bromochloroacetic-acid and Helicobacter-Infections

Esophagogastric ulcer is an independent disease in swine that is characterized by ulcerous autodigestion of the cutaneous mucosa, which does not exhibit a tendency to recover, but, on the contrary, a tendency toward severe hemorrhaging, with a predominantly lethal outcome. Since it develops in the part of the stomach that is morphologically and functionally different from other glandular mucosa, it was questioned earlier whether it could be a peptic ulcer based on its nature. Spontaneous ulcers, usually of the stomach, commonly occur in many domestic animals. Some of these lesions are chronic and they may occur in either the glandular or squamous-lined regions of the stomach. As with the human disease, the pathogenesis in domestic animals is multifactorial, poorly understood, and variable between and within species. Environmental stress and dietary factors are very important in the ulcer disease in swine. It has been shown that the Helicobacter spp. is strongly associated with naturally occurring ulcer and preulcer lesions of the pars esophagea in swine, which raises the possibility that Helicobacter spp. is an important factor in the pathogenesis of these lesions. The dynamics of the development of esophagogastric ulcers imply hyperplastic lesions (parakeratosis and hyperkeratosis), keratolysis, erosions, peptic necrosis, and the development of ulcers with all the characteristics of peptic ulcerations in other localities. In addition, K6 is expressed in association with the mucosal changes. The pattern of the intermediate filaments of keratin suggests that epithelial proliferation, which leads to visible hyperkeratosis, constitutes the essence of gastric ulcers in swine.

Topics: Animals; Cell Proliferation; Chronic Disease; Diagnosis, Differential; Diet; Esophageal Diseases; Esophagogastric Junction; Helicobacter Infections; Humans; Intermediate Filaments; Keratins; Stomach; Stomach Ulcer; Swine

To investigate the expression of different cytokeratins (CKs) in gastric epithelium of adult patients with chronic gastritis infected with Helicobacter pylori (H pylori) cagA+ strains.. 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+H pylori gastritis (57 cases), non-H pylori gastritis (17 cases) and normal gastric mucosa (10 cases).. 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 H pylori-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 H pylori infection, CK20 was expressed strongly/moderately and homogeneously in surface epithelium and upper foveolar region, but in H pylori -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.. 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.

Topics: Adult; Antigens, Bacterial; Bacterial Proteins; Chronic Disease; Female; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Keratins; Male; Middle Aged; Prospective Studies

Helicobacter pylori (H. pylori) is a "slow" bacterial pathogen, which induces several gastroduodenal diseases. Varying degrees of inflammation can be present in the gastric mucosa of patients infected with H. pylori. The case presented here is a male patient suffering from dyspepsia and nausea. His upper gastrointestinal endoscopy revealed pan gastritis. Histological examination of multiple gastric biopsies taken from the body and antrum showed a rare morphological expression of H. pylori gastritis characterized by diffuse plasma cell infiltration with extensive Russell body formation. Diffuse infiltration of plasma cells with Russell bodies in gastric mucosa can cause difficulties in differentiation from neoplastic processes. However, immunohistochemically, the infiltrating cells in the gastric mucosa stained negatively with cytokeratins while they expressed both kappa and lambda light chains showing their polyclonal nature. The presence of diffuse plasma cells with Russell bodies in the gastric mucosa may represent a different presentation of H. pylori gastritis. There are only two case reports of similar presentation and both have been called "Russell body gastritis".

Topics: Aged; Biomarkers; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunoenzyme Techniques; Immunoglobulin Heavy Chains; Immunoglobulin Light Chains; Inclusion Bodies; Keratins; Male; Plasma Cells

Both Helicobacter pylori and gastro-oesophageal reflux disease (GORD) may cause inflammation in cardiac mucosa. Intestinal metaplasia (IM) is found more often in GORD associated inflammation than in inflammation caused by H pylori, especially in young individuals.. To examine morphological differences in chronic inflammation in these two conditions by immunohistochemistry.. Tissue blocks from cardiac mucosa of patients <45 years were available as follows: 10 patients with chronic inflammation of cardiac mucosa (carditis) and H pylori gastritis (group 1); 10 patients with (possibly GORD related) carditis, but normal antrum and corpus (group 2); and 10 patients with non-inflamed cardiac mucosa and normal antrum and corpus (group 3). Haematoxylin and eosin staining and immunohistochemical staining for various inflammatory cells were performed for patients in groups 1 and 2 as follows: CD20 (B cells), CD3 (T cells), CD4 (T helper cells), CD8 (T suppressor cells), CD163 (macrophages), CD138 (plasma cells), and CD117 (mast cells). For all patients, cytokeratin 7/20 (CK7/20) staining was performed.. No clear differences were seen in the morphology of chronic inflammation between groups 1 and 2. In both, plasma cells were most abundant. CK7/20 staining showed no differences between these groups.. Helicobacter pylori negative (possibly GORD associated) and H pylori related carditis cannot be distinguished on a morphological basis. The stronger tendency towards IM in the first entity cannot be explained by differences in the type of inflammation. Barrett-type CK7/20 staining seems typical for cardiac mucosa, irrespective of the type of inflammation or presence of IM.

Topics: Adult; Antigens, CD; Biomarkers; Chronic Disease; Connective Tissue Cells; Female; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Intermediate Filament Proteins; Keratin-20; Keratin-7; Keratins; Male; Mucous Membrane; Myocarditis; Plasma Cells; T-Lymphocytes

Intestinal metaplasia and gastro-oesophageal reflux disease typify classical Barrett's oesophagus. Cytokeratin (CK) 7 and 20 phenotypes differentiate intestinal metaplasia in long segment Barrett's oesophagus from gastric intestinal metaplasia. This study examines the relationship between CK7/20 phenotypes and reflux disease in intestinal metaplasia of the distal oesophagus.. Eighty patients with oesophageal pH studies included 30 with long segment Barrett's, 16 with short segment Barrett's and 34 with intestinal meatplasia of the gastro-oesophageal junction. Representative biopsy specimens were immunostained for CK7 and CK20. All 30 long segment patients demonstrated a Barrett's CK7/20 phenotype. All nine short segment patients with gastro-oesophageal reflux had a Barrett's CK7/20 phenotype, while four of seven short segment patients without reflux had a gastric CK7/20 phenotype (P = 0.019). Of 14 patients with intestinal metaplasia of the gastro-oesophageal junction and reflux, 10 (71%) had a Barrett's CK7/20 phenotype, compared with 11 (55%) of the 20 non-reflux patients.. CK7/20 immunoreactivity for patients with intestinal metaplasia of the distal oesophagus without long segment Barrett's oesophagus suggests a heterogeneous group, with an association between Barrett's CK7/20 pattern and gastro-oesophageal reflux disease in both short segment Barrett's and intestinal metaplasia of the gastro-oesophageal junction.

Topics: Barrett Esophagus; Esophagus; Female; Gastric Mucosa; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Intermediate Filament Proteins; Keratin-20; Keratin-7; Keratins; Male; Metaplasia; Middle Aged

To investigate the roles of mucin histochemistry, cytokeratin 7/20 (CK7/20) immunoreactivity, clinical characteristics and endoscopy to distinguish short-segment Barrett's esophageal (SSBE) from cardiac intestinal metaplasia (CIM).. High iron diamine/Alcian blue (HID/AB) mucin-histochemical staining and immunohistochemical staining were used to classify intestinal metaplasia (IM) and to determine CK7/20 immunoreactivity pattern in SSBE and CIM, respectively, and these results were compared with endoscopical diagnosis and the positive rate of gastroesophageal reflux disease (GERD) symptoms and H pylori infection. Long-segment Barrett's esophageal and IM of gastric antrum were designed as control.. The prevalence of type III IM was significantly higher in SSBE than in CIM (63.33% vs 23.08%, P< 0.005). The CK7/20 immunoreactivity in SSBE showed mainly Barrett's pattern (76.66%), and the GERD symptoms in most cases which showed Barrett's pattern were positive, whereas H pylori infection was negative. However, the CK7/20 immunoreactivity in CIM was gastric pattern preponderantly (61.54%), but there were 23.08% cases that showed Barrett's pattern. H pylori infection in all cases which showed gastric pattern was significantly higher than those which showed Barrett's pattern (63.83% vs 19.30%, P< 0.005), whereas the GERD symptoms in gastric pattern were significantly lower than that in Barrett's pattern (21.28% vs 85.96%, P< 0.005).. Distinction of SSBE from CIM should not be based on a single method; however, the combination of clinical characteristics, histology, mucin histochemistry, CK7/20 immunoreactivity, and endoscopic biopsy should be applied. Type III IM, presence of GERD symptoms, and Barrett's CK7/20 immunoreactivity pattern may support the diagnosis of SSBE, whereas non-type III IM, positive H pylori infection, and gastric CK7/20 immunoreactivity pattern may imply CIM.

Topics: Barrett Esophagus; Cardia; Diagnosis, Differential; Esophageal Diseases; Esophagogastric Junction; Gastroesophageal Reflux; Gastrointestinal Diseases; Gastroscopy; Helicobacter Infections; Humans; Intestines; Keratin-20; Keratin-7; Keratins; Metaplasia; Mucins

Epithelial cancers are believed to originate from transformation of tissue stem cells. However, bone marrow-derived cells (BMDCs), which are frequently recruited to sites of tissue injury and inflammation, might also represent a potential source of malignancy. We show that although acute injury, acute inflammation, or transient parietal cell loss within the stomach do not lead to BMDC recruitment, chronic infection of C57BL/6 mice with Helicobacter, a known carcinogen, induces repopulation of the stomach with BMDCs. Subsequently, these cells progress through metaplasia and dysplasia to intraepithelial cancer. These findings suggest that epithelial cancers can originate from marrow-derived sources and thus have broad implications for the multistep model of cancer progression.

Topics: Animals; Apoptosis; Bone Marrow Cells; Bone Marrow Transplantation; Carcinoma in Situ; Cell Differentiation; Cell Fusion; Disease Progression; Female; Gastric Mucosa; Gastritis; Helicobacter felis; Helicobacter Infections; Keratins; Male; Mesenchymal Stem Cells; Metaplasia; Mice; Mice, Inbred C57BL; Mice, Transgenic; Mucins; Muscle Proteins; Parietal Cells, Gastric; Peptides; Phenotype; Stem Cells; Stomach Neoplasms; Trefoil Factor-2

Intestinal metaplasia occurs in the esophagus as a consequence of gastroesophageal reflux disease and in the stomach secondary to H. pylori infection. The etiology of intestinal metaplasia limited to the gastroesophageal junction or cardia (CIM) is disputed. We hypothesized that CIM has dual etiologies: gastroesophageal reflux in some, H. pylori infection in others, and that cytokeratin immunostaining can help to differentiate between these two etiologies.. We defined CIM as the presence of intestinal metaplasia within cardiac mucosa on biopsy from an endoscopically normal-appearing gastroesophageal junction. Thirty patients with CIM who had multiple biopsy specimens taken from the esophagus, gastroesophageal junction, and stomach were identified. Tissue blocks from biopsy specimens taken at the gastroesophageal junction were sectioned and immunostained for cytokeratins 7 and 20. The cytokeratin 7/20 staining of the CIM in each patient was determined to be either a Barrett's or non-Barrett's pattern. H. pylori infection was assessed by Giemsa staining of antral biopsy specimens.. H. pylori infection was present in 16 patients. A Barrett's cytokeratin 7/20 staining pattern in the CIM was present in only 46% of the H. pylori-positive patients, as compared to 86% in the 14 patients with CIM and no H. pylori (p = 0.025). Objective evidence of reflux disease was present in 71% of patients with CIM and no H. pylori, as compared to 31% of patients with H. pylori.. The two different patterns of cytokeratin 7/20 staining found in patients with CIM support the concept of dual etiologies for CIM. A Barrett's staining pattern was associated with objective evidence of gastroesophageal reflux and the absence of H. pylori, suggesting that cytokeratin 7/20 immunostaining is useful to determine the likely etiology of CIM.

Topics: Biopsy; Esophagitis; Esophagus; Gastric Mucosa; Gastroesophageal Reflux; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Intermediate Filament Proteins; Keratin-20; Keratin-7; Keratins; Metaplasia

The normal histology at the gastroesophageal junction, and in particular the nature of cardiac mucosa, remains in dispute. Likewise, the relationship of intestinal metaplasia at the gastroesophageal junction (CIM) to Barrett's and intestinal metaplasia of the stomach (GIM) is unclear. The aim of this study was to assess the immunostaining characteristics of cardiac mucosa and CIM and compare their staining pattern with that of other foregut mucosal types. We hypothesized that the immunostaining patterns of these foregut tissues would provide insight into the nature and etiology of cardiac mucosa and CIM.. Paraffin-embedded biopsy specimens from 50 patients with normal antral or fundic mucosa, cardiac mucosa, squamous mucosa, CIM, GIM, or Barrett's were obtained and immunostained with a panel of monoclonal antibodies including those for cytokeratins 7 and 20 (CK7/CK20) and DAS-1.. Biopsies from normal gastric antral and fundic mucosa and squamous esophageal mucosa all showed a non-Barrett's type CK7/CK20 immunostaining pattern, whereas in 85% of patients, cardiac mucosa had a Barrett's type CK7/CK20 pattern (p < 0.001). A Barrett's type CK7/ CK20 staining pattern was seen in 100% of Barrett's, 78% of CIM, and 0% of GIM patients. Likewise, DAS-1 staining was similar in patients with CIM and Barrett's and significantly different in patients with GIM.. Cytokeratin immunostaining of cardiac mucosa demonstrates significant differences from recognized normal gastric and esophageal mucosa but a similarity to Barrett's. This suggests that cardiac mucosa, like Barrett's, may be acquired. Likewise, immunostaining similarities between CIM and Barrett's biopsies point to the possibility of a reflux etiology for CIM in some patients.

Topics: Antibodies; Barrett Esophagus; Biopsy; Cardia; Esophagogastric Junction; Gastric Fundus; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Intermediate Filament Proteins; Keratin-20; Keratin-7; Keratins; Metaplasia; Mucous Membrane; Pyloric Antrum

Distinguishing histological features between non-steroidal anti-inflammatory drug (NSAID) gastropathy and Helicobacter pylori gastritis have been accepted. However, the molecular basis explaining these dissimilar histologies has not been elucidated. In an attempt to clarify this question we investigated the differences in the structural cytoskeleton and proliferative activity of these two gastropathies.. We assessed the distribution of five cytokeratins (CK) (CK7, 8, 18, 19 and 20) and Ki67 for the ability to distinguish NSAID from H. pylori gastropathies. In H. pylori gastritis, CK7, 8, 18 and 19 were expressed comparably to normal mucosa from the deep foveolae up to the tips of the glands. The detection of CK20, normally expressed in the upper foveolar region and surface, was decreased with only an epithelial surface reaction. In NSAID gastropathy, CK expression was increased in intensity, with normal distribution for CK8, 18 and 19. Modification of localization was noted for CK7 and 20, with labelling extending toward the deep foveolar region. Unlike H. pylori gastritis, no surface epithelial labelling with Ki67 was noted with NSAID gastropathy but downward elongation of the proliferative zone occurred instead.. Contrasting cytostructural alterations and distinct proliferative patterns distinguish NSAID gastropathy from H. pylori gastritis, possibly reflecting different injury pathways.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Cytoskeleton; Diagnosis, Differential; Epithelium; Gastric Mucosa; Gastritis; Gastrointestinal Diseases; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Intermediate Filament Proteins; Keratin-20; Keratin-7; Keratins; Ki-67 Antigen

Cytokeratin (CK) 7 and 20 patterns are specific for long and short segments of Barrett's oesophagus but their use has not been assessed in intestinal metaplasia arising in macroscopically normal gastro-oesophageal junction (GOJ).. This study was carried out in a large prospective series of 254 patients who underwent upper endoscopy, had normal gastro-oesophageal anatomy, and who had biopsies of the antrum, fundus, cardia, GOJ, and lower oesophagus. Intestinal metaplasia of the GOJ was typed by histochemistry with high iron diamine-alcian blue staining and by immunohistochemistry using CK7 and CK20 antibodies. Results were correlated with clinical, endoscopic, and pathological data.. Sixty (23.6%) of our patients presenting with a normal GOJ had intestinal metaplasia. The CK7/CK20 pattern identified two groups of patients: one highly correlated with Barrett's and the other with characteristics of Helicobacter pylori gastritis. The Barrett's type CK7/CK20 pattern was related to a high frequency of gastro-oesophageal reflux symptoms (p<0.02) and normal endoscopic appearance of the stomach (p<0.03). In contrast, the gastric type CK7/CK20 pattern was linked to atrophic (p<0.02) or erythematous (p<0.05) appearance of the stomach (p<0.03), high frequency of H pylori infection (p<0.04), antral inflammation (p<0.006) with atrophy (p<0.02), and intestinal metaplasia (p<0.02).. In patients presenting with intestinal metaplasia in normal appearing GOJ, the cytokeratin pattern identifies two groups of patients, one with features identical to those of long segment Barrett's oesophagus and one with features seen in H pylori gastritis. These data may be used by clinicians and should result in improved endoscopic surveillance strategies targeted specifically at patients at increased risk of Barrett's oesophagus and thus cancer.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Barrett Esophagus; Biomarkers; Esophagogastric Junction; Female; Gastritis; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Histocytochemistry; Humans; Immunohistochemistry; Intermediate Filament Proteins; Intestines; Keratin-20; Keratin-7; Keratins; Male; Metaplasia; Middle Aged; Prospective Studies; Statistics, Nonparametric

Cancer presumably arises from stem cells, preserved in an undifferentiated status since fetal development, or from a dedifferentiation of mature cells that return into a fetal phenotype with the potential for proliferation and renewal. Dedifferentiation in this context could represent a transient phase, passed through by cells, before they switch to redifferentiation, metaplasia or neoplasia. Cytokeratin-7 (CK7) is present in fetal, largely absent in normal adult, and transiently neoexpressed in metaplastic and neoplastic epithelial cells of the stomach according to previous observations. CK7 neoexpression in the stomach could, hence, define a fetal-like, dedifferentiated, cellular phenotype during the development of metaplasia and neoplasia. To test this hypothesis, we investigated CK7 expressions in fetal stomachs, non-neoplastic control stomachs, and neoplastic stomachs exhibiting metaplasia, intraepithelial neoplasia, and early cancer. Proliferation and beta-catenin expression of CK7-positive cells were also evaluated. The chronology of CK7 expression was studied during the experimental gastritis-cancer sequence in Mongolian gerbils. Our results show that metaplastic and neoplastic changes in the gastritis-cancer sequence are related to dedifferentiated epithelial cells which are defined by CK7 expression and can phenotypically be linked to fetal cells at the start of gastric pit development. The dedifferentiated cells exhibit a low proliferation and beta-catenin accumulation, similar to stem cells. Thus, the "stem cell" and "dedifferentiation" hypotheses for cancer origin could complement one another, and dedifferentiation-redifferentiation processes might be decisive for carcinogenesis in the stomach.

Topics: Adenocarcinoma; Adolescent; Adult; Aged; Aged, 80 and over; Animals; Carcinoma in Situ; Cell Transformation, Neoplastic; Child; Disease Models, Animal; Epithelial Cells; Female; Fetus; Gastric Mucosa; Gastritis; Gerbillinae; Gestational Age; Helicobacter Infections; Helicobacter pylori; Humans; Keratin-7; Keratins; Male; Metaplasia; Middle Aged; Stomach; Stomach Neoplasms

Based on the histological criteria proposed by the REAL and adopted by the WHO Classification, 30 cases of MALT type lymphoma, 18 cases of diffuse large B cell lymphoma (DLCL), and 17 cases of DLCLs, associated with a MALT type, were identified in a series of 65 surgically treated primary gastric lymphomas. The clinical records of the patients were analyzed retrospectively and the resected specimens were immunostained for bcl-2, p53 and Ki-67. Primary gastric DLBCLs, with or without a MALT type component, disclosed a higher stage of local extension, a more frequent nodal involvement and a significantly worse survival than pure MALT types. High p53 expression and high proliferation rate correlated with the presence of a large cell component and appeared useful for its identification in mixed forms. Low bcl-2 expression discriminated DLCL from DLCL/MALT. Tumor size, stage and Mib-1 index revealed a value in predicting prognosis.

Topics: Adult; Aged; Aged, 80 and over; Antigens, Bacterial; Antigens, CD; Antigens, Nuclear; Biomarkers, Tumor; Combined Modality Therapy; Female; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Italy; Keratins; Ki-67 Antigen; Life Tables; Lymphoma, B-Cell, Marginal Zone; Lymphoma, Large B-Cell, Diffuse; Male; Middle Aged; Neoplasm Invasiveness; Neoplasm Proteins; Neoplasm Staging; Nuclear Proteins; Phenotype; Proto-Oncogene Proteins c-bcl-2; Retrospective Studies; Stomach Neoplasms; Survival Analysis; Tumor Suppressor Protein p53

In humans, low-grade B-cell mucosa-associated lymphoid tissue (MALT) lymphomas of the stomach regress when Helicobacter pylori infection is cured by antimicrobial therapy. Using an animal model of human gastric MALT lymphoma, we observed the effects of Helicobacter felis eradication and the relationship between infection and disease progression. Antimicrobial therapy was given to one-half of the BALB/c mice infected with H. felis for 20 months. Groups of antibiotic-treated and untreated mice were killed 2, 3, and 4 months after antimicrobial therapy (ie, 22, 23, and 24 months after infection). The numbers of mice with MALT decreased after H. felis eradication with no lymphoid follicles seen 4 months after treatment. MALT lymphoma was present in a total of 23% (11/48) of antibiotic-treated infected mice compared with 75% (27/36) in untreated infected mice. These lymphomas were further graded into low-, intermediate-, and high-grade lymphoma. In the untreated mice, lymphoma development was more advanced with 36% low-grade (13/36), 39% intermediate-grade (14/36), and 6% high-grade (large B-cell) lymphoma (2/36) whereas in the treated mice the incidence was 21% (10/48), 6% (3/48), and 0% (0/48), respectively. These observations suggest that antigenic stimulation by H. felis sustained growth and progression of low-grade MALT lymphoma and that primary high-grade gastric lymphomas can evolve from the transformation of these tumors. Eradication of the organism caused low-grade tumors to regress, with inhibition or slowing down of lymphoma development toward high-grade lymphoma. The H. felis mouse model of gastric MALT lymphoma presents an opportunity to address the issues arising from antimicrobial treatment of these tumors in humans.

Topics: Animals; Anti-Bacterial Agents; CD3 Complex; Female; Helicobacter Infections; Immunohistochemistry; Keratins; Lymphoma, B-Cell, Marginal Zone; Mice; Mice, Inbred BALB C; Specific Pathogen-Free Organisms; Stomach Neoplasms; Time Factors

To clarify structural changes in the gastric foveolar epithelium in Helicobacter pylori (Hp)-positive gastritis, the expression rates of keratins 8, 18, 19, and 20 were assessed immunohistochemically in normal tissue and chronic gastritis. In normal tissue, keratin 8 was found in 100% of the cells. Staining for keratins 18 and 19 was abundantly positive. Keratin 20 was not expressed in the deep foveolae, but present in the upper foveolae and on the tips. No differences were found between the antrum and the body. In chronic gastritis, both Hp-positive and -negative, keratins 8, 18, and 19 were expressed comparably to normal tissue. Keratin 20 expression in the antrum was significantly lower in Hp-positive compared with Hp-negative gastritis (P < .05) and normal tissue (P < .05). In the body, staining for keratin 20 did not differ significantly between all groups. The difference in keratin 20 expression between the antrum and the body in Hp-positive gastritis was significant (P < .05). After successful eradication, staining for keratin 20 in the antrum normalized within 6 months (P < .05). These findings indicate structural changes in the gastric foveolar epithelium in Hp-positive gastritis. They predominantly include the antral region and show full reversibility after eradication.

Topics: Adult; Aged; Biopsy; Female; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Keratins; Male; Middle Aged

The expression of the cytokeratins (CK) 1, 5, 6, 7, 10, 13 and 14 was studied immunohistochemically in gastric biopsies from both the antrum and the body of 70 patients. Normal gastric foveolar epithelium (9 cases) Helicobacter pylori gastritis (23) and intestinal metaplasia (38) were examined. Positive staining results for CK 1, 5, 10 and 14 were not observed using the 34 beta E12 antibody. With antibodies to CK 5/6, 7 and 13 some, but not all cases, were immunoreactive. Predominantly positive staining included less than 10% of the cells and was always restricted to the tips and the juxtaluminal areas of the foveolae. No difference was seen between the antrum and the body. Comparing normal gastric mucosa with gastritis and intestinal metaplasia, cases positive for CK 5/6 were observed less frequently in intestinal metaplasia types II and II compared to the other groups. CK 7 was expressed exclusively in intestinal metaplasia. CK 13 was seen in all groups of specimens. Thus, cytokeratins typical for ductal structures (CK 7) and squamous epithelia (CK 5/6, CK 13) can be regarded as an inconstant, but not unusual observation in the gastric mucosa. Their expression may be controlled by both differentiation-related as well as environmental factors.

Topics: Adult; Carcinoma, Squamous Cell; Epithelium; Female; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Neoplasms; Keratins; Male; Middle Aged; Pyloric Antrum; Stomach Neoplasms