ABSTRACT
OBJECTIVE: Recently, hepatocyte antigen (Hep) was introduced as a sensitive and reliable marker of intestinal metaplasia (IM). However, the distribution of Hep expression in subtypes of IM was not described. METHODS: We examined the expression of Hep in 58 cases of chronic gastritis associated with IM by immunohistochemical staining. Cases were classified as: 19 of IM Type I (complete) cases, 16 cases of IM Type II (incomplete) and 23 cases of IM Type III (incomplete). The distribution of Hep expression was classified into four groups according to the intensity of Hep expressing metaplastic cells: negative, low, moderate and high. We also compared expression of Hep with that of MUC-1, MUC-2 and MUC-5AC. RESULTS: Hep expression showed granular cytoplasmic staining and was specifically identified in columnar cells, but not in goblet cells. There was no significant difference between Hep expression and subtypes of IM (p > 0.005). However, the difference between the distribution of Hep expression among three subtypes of IM was significant (p < 0.001). No relationship was observed among the expression of Hep, MUC-1, MUC-2 and MUC-5AC. CONCLUSION: Results of the present study revealed that the distribution of Hep expression is high in the majority of the complete type (Type I) IM cases, moderate in the majority of the incomplete Type II IM cases and low in all of the incomplete Type III IM cases and suggest that besides its role as a sensitive marker in IM, the evaluation of the distribution of Hep expression might be useful in the classification of IM.
OBJETIVO: El antígeno del hepatocito (Hep) se introdujo recientemente como un marcador sensible y confiable de la metaplasia intestinal (MI). Sin embargo, no se describe la distribución de la expresión de Hep en los subtipos de MI. MÉTODOS: Se examinó la expresión de Hep en 58 casos de gastritis crónica asociados con MI mediante tinción inmunohistoquímica. Los casos fueron clasificados como: 19 casos de tipo MI (completo), 16 casos de tipo MI II (incompleto), y 23 casos de tipo MI III (incompleto). La distribución de la expresión del Hep se clasificó en cuatro grupos según la intensidad de Hep, que expresa las células metaplásticas: negativa, baja, moderada y alta. También se comparó la expresión de Hep con la de MUC-1, MUC-2 y MUC-5AC. RESULTADOS: La expresión de Hep mostró tinción citoplasmática granular, específicamente identificada en las células columnares, pero no en las células caliciformes. No hubo ninguna diferencia significativa entre la expresión de Hep y los subtipos de MI (p > 0.005). Sin embargo, la diferencia entre la distribución de la expresión del Hep entre tres subtipos de MI fue significativa (p < 0.001). No se observó relación alguna entre la expresión de Hep, MUC-1, MUC-2 y MUC-5AC. CONCLUSIÓN: Los resultados del presente estudio revelaron que la distribución de la expresión de Hep es alta en la mayoría de los casos MI de tipo completo (tipo I), moderada en la mayoría de los casos MI de tipo II, y baja en todos los casos MI de tipo III incompleto. Los resultados sugieren que además de su papel como marcador sensible en MI, la evaluación de la distribución de expresión del Hep podría ser útil en la clasificación de MI.
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Adenocarcinoma/metabolism , Gastritis/metabolism , Hepatocytes/immunology , Precancerous Conditions/metabolism , Stomach Neoplasms/metabolism , Adenocarcinoma/classification , Adenocarcinoma/pathology , Gastric Mucosa/immunology , Gastric Mucosa/pathology , Gastritis/pathology , Immunohistochemistry , Metaplasia/immunology , /metabolism , Mucin-1/metabolism , /metabolism , Precancerous Conditions/immunology , Precancerous Conditions/pathology , Stomach Neoplasms/immunology , Stomach Neoplasms/pathology , Biomarkers, Tumor/metabolismABSTRACT
No abstract availble.
Subject(s)
Humans , Gastric Mucosa/metabolism , Gastritis/metabolism , Helicobacter Infections/metabolism , Helicobacter pylori , PPAR gamma/metabolism , Predictive Value of TestsABSTRACT
BACKGROUND/AIMS: Peroxisome proliferator-activated receptorgamma (PPARgamma), a nuclear transcription factor, plays a critical role in the regulation of gene expression associated with inflammation and cancer. PPARgamma is expressed in human gastric cancer as well as in colon cancer. Activation of PPARgamma by ligand produces pro-apoptotic effect and ameliorate growing of cancer cells. Helicobacter pylori (H. pylori) is a main etiologic agent for gastric inflammation, and raises cell turnover in gastric epithelium. Longstanding infection with this organism is related with the development of non-cardiac gastric cancer. The aim of this study was to investigate the effect of H. pylori on the expression of PPARgamma protein and mRNA in chronic gastritis. METHODS: Gastric biopsy samples were taken from H. pylori infected (n=18) and non-infected (n=21) patients during endoscopic examination. PPARgamma expressions were assessed by real time polymerase chain reaction and immunohistochemistry. RESULTS: PPARgamma was localized to the nuclei of the foveolar epithelial cells in both infected and non-infected mucosa. PPARgamma protein expression was higher in H. pylori infected patients than in non-infected patients (3.8+/-0.4 vs. 2.6+/-1.0, H. pylori infected and non-infected, respectively; p<0.05). However, PPARgamma mRNA levels were not significantly different between the two groups (24+/-18 vs. 29+/-25, H. pylori infected and noninfected, respectively). CONCLUSIONS: PPARgamma expression is increased in the gastric mucosa of H. pylori infected chronic gastritis, which suggests a certain role of PPARgamma in the mucosal inflammatory reaction to H. pylori infection.
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Colonic Neoplasms/metabolism , Computer Systems , Gastric Mucosa/metabolism , Gastritis/metabolism , Helicobacter Infections/metabolism , Helicobacter pylori , Immunohistochemistry , PPAR gamma/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Stomach Neoplasms/metabolismABSTRACT
Recently, gastric Helicobacter pylori (H. pylori) colonization has been shown to affect the expression of leptin and ghrelin, hormones that control appetite and satiety. Gastric leptin, produced by chief and parietal cells and released in response to meals, may play a role in weight gain after eradication of H. pylori infection, whereas ghrelin, produced by X/A-like enteroendocrine cells in oxyntic gland, is released during fasting, and suppressed by feeding and leptin. Whether either that H. pylori genes represent microbial contributions to the complement of thrifty genes of humans, or that H. pylori disappearance plays a role in adiposity remains to be determined. Simply, ghrelin-leptin might tango in body weight regulation, gastric inflammation, and gastric motility. In the current review about the possible role of ghrelin in gastric inflammation, we found that high serum albumin condition decreased ghrelin expression, whereas serum albumin deprivation significantly increased ghrelin expression, however, of which regulation was abolished after H. pylori infection. Ghrelin significantly attenuated the inflammatory stimuli imposed after H. pylori, shown with inactivation of phospho-extracellular signal-regulated kinase (p-ERK) and nuclear factor-KappaB (NF-KappaB)-DNA binding activities. Conclusively, besides orexigenic and weight gaining actions of gastric hormone, ghrelin, it likely endows the stomach the protective effect from exogenous damages.
Subject(s)
Humans , Amino Acid Sequence , Appetite Stimulants , Gastritis/metabolism , Ghrelin/blood , Helicobacter Infections/metabolism , Helicobacter pylori , Insulin-Like Growth Factor I/analysis , Leptin/blood , Mitogen-Activated Protein Kinases/metabolism , Molecular Sequence Data , NF-kappa B/metabolism , Neurosecretory Systems/metabolism , Peptide Hormones/blood , Signal Transduction , Weight GainABSTRACT
OBJECTIVES: Helicobacter pylori infection induces selective reduction of the number of antral D-cells and results in abnormal regulation of serum gastrin secretion. The purpose of this study was to investigate the relationship between H. pylori infection and the numbers of G-cells and D-cells. METHODS: The numbers of antral G-cells and D-cells, the ratio of G-cells to D-cells and fasting serum gastrin concentrations were compared between 37 patients with (29 with duodenal ulcers and 8 with gastric ulcers) and 33 without H. pylori infection (22 with duodenal ulcers and 11 with gastric ulcers). Serum gastrin concentrations were measured using the radioimmunoassay technique. Antral mucosal biopsy specimens were examined using immunohistochemical staining with antibodies specific for gastrin and somatostatin and the numbers of G-cells and D-cells per gastric gland were counted. RESULTS: Fasting serum gastrin concentrations were significantly higher in patients with H. pylori infection compared to patients without infection (80.3 +/- 23.5 vs 47.6 +/- 14.1 pg/ml, p 0.5). The number of D-cells was significantly lower in patients with H. pylori infection than in uninfected patients in both duodenal and gastric ulcer patients (1.3 +/- 0.4 vs 2.5 +/- 1.6, respectively, p < 0.001). The ratio of G-cells to D-cells was also significantly higher in infected patients compared with uninfected patients for both gastric and duodenal ulcers (5.7 +/- 2.7 vs 3.5 +/- 1.9, respectively, p < 0.001). CONCLUSIONS: These results strongly suggest that Helicobacter pylori infection induces reduction of the number of antral D-cells. The resulting relative hypofunction of the inhibitory action of D-cells against G-cells may be responsible for increased serum gastrin secretion.
Subject(s)
Humans , Case-Control Studies , Somatostatin-Secreting Cells/pathology , Somatostatin-Secreting Cells/metabolism , Gastrin-Secreting Cells/pathology , Gastrin-Secreting Cells/metabolism , Gastrins/metabolism , Gastrins/blood , Gastritis/pathology , Gastritis/metabolism , Helicobacter Infections/pathology , Helicobacter Infections/metabolism , Helicobacter pylori , Somatostatin/metabolismABSTRACT
Gastric biopsies (42) from patients with peptic ulcer disease were classified into Helicobacter pylori positive (32) and negative (10) groups, based on the results of tissue urease test and microscopic demonstration of spiral bacteria. A statistically significant difference in peanut agglutinin (PNA) binding between the two groups was observed, attributable to exposure of sialic acid residues on gastric epithelium in the H. pylori positive group. That the negative binding was due to sialic acid, was further confirmed by application of sialidase digestion technique. These results support the existing biochemical evidence for exposure of sialic acid residues on H. pylori colonized epithelium.
Subject(s)
Adolescent , Adult , Aged , Arachis/metabolism , Female , Gastric Mucosa/cytology , Gastritis/metabolism , Helicobacter pylori/isolation & purification , Humans , Lectins/metabolism , Male , Middle Aged , Peanut Agglutinin , Plant Lectins , Protein Binding , Sialic Acids/metabolismABSTRACT
Os autores realizaram estudo experimental em caes em que a mucosa gastrica foi exposta a acao da bile e do acido cloridrico. Atraves de colecistogastrostomia, apos ligaduras do coledoco, direcionaram a bile para o antro gastrico em 20 animais e para o corpo em outros 20. Em 10 caes de cada grupo realizaram vagotomia troncular bilateral.Sacrificaram os animais 180 dias de pos-operatorio. Concluiram que a gastrite ocorreu com mais frequencia e intensidade nos animais com anastomose a nivel do antro do que naqueles com anastomose no corpo do estomago. Concluiram ainda que a vagotomia protegeu a mucosa gastrica contra o efeito lesivo da bile
Subject(s)
Animals , Dogs , Gastritis/metabolism , Gastric Mucosa/physiopathology , Hydrochloric Acid/metabolism , Bile/metabolism , Cholecystostomy , Gastrostomy , Vagotomy, TruncalABSTRACT
Existen diversas técnicas histoquímicas para identificar el Campylobacter pilórico en el tejido, siendo la coloración de Warthin Starry la más conocida y usada. Con la finalidad de buscar otra coloración con igual eficacia que la mencionada, utilizamos la coloración de Waysson con una técnica sensilla y de bajo costo, que se basa en la reacción química específica de los colorantes. De los especímenes biópsicos conocidos con diagnóstico positivo a Cambylobacter pilórico (75), se realizaron nuevos cortes para ser colorados con ambas técnicas, (Warthin Starry y Waysson) en cada caso. Se demuestra que ambas coloraciones identifican adecuadamente a la bacteria en el tejido, y que la coloración de Waysson) en cada caso. Se demuestra que ambas coloraciones identifican adecuadamente a la bacteria en el tejido, y que la coloración de Waysson es más fácil de procesar, usa menos tiempo y es menos costosa