruited, aged between 17-63 years(mean 37.6 ± 8.9 years). H. pyloriseropositivity (IgG ≥30 EIU) was detected in 68(81.0%) of the subjects. H. pyloriseropositivity was closely associated with low CD4 counts (p = 0.01). Altogether, 26(31.0%) of the subjects presented with AG of the corpus while, hypochlorhydria (acid-free stomach) was detected in 32(38.1%) of the patients. AG and hypochlorhydria were associated with low CD4 counts<200 μl/l (p = 0.01) and (p = 0.005), respectively. Conclusion: H. pylori infection, AG and acid-free stomach were common among HIV/AIDS patients, associated with an increased risk for GC and impaired absorption of micronutrients and some medicines.

Clopidogrel-Induced Gastric Injury in Rats is Attenuated by Stable Gastric Pentadecapeptide BPC 157.

AimAlthough Clopidogrel is safe in healthy volunteers, it can induce recurrence of gastric ulcers in high-risk patients. Here, we investigated the protective effect of the natural product, stable gastric pentadecapeptide 157 (BPC 157) on Clopidogrel-induced gastric injury.MethodsWe used acetic acid to induce gastric ulcer in Sprague Dawley rats. Clopidogrel alone or in combination with BPC 157 or L-NAME (nitric oxide system blockade) were administered after healing of acetic acid-induced ulcer. One percent methylcellulose solution was used as control. Ulcer recurrence rate and the ulcer index were compared between these groups. Gastric mucosal apoptosis rate, microscopic inflammation activity and angiogenesis markers vascular endothelial growth factor A (VEGF-A) and CD34 were examined by TUNEL, histological evaluations (HE) and immunohistochemistry (IHC). Pathways involved, expressions of endoplasmic reticulum (ER) stress apoptosis marker CHOP, angiogenic markers VEGF-A and its receptor VEGFR1, and endothelial NO synthase (eNOS) were all analyzed by Western blot.ResultsThis study indicated that Clopidogrel significantly induced the gastric ulcers recurrence, severe inflammation and ER stress related apoptosis of the gastric mucosa, suppressed the synthesis of angiogenic markers and eNOS. Furthermore, Clopidrogel intervention resulted in the activation of protein kinase B (AKT) and p38 mitogen-activated protein kinase (p38/MAPK). BPC 157 attenuated the gastric mucosal damage caused by Clopidogrel and reversed these molecular effects. However, NO blockade L-NAME weakened the protective effect and thus the molecular effects of BPC 157 on gastric mucosa.ConclusionIn conclusion, these results suggest that BPC 157 inhibited Clopidogrel-induced gastric mucosa injury partially by inhibition of gastric mucosa cell ER stress-mediated apoptosis and inflammation, and promoting gastric mucosa angiogenesis via VEGF-A/VEGFR1 mediated-AKT/p38/MAPK signaling pathways.

Wheat peptide protects against ethanol-induced gastric mucosal damage through downregulation of TLR4 and MAPK

• Excessive alcohol consumption can lead to gastric mucosal damage. • Wheat peptides repressed gastric inflammation through the reduction of inflammatory factor. • Wheat peptides prevented gastric oxidative stress through the inhibition of lipid peroxides. • Wheat peptides down-regulated protein expression levels of TLR4, MAPK and ERK. • Ethanol-induced gastric mucosal damage in rats can be prevented by wheat peptides. Excessive alcohol consumption can induce gastric mucosal damage. The present work aimed to examine the protective effect of wheat peptides against ethanol-induced gastric mucosal damage in rats. Wheat peptides (WP) were administered daily by gavage for 30 days before the rats were treated with anhydrous ethanol (1 mL). Histological observations were performed, as well as the anti-oxidation effect and anti-inflammatory action. WP increased the superoxide dismutase activity and prostaglandin E-2 (PGE2) levels and decreased the malondialdehyde and interleukin-8 (IL-8) levels. WP suppressed gastric mucosa inflammation through the reduction of TNF-α, MPO, IL-6, and IL-1β. WP repressed the expression of caspase-3, and enhanced the expression of anti-apoptotic protein EGFR. Furthermore, WP down-regulated protein expression levels of TLR4, MAPK and ERK, suggesting that WP have a potential effect to inhibit ethanol-induced inflammatory responses via blocking TLR4/MAPK/ERK signal transduction. The potential mechanism may be associated with enhancement of antioxidation, anti-inflammatory action and anti-apoptosis function.

Multispectral imaging detects gastritis consistently in mouse model and in humans

Gastritis constitutes the initial step of the gastric carcinogenesis process. Gastritis diagnosis is based on histological examination of biopsies. Non-invasive real-time methods to detect mucosal inflammation are needed. Tissue optical properties modify reemitted light, i.e. the proportion of light that is emitted by a tissue after stimulation by a light flux. Analysis of light reemitted by gastric tissue could predict the inflammatory state. The aim of our study was to investigate a potential association between reemitted light and gastric tissue inflammation. We used two models and three multispectral analysis methods available on the marketplace. We used a mouse model of Helicobacter pylori infection and included patients undergoing gastric endoscopy. In mice, the reemitted light was measured using a spectrometer and a multispectral camera. We also exposed patient’s gastric mucosa to specific wavelengths and analyzed reemitted light. In both mouse model and humans, modifications of reemitted light were observed around 560 nm, 600 nm and 640 nm, associated with the presence of gastritis lesions. These results pave the way for the development of improved endoscopes in order to detect real-time gastritis without the need of biopsies. This would allow a better prevention of gastric cancer alongside with cost efficient endoscopies.

Russelioside B; A pregnane glycoside for treatment of gastric ulcer via modulation of heat shock protein-70 and vascular endothelial growth factor

Gastric ulcers are a very common public health problem affecting up to 10% worldwide. Russelioside B is a steroidal glycoside isolated from several Caralluma species. No study tested the ulcer healing potential of the compound. The current study aimed to assess the protective effect of russelioside B against ethanol-induced gastric mucosal injury in rats. Ulcer was induced on rats by a single intragastric dose of absolute ethanol (5 mL/kg). Rats were randomly assorted into four groups (n = 8) and given treatments (Antodine, 20 mg/kg or russelioside B, 50 mg/kg) by oral gavage 1 h before ulcer induction. Pretreatment with russelioside B (50 mg/kg) attenuated the gastric mucosal injury as proved by a decrease of ulcer index, and histological scores. It suppressed the gastric inflammation by a significant lowering the tumor necrosis factor-α and interleukin-6 levels with myeloperoxidase activity (which are also aggravating factors in the case of Covid-19 infection). In addition, administration of russelioside B halted the gastric oxidative stress via inhibition of lipid peroxides by maintaining reduced glutathione and by decreasing malondialdehyde. It was able also to restore the sharp drop in the levels of heat shock protein-70, vascular endothelial growth factor and prostaglandin E2 induced by ethanol. Additionally, it showed carbonic anhydrase inhibition activity. The gastroprotective action of russelioside B was umpired through multi mechanistic actions; suppression of gastric oxidative stress, inflammation, anti-apoptotic activities and enhanced gastric mucosal protection by up-regulation of endothelial growth factor, normalization of heat shock protein-70 and prostaglandin E2. These actions were comparable in part to some classical antiulcer drugs such as Antodine.

Helicobacter pyloriin Pediatric Patients

Helicobacter pylori causes one of the most common chronic bacterial infections. Clinical manifestations include asymptomatic chronic gastritis, gastric and duodenal ulcers, adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma in adults. In children, most H pylori infections are asymptomatic despite being associated with microscopic gastric inflammation, and children rarely develop complications associated with infection. Due to rising resistance and lack of symptomatic improvement in the absence of peptic ulcer disease, testing and eradication therapy are recommended only for the subset of patients in whom there is a high suspicion of peptic ulcer disease. Studies do not support the role of H pylori infection in functional disorders such as recurrent abdominal pain. A variety of diagnostic modalities exist; therefore, it is important to understand the appropriate approach to diagnosing H pylori infection. The joint European Society for Pediatric Gastroenterology, Hepatology, and Nutrition/North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition guidelines were updated in 2016. Antibiotic and proton pump inhibitor weight-based dosing guidelines have changed to prevent ineffective treatment from increasing antimicrobial resistance. Treatment can also be guided by antibiotic sensitivities obtained from H pylori culture. Patients should be tested again after treatment to confirm eradication.

L-Glutamine and Physical Exercise Prevent Intestinal Inflammation and Oxidative Stress Without Improving Gastric Dysmotility in Rats with Ulcerative Colitis.

The aim of this study was to evaluate the effects of glutamine supplementation or exercise on gastric emptying and intestinal inflammation in rats with ulcerative colitis (UC). Strength exercise consisted of jump training 4 × 10 repetitions/5 days a week/8 weeks with progressive overload. Endurance exercise consisted of swimming without overload for a period of 1 h a day/5 days a week/8 weeks. Another group (sedentary) of animals was supplemented with L-glutamine (1 g/kg of body weight) orally for 8 weeks before induction of UC. Colitis was induced by intra-colonic administration of 1 mL of 4% acetic acid. We assessed gastric emptying, macroscopic and microscopic scoring, oxidative stress markers, and IL-1β, IL-6, and (TNF-α) levels. The UC significantly increased (p < 0.05) the gastric emptying compared with the saline control group. We observed a significantly decrease (p < 0.05) in body weight gain in UC rats compared with the control groups. Both exercise interventions and L-glutamine supplementation significantly prevented (p < 0.05) weight loss compared with the UC group. Strength and endurance exercises significantly prevented (p < 0.05) the increase of microscopic scores and oxidative stress (p < 0.05). L-glutamine supplementation in UC rats prevented hemorrhagic damage and improved oxidative stress markers (p < 0.05). Strength and endurance exercises and glutamine decreased the concentrations of inflammatory cytokines IL-1β, IL-6, and TNF-α compared with the UC group (p < 0.05). Strength and endurance exercises and L-glutamine supplementation prevented intestinal inflammation and improved cytokines and oxidative stress levels without altering gastric dysmotility in rats with UC.

Pre-existing Helicobacter pylori serum IgG enhances the vibriocidal antibody response to CVD 103-HgR live oral cholera vaccine in Malian adults

Accumulating evidence indicates that persistent Helicobacter pylori gastric infection influences immune responses to oral enteric vaccines. We studied the association between pre-existing H. pylori serum IgG and serum pepsinogens levels (PGs) as markers of gastric inflammation and the immune response to single-dose live oral cholera vaccine CVD 103-HgR in Malian adults. Baseline sera obtained during a phase 2 safety/immunogenicity clinical trial of cholera vaccine CVD 103-HgR among 93 healthy Malian adults were tested for H. pylori IgG antibodies and PGI and PGII levels using enzyme linked immunosorbent assays. Overall 74/93 (80%) vaccine recipients were H. pylori IgG seropositive at baseline. Vibriocidal antibody seroconversion (≥ fourfold increase 14 days following administration of CVD 103-HgR compared to baseline) among vaccine recipients was 56%. However, vibriocidal antibody seroconversion was markedly higher among H. pylori seropositives than seronegatives 64% vs. 26% (p = 0.004); adjusted relative risk: 2.20 (95% confidence intervals 1.00–4.80; p = 0.049). Among H. pylori seropositive vaccine recipients, there were no significant associations between PGI, PGII and PGI:PGII levels and vibriocidal seroconversion. The enhanced seroconversion to oral cholera vaccine CVD 103-HgR among H. pylori seropositive African adults provides further evidence of the immunomodulating impact of H. pylori on oral vaccine immunogenicity.

S2977 Incidental Finding of Helicobacter Heilmannii in Two Asymptomatic Individuals

INTRODUCTION: Helicobacter heilmannii previously known as Gastrospirillum hominis is commonly seen in animals and may have zoonotic potential. It contributes to about 5% of human gastric infections, resulting in chronic gastritis, peptic ulceration, and rarely gastric carcinoma or mucosa-associated lymphoid tissue lymphoma. Most patients are symptomatic and present with dyspepsia, epigastric pain, or acid reflux. We report two cases in which incidental H.Heilmannii was found in the pathological report. CASE DESCRIPTION/METHODS: Both our patients had undergone esophagogastroduodenoscopy (EGD) in anticipation of bariatric surgery. One is a 22-year-old morbidly obese female without significant medical illness, who had mild patchy erythematous mucosa in the gastric antrum. Biopsy revealed moderate to severe chronic active gastritis. Both H.pylori and H.heilmannii organisms were identified on the Hematoxylin and eosin (H&E) stain. Next is a 25-year-old morbidly obese female with gastroesophageal reflux disease. Her EGD also revealed mild patchy erythematous mucosa in the gastric antrum and biopsy showed moderate inactive gastritis, reactive lymphoid follicles, and frequent long tightly coiled bacteria highlighted on H&E stain consistent with H.heilmannii. They were both treated with a 2-week course of amoxicillin, clarithromycin, and omeprazole. They remained asymptomatic during subsequent office visits and are scheduled for follow up EGD after their bariatric surgery. DISCUSSION: Gastric inflammation in humans infected with H.heilmannii is less severe and usually involves the gastric antrum like seen in our patients. Co-infection of H.heilmannii and H.pylori is often seen and is believed to have a higher prevalence of intestinal metaplasia than does infection with either strain alone. Studies have highlighted that H.heilmannii like H.pylori, is effectively eradicated with similar antimicrobial therapy. We are however unable to detect the presence or confirm eradication via ancillary tests such as urea breath test, serum antibody testing, or stool testing as with H.pylori. Whether in symptomatic patients or with incidental chronic gastritis findings, it is prudent to look for H.heilmannii in the absence of, or concomitant with H.pylori infection and treat them adequately to prevent further complications.Figure 1.: Antral mild chronic active gastritis - H&E stain, 10x.Figure 2.: Antral moderate chronic active gastritis - H&E stain, 10x.Figure 3.: Long tightly coiled organisms with corkscrew appearance, consistent with Helicobacter heilmannii - H&E stain, 100x, oil.