			Home About us Contact

Gastric Infection (gastric + infection)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Oral vaccination of mice against Helicobacter pylori with recombinant Lactococcus lactis expressing urease subunit B

FEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 3 2009
Qing Gu
Abstract To determine whether a protective immune response could be elicited by oral delivery of a recombinant live bacterial vaccine, Helicobacter pylori urease subunit B (UreB) was expressed for extracellular expression in food-grade bacterium Lactococcus lactis. The UreB-producing strains were then administered orally to mice, and the immune response to UreB was examined. Orally vaccinated mice produced a significant UreB-specific serum immunoglobulin G (IgG) response. Specific anti-UreB IgA responses could be detected in the feces of mice immunized with the secreting lactococcal strain. Mice vaccinated orally were significantly protected against gastric Helicobacter infection following a challenge with H. pylori strain SS1. In conclusion, mucosal vaccination with L. lactis expressing UreB produced serum IgG and UreB-specific fecal IgA, and prevented gastric infection with H. pylori. [source]

Helicobacter pylori Infection and Gastric Autoimmune Diseases: Is There a Link?

HELICOBACTER, Issue 6 2003
Fabio Presotto
ABSTRACT Background.,Helicobacter pylori is thought to be involved in atrophic body gastritis. We explored the prevalence of H. pylori infection in asymptomatic subjects with gastric parietal cell antibodies, as well as in patients with pernicious anemia, to evaluate a possible role of H. pylori gastric infection in gastric autoimmunity. Patients and Methods., We studied 79 consecutive asymptomatic subjects with parietal cell antibodies, 24 patients with pernicious anemia, and 66 parietal cell antibody-negative controls. All patients underwent gastric biopsies for histology and detection of H. pylori. Red blood cell count and volume, serum levels of gastrin, pepsinogen I, iron, folic acid, vitamin B12, and circulating antibodies to H. pylori and to intrinsic factor were also determined. Results., We found an atrophic body gastritis in 14 of the 79 asymptomatic subjects with parietal cell antibodies (18%) and in 2 of the 66 controls (3%) (p = .01). Mean levels of gastrin were increased (p < .0001), while those of pepsinogen were reduced (p < .001) compared with controls. H. pylori was identified at the gastric level and/or circulating anti- H. pylori antibodies were detected in 46 parietal cell antibody-positive subjects (58%) compared with 26 controls (39%) (p = .03). In patients with pernicious anemia we found an atrophic body gastritis in 18 of 24 cases (75%) (p < .001 vs. controls). Mean levels of gastrin were markedly increased (p < .0001) and those of pepsinogen I decreased (p < .0001) relative to controls. Only five of these patients (21%) had evidence of H. pylori infection compared with 46 of the parietal cell antibody-positive subjects (58%) (p = .003) and 26 of the controls (39%). Considering all patients with gastric autoimmunity (i.e. with parietal cell antibodies and/or with pernicious anemia), H. pylori was found in 44 of 72 of those without atrophy (61%) but in 6 of 31 with gastric body atrophy (19%) (p < .001), indicating that H. pylori infection is greatly reduced when gastric acid secretion decreases. Conclusions., The frequent detection of H. pylori infection in subjects with early gastric autoimmunity, indicated by the presence of parietal cell antibodies, suggests that H. pylori could have a crucial role in the induction and/or the maintenance of autoimmunity at the gastric level. [source]

Double gastric infection with Helicobacter pylori and non- Helicobacter pylori bacteria during acid-suppressive therapy: increase of pro-inflammatory cytokines and development of atrophic gastritis

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2001
S. Sanduleanu
Background: Long-term acid suppression may accelerate the development of atrophic gastritis in Helicobacter pylori -positive subjects. The pathogenetic mechanism remains unclear. Aim: To test the hypothesis that gastric double infection with H. pylori and non -H. pylori bacterial species,during acid suppression,may result in an enhanced inflammatory response, contributing to the development of atrophic gastritis. Patients and methods: A consecutive series of patients with gastro-oesophageal reflux disease undergoing treatment with proton pump inhibitors (n=113) or histamine2 -receptor antagonists (H2 -RAs) (n=37), and 76 non-treated dyspeptic controls were investigated. Gastric mucosal H. pylori and non- H. pylori bacteria, histological gastritis, H. pylori serology, and circulating interleukin (IL)-1,, IL-6, and IL-8 were examined. Results: Patients on acid suppression with either proton pump inhibitors or H2 -RAs had a similar prevalence of H. pylori infection to the controls, but a higher prevalence of non- H. pylori bacteria (61% and 60% vs. 29%, P < 0.0001 and P < 0.002). Both the presence of H. pylori and non- H. pylori bacteria were independent risk factors of atrophic gastritis (antrum: relative risks (RRs), 10.1 and 5.07; corpus: RRs, 11.74 and 6.38). A simultaneous presence of H. pylori and non- H. pylori bacteria was associated with a markedly increased risk of atrophic gastritis (antrum: RR, 20.25; corpus: RR, 20.38), compatible with a synergistic effect. Furthermore, the simultaneous presence of both types of bacteria was associated with higher cytokine levels than in patients without any type of bacteria. This increase was also greater than in patients with H. pylori infection alone (P < 0.001, for both IL-1, and IL-8). Summary and conclusions: H. pylori -positive patients on long-term acid inhibition displayed three features: non- H. pylori bacterial growth; increased cytokine levels; and a higher risk of atrophic gastritis. We suggest that double infection with H. pylori and non- H. pyloribacteria is a major factor in the development of atrophic gastritis during gastric acid inhibition. [source]

Ocular adnexal lymphoma and Helicobacter pylori gastric infection,

AMERICAN JOURNAL OF HEMATOLOGY, Issue 9 2010
Didier Decaudin
There is a causal association between Helicobacter pylori (Hp) gastric infection and the development of gastric MALT lymphoma. In contrast, the link between Hp gastric infection and the development of extragastric lymphoma has not been thoroughly investigated. We, therefore, studied the prevalence of gastric Hp infection at initial diagnosis of ophthalmologic and nonophthalmologic extragastric lymphoma patients. Three cohorts of patients were studied: a first one of 83 patients with OAL, a second one of 101 patients with extraophthalmologic extragastric lymphoma, and a third one of 156 control individuals (control) without malignant lymphoma. Gastric Hp infection was investigated by histopathological analysis and Hp -specific PCR assay on gastric biopsy tissue samples. We found gastric Hp infection in 37 OAL patients (45%), in 25 extraophthalmologic extragastric lymphoma cases (25%), and in 18 controls individuals (12%) (P < 0.0001 OAL/C and P < 0.01 OAL/extra-OAL cases). Gastritis was found in 51% and 9% of Hp -positive and Hp -negative lymphoma patients, respectively (P < 10,4). Gastric Hp infection only correlated with MALT/LPL lymphoma (P = 0.03). There is a significant association between gastric Hp infection and MALT/LPL OAL. This suggests a novel mechanism of indirect infection-associated lymphomagenesis whereby chronic local antigen stimulation would lead to the emergence of ectopic B-cell lymphoma. © 2010 Wiley-Liss, Inc. Am. J. Hematol. [source]

Determination of Helicobacter pylori in patients with chronic nonspecific pharyngitis

THE LARYNGOSCOPE, Issue 8 2009
Zeynep K, lkaya Kaptan MD
Abstract Objectives/Hypothesis: To determine if there is a relationship between Helicobacter pylori colonization in the pharynx mucous membrane and chronic nonspecific pharyngitis. Study Design: A prospective clinical study. Methods: Seventy patients with chronic pharyngitis and 20 healthy control subjects were examined with polymerase chain reaction (PCR) and culture for H. pylori colonization in the pharynx mucous membrane between March 2008 and October 2008. Patients with pharyngitis were seperated into two groups (35 patients in each) by using C-14 urea breath test, according to the presence of gastric H. pylori infection. Results: In the control group, none of the patients had H. pylori in the pharynx. In the chronic pharyngitis group, in 12 patients (34.3%) with gastric H. pylori infection and in seven patients (20%) without gastric infection, H. pylori colonization in pharynx mucosa was determined with the PCR method. In only two of chronic pharyngitis patients (5.8%), H. pylori infection was detected with culture. In the pharynx mucosa, the H. pylori infection rate was significantly higher in the chronic pharyngitis groups than in the control group (P = .002 between C-14 positive and control groups, P = .040 between C-14 negative and control groups). There was not a significant difference in H. pylori colonization in the pharynx of patients who had chronic pharyngitis with or without gastric ailments and H. pylori infection (P = .179). Conclusions: Chronic nonspecific pharyngitis without gastric H. pylori infection is significantly related to H. pylori colonization in the pharynx, and gastric involvement increases the rate of this spread. The gold standart for detection of H. pylori infection is the PCR method. Laryngoscope, 2009 [source]