Chronic gastritis and Helicobacter pylori in digestive form of Chagas' disease

Patients with the digestive form of Chagas'disease frequently present chronic gastritis. As the microorganism Helicobacter pylori is now accepted as the most common cause of human chronic gastritis, the present work was undertaken to verify a possible relationship between the presence of this bacterium and inflammatory changes of antral mucosa in chagasic patients. Seventeen chagasics, with megaesophagus and or megacolon were studied. Fragments from two different regions of antral mucosa were obtained by endoscopy, fixed in 4% neutral formaldehyde and embedded in paraffin. The sections were stained by haematoxylin and eosin for histology analysis, and by carbolfuchsin for H. pylori identification. H. pylori was found in 16 (94.1%) chagasic patients, all of them presenting chronic gastritis. Superficial gastritis was seen in 9 (52.9%) while atrophic gastritis was present in 8 (47.1%) patients. H. pylori was present on gastric mucosa of 8 (100%) patients with atrophic gastritis and of 8 (88.8%) patients with superficial gastritis. We concluded that the microorganism H. pylori should be considered a possible factor connected with the etiopathogenesis of chronic superficial and atrophic gastritis frequently observed in patients with the digestive form of Chagas' disease.

Comparative analysis of two-dimensional electrophoresis maps (2-DE) of Helicobacter pylori from Brazilian patients with chronic gastritis and duodenal ulcer: a preliminary report

Helicobacter pylori is a bacterium recognized as the major cause of peptic ulcer and chronic gastritis. Recently, a proteome-based approach was developed to investigate pathogenic factors related to H. pylori. In this preliminary study, H. pylori strains were isolated from gastric biopsies of patients with chronic gastritis and duodenal ulcers. A partial proteomic analysis of H. pylori strains was performed by bacterial lyses and proteins were separated by two-dimensional gel electrophoresis (2-DE). A comparative analysis was performed to verify a differential protein expression between these two 2-DE maps. These data should be useful to clarify the role of different proteins related to bacterial pathogenesis. This study will be completed using a larger number of samples and protein identification of H. pylori by MALDI-TOF mass spectrometry.

A Case of Post-Radiotherapy Gastritis: Radiation Does Not Explain Everything

Hemorrhagic gastritis is a possible late toxicity outcome after radical radiotherapy but it is nowadays a very rare condition and most likely depends on other clinical factors. We report the case of a 77-year-old woman with a symptomatic solitary extramedullary intra-abdominal plasmacytoma and multiple gastric comorbidities, treated with external beam radiotherapy. Despite the good response to radiotherapy, the patient experienced multiple gastric bleeding a few months later, with the need of multiple treatments for its control. In this paper we will discuss in detail all aspects related to the different causes of hemorrhagic gastritis.

Mouse mammary tumor virus superantigens and murine autoimmune gastritis.

BACKGROUND/AIMS: Neonatal thymectomy induces autoimmune gastritis in BALB/c (minor lymphocyte-stimulating antigen [Mls]-1b) mice, whereas DBA/2 (Mls-1a) mice are resistant. Resistance has been linked to the Mls-1a locus, which encodes a retroviral superantigen, and to superantigen reactive T cells that express V beta 6+ T-cell receptors. V beta 6+ T cells are known to be deleted in mice expressing Mls-1a superantigens. METHODS: Neonatal thymectomized BALB/c and Mls-1a congenic BALB.D2.Mls-1a mice were analyzed to examine directly the role of Mls-1a self-superantigens and V beta 6+ T cells in autoimmune gastritis. RESULTS: Autoimmune gastritis was detected in thymectomized BALB.D2.Mls-1a mice with high incidence. Autoantibodies to the gastric H+,K(+)-adenosine triphosphatase were present independent of the Mls phenotype in sera of gastritic mice. Severe gastritis had already appeared 1 month after thymectomy in BALB.D2.Mls-1a mice. V beta 6+ T cells were deleted in the stomach lymph nodes of 1-month-old gastritic BALB.D2.Mls-1a mice but could be detected by immunocytochemistry in the stomach lesions. CONCLUSIONS: Endogenous Mls-1a self-superantigens and Mls-1a reactive V beta 6+ T cells are not involved in resistance to autoimmune gastritis in BALB.D2 mice.

Functional renal failure and haemorrhagic gastritis associated with endotoxaemia in cirrhosis

Forty-three patients with cirrhosis and ascites, 21 with normal renal function, 10 with a progressive functional renal failure (FRF), and 12 with a steady FRF, were investigated for the presence of endotoxaemia by the Limulus lysate test. Endotoxaemia was found in nine patients with FRF and in none of the 21 with normal renal function (P less than 0-01). A positive Limulus test was almost exclusively associated with a progressive FRF (eight of 10 patients) and all but one of them died. Renal function improved as endotoxaemia disappeared in the survivor. Endotoxaemia was also associated with haemorrhage due to acute erosions of the gastric mucosa, being present in six of the seven patients who had this complication. Intravascular coagulation was not found in any patient. The Limulus test was positive in the ascitic fluid in 18 of 21 patients tested, although only two of them had peritonitis. These results suggest that endotoxaemia may play a critical role in the development of progressive renal failure and haemorrhagic gastritis in cirrhosis, and emphasise the potential risk of procedures involving reinfusion of ascitic fluid.

Immunoexpression of CD95 in chronic gastritis and gastric mucosa-associated lymphomas

CD95 (Fas/APO-1)-mediated apoptosis plays an important role in immunological regulation and is related to the pathogenesis of autoimmune diseases. Immunoexpression of CD95 has been reported to frequently occur in low grade non-Hodgkin lymphomas, especially of post-germinal center histogenesis, among which those originating in mucosa-associated lymphoid tissue (MALT lymphomas). However, there is no report comparing in situ immunoexpression of this marker in lymphomas and the hyperplastic lymphoid reaction (chronic gastritis) related to Helicobacter pylori infection. The purpose of the present research was to compare the intensity of lymphoid CD95 immunoexpression in 15 cases of H. pylori-related chronic gastritis and 15 gastric MALT lymphomas. CD95 (anti-CD95) was detected by an immunoperoxidase technique in paraffin sections using the catalyzed amplification system. Graduation of reaction intensity (percentage of CD95-positive cells) was semiquantitative, from 1+ to 4+. Nine cases of chronic gastritis were 4+, five 2+ and one 1+. Three lymphomas were 4+, three 3+, four 2+, four 1+, and one was negative. Although 14 of 15 lymphomas were positive for CD95, the intensity of the reaction was significantly weaker compared to that obtained with gastric tissue for patients with gastritis (P = 0.03). The difference in CD95 immunoexpression does not seem to be useful as an isolated criterion in the differential diagnosis between chronic gastritis and MALT lymphomas since there was overlapping of immunostaining patterns. However, it suggests the possibility of a pathogenetic role of this apoptosis-regulating protein in MALT lymphomas.

Comparative proteomics analysis of chronic atrophic gastritis: changes of protein expression in chronic atrophic gastritis without Helicobacter pylori infection

Chronic atrophic gastritis (CAG) is a very common gastritis and one of the major precursor lesions of gastric cancer, one of the most common cancers worldwide. The molecular mechanism underlying CAG is unclear, but its elucidation is essential for the prevention and early detection of gastric cancer and appropriate intervention. A combination of two-dimensional gel electrophoresis and mass spectrometry was used in the present study to analyze the differentially expressed proteins. Samples from 21 patients (9 females and 12 males; mean age: 61.8 years) were used. We identified 18 differentially expressed proteins in CAG compared with matched normal mucosa. Eight proteins were up-regulated and 10 down-regulated in CAG when compared with the same amounts of proteins in individually matched normal gastric mucosa. Two novel proteins, proteasome activator subunit 1 (PSME1), which was down-regulated in CAG, and ribosomal protein S12 (RPS12), which was up-regulated in CAG, were further investigated. Their expression was validated by Western blot and RT-PCR in 15 CAG samples matched with normal mucosa. The expression level of RPS12 was significantly higher in CAG than in matched normal gastric mucosa (P < 0.05). In contrast, the expression level of PSME1 in CAG was significantly lower than in matched normal gastric mucosa (P < 0.05). This study clearly demonstrated that there are some changes in protein expression between CAG and normal mucosa. In these changes, down-regulation of PSME1 and up-regulation of RPS12 could be involved in the development of CAG. Thus, the differentially expressed proteins might play important roles in CAG as functional molecules.

Influence of Helicobacter pylori infection on the expression of MLH1 and MGMT in patients with chronic gastritis and gastric cancer

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effect of Helicobacter pylori infection on IL-8, IL-1 and COX-2 expression in patients with chronic gastritis and gastric cancer

Objective. Helicobacter pylori infection is related to gastric cancer development, and chronic inflammation is presumed to be the main cause. The aim of the present study was to evaluate the influence of H. pylori cagA, vacA, iceA, and babA genotypes on COX-2, IL-1, and IL-8 expression. Material and methods. of the 217 patients included in the study, 26 were uninfected, 127 had chronic gastritis and were H. pylori-positive, and 64 had gastric cancer. Bacterial genotypes were evaluated by polymerase chain reaction (PCR), and the expression values were determined by quantitative real-time PCR and immunohistochemistry. Results. An association was found between the infection with cagA, vacA s1m1 strains and gastric cancer development. Regarding the 3' region of the cagA gene, we also found an association between the infection with cagA EPIYA-ABCCC strains and clinical outcome. Higher levels of IL-8, IL-1, and COX-2 were detected in gastric mucosa from infected patients with chronic gastritis, and they were also associated with the infection by cagA, vacA s1m1 strains. The IL-8 and IL-1 levels decrease significantly from chronic gastritis to gastric cancer, while the relative expression remained unaltered when COX-2 expression was analyzed among patients with gastritis and cancer. Conclusions. Since inflammatory response to H. pylori infection plays an important role in cellular proliferation and gastric mucosal damage, the up-regulation of IL-1, IL-8, and COX-2 in patients with chronic gastritis has an important clinical implication in gastric carcinogenesis.

Effects of Helicobacter pylori Infection on the Expressions of Bax and Bcl-2 in Patients with Chronic Gastritis and Gastric Cancer

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

IL-1ra anti-inflammatory cytokine polymorphism is associated with risk of gastric cancer and chronic gastritis in a Brazilian population, but the TNF-beta pro-inflammatory cytokine is not

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Methylation status of CDH1 gene in samples of gastric mucous from brazilian patients with chronic gastritis infected by Helicobacter pylori

CONTEXTO:O câncer gástrico é uma das principais neoplasias que causam o óbito no Brasil e no mundo. Helicobacter pylori é um carcinógeno do tipo I relacionado à gastrite crônica. Diferenças no grau de virulência de suas cepas levam a maior risco de desenvolvimento de doenças gástricas. A metilação de ilhas CpGs está envolvida com o processo de tumorigênese em diferentes tipos de câncer. CDH1 é um gene supressor tumoral que, quando inativado, pode aumentar as chances de metástase. A metilação deste gene em estágios precoces da carcinogênese gástrica ainda não é totalmente compreendida. OBJETIVO: Investigar o padrão de metilação do gene CDH1 em amostras de gastrites crônicas e correlacionar com a presença do H. pylori. MÉTODOS: Foram usadas 60 biopsias de mucosas gástricas. A detecção de H. pylori foi realizada por PCR para o gene da urease C e a genotipagem com PCR para os genes cagA e vacA (região s e m). O padrão de metilação do gene CDH1 foi analisado usando a técnica de PCR e específica para a metilação e sequenciamento direto dos produtos de PCR. RESULTADOS: A bactéria H. pylori foi detectada em 90% das amostras de gastrites crônicas; destas, 33% portavam o gene cagA e 100% vacA s1. O genótipo vacA s2/m1 não foi detectado nas amostras analisadas. Metilação de CDH1 foi detectada em 63,3% das amostras de gastrites e 95% delas eram portadoras de H. pylori. CONCLUSÃO: Os resultados deste estudo sugerem que a metilação em CDH1 e a infecção pelo H. pylori são eventos frequentes em amostras de pacientes brasileiros com gastrite crônica e reforça a correlação entre infecção por H. pylori e inativação do gene CDH1 em estágios precoces da tumorigênese gástrica.