Role of Th22 cells in Helicobacter pylori-related gastritis and peptic ulcer diseases.

Helicobacter pylori (H. pylori) has been shown to be one of the leading causes of peptic ulcer diseases (PUDs) and gastritis. T helper-22 (Th22) cells and its most important cytokine, interleukin-22 (IL-22) are importantly active in inflammation and inflammatory tissues. Since inflammation is one of the main attributes of infection caused by H. pylori and resulting complications (gastritis and gastrointestinal ulcer), this study was designed to evaluate the Th22 cells count and the IL-22 protein expression in people suffering from PUD and gastritis. The present study was conducted on 55 patients with gastritis, 47 patients with PUD and 48 uninfected subjects. After preparation of section and extraction of protein from antral biopsies, immunohistochemistry and western blot methods were used to evaluate the Th22 cells and IL-22 protein expression level, respectively. According to findings, the Th22 cells count and the IL-22 protein expression level in the infected subjects were siginficantly more than in the uninfected subjects. It should be noted that the Th22 cells count and the IL-22 protein expression level in the infected subjects with PUD were significantly greater than those in the infected subjects with gastritis. In addition, the Th22 cells count had positive correlation with the density of H. pylori, chronic inflammation score and acute inflammatory score in the infected subjects with PUD. The Th22 cells count had positive correlation with the Th17 cells count and inverse correlation with the Treg cells count in the infected subjects with PUD and gastritis. Our data demonstrated that abnormal hyper-activation of Th22 cells as well as its correlation with the Th17 cells during infection caused by H. pylori might damage tissues through immunopathological responses.

Arginase-1 and Treg Profile Appear to Modulate Inflammatory Process in Patients with Chronic Gastritis: IL-33 May Be the Alarm Cytokine in H. pylori-Positive Patients.

Helicobacter pylori (H. pylori) is a highly prevalent bacterium in our environment, directly involved in various upper digestive tract diseases, such as gastritis, peptic ulcer, and gastric cancer. Several molecules activating the immune system have been reported to be involved in containing H. pylori infection. This study is aimed at analyzing the mRNA expression of the cytokines IFN-γ, IL-17, IL-10, TGF-ß, IL-6, IL-22, IL-23, and IL-33; transcription factors T-bet, RORC, and FOXP3; enzymes ARG1, ARG2, and NOS2; and neuropeptides VIP and TAC and their respective receptors VIPR1 and TACR1 in the stomach lining of patients with severe digestive disorders. One hundred and twenty six patients have been evaluated, presenting with symptoms in the upper digestive tract, with the clinical indication for an Upper Digestive Endoscopy exam. Two fragments of the mucosa of the gastric body and antrum have been collected for anatomopathological examination and to analyze the expression of enzymes, cytokines, and transcription factors using qPCR. Expression of the ARG1 gene was seen as significantly higher in the group of patients with chronic inactive gastritis than in the control group. Expression of the TGF-ß gene and its FOXP3 transcription factor was significantly higher in the group of chronic inactive gastritis patients than in the control. Expression of IFN-γ, IL-17, IL-10, and TGF-ß and the transcription factors, T-bet and RORC, in the presence or absence of H. pylori showed no significant difference. However, the expression of FOXP3 was significantly lower in H. pylori-positive patients than that in H. pylori-negative patients. ARG1 and Treg profile appeared to be modulating the inflammatory process, protecting patients from the tissue lesions with chronic inactive gastritis. Furthermore, we suggest that IL-33 may be a crucial mediator of the immune response against an infection, after gastric mucosal damage.

T Cell-Dependent Maturation of Pathogen-Specific Igs in the Antrum of Chronically Helicobacter pylori-Infected Patients.

Mucosal plasma cells (PC) and Ig production are essential to fend pathogens and to maintain mucosal homeostasis. In human Helicobacter pylori infection, mucosal PC express inducible NO synthase (iNOS), which positively correlates with clearance of experimental human infection. To characterize Ig genes and specificities of antral mucosal iNOS+ and iNOS- PC in H. pylori infection, we sequenced rearranged Ig genes from single cell-sorted PC from biopsy specimens of chronically infected patients and analyzed them with respect to their molecular features. The binding specificity of individual PC's Ig was determined following recombinant expression. We identified high rates of somatic hypermutations, especially targeting RGYW/WRCY hotspot motifs in the individual Ig genes, indicating T cell-dependent maturation. For seven of 14 recombinantly expressed Ig, Ag specificity could be determined. Two clones reacted to H. pylori proteins, and five were found to be polyreactive against LPSs, dsDNA, and ssDNA. All specific Ig originated from iNOS+ PC. H. pylori-specific Ig are encoded by V and J family genes previously shown to be also used in rearranged Ig loci of MALT B cell lymphomas. In summary, mucosal iNOS+ PC producing H. pylori-specific Ig accumulate in infection and appear to be a product of T cell-dependent B cell maturation. Moreover, the Ig's molecular features partly resembled that of MALT B cell lymphoma Ig genes, suggestive of a mechanism in which a progressive molecular evolution of pathogen-specific B cells to MALT B cell lymphoma occurs.

Increased Proliferative Activity Accompanies the Local Inflammatory Response of Gastric Mucosa After Intragastric Balloon Insertion.

BACKGROUND AND AIM: The use of BioEnterics intragastric balloon (BIB) is progressively increasing, owing to the fact that morbid obesity becomes a global epidemic together with risks of bariatric surgery. Yet, the possible local BIB effect on gastric mucosa is not clearly elucidated. The aim of the current study was to assess the histological changes occurring in the gastric mucosa post-BIB insertion. METHODS: Gastric mucosa biopsy was obtained from 87 cases of morbid obesity both pre-BIB and 6 months post-BIB insertion to compare the local changes by histological and immunohistochemical analysis. RESULTS: An inflammatory reaction was detected in the post-BIB mucosa which displayed a positive CD20, CD3 (p < 0.05), and the proliferation index (Ki67) increased significantly compared with that of the pre-BIB cases. The Ki67 index showed a significant positive correlation with CD20 and CD3 immunoexpression in the post-BIB gastric mucosae. CONCLUSION: Our results demonstrated a possible increase in the gastric proliferative activity after BIB insertion accompanied with a remarkable local inflammatory reaction. Although these findings may be reactive and transient, endoscopic follow-up is recommended for early detection of further pathological changes.

Monoclonal light chain deposits within the stomach manifesting as immunotactoid gastropathy.

Immunotactoid deposits are defined by their ultrastructural appearance and are characterized by microtubular or cylindrical structures typically measuring greater than 30 nm in diameter. Although a rare entity, immunotactoid deposition most often manifests as immunotactoid glomerulopathy and is associated with underlying lymphoplasmacytic disorders. Corneal immunotactoid deposition known as immunotactoid keratopathy has also been reported in patients with paraproteinemia. Here, we describe the first reported case of immunotactoid deposition in the stomach. The deposits were composed solely of kappa immunoglobulin light chains without significant lambda light chain or immunoglobulin heavy chain components. The patient displayed no renal signs or symptoms, and additional thorough clinical examination failed to detect any evidence of a paraproteinemia or plasma cell dyscrasia. Thus, the gastric immunotactoid deposits in this case appear to be an isolated finding of light chain deposition, of which the significance and etiology are unclear.

Immunoreactivity to cocaine- and amphetamine-regulated transcript in the enteric nervous system of the pig and wild boar stomach.

Cocaine- and amphetamine-regulated transcript (CART) is a recently discovered peptide inducing strong anxiogenic-like effect. CART distribution and its role(s) at periphery are not well understood. Immunohistochemisty was utilized to investigate the distribution patterns of CART in the stomach of the pig and wild boar. Double immunohistochemisty was applied to elucidate whether CART-immunoreactive (IR) neuronal elements coexpress galanin, substance P (SP) and neuropeptide Y (NPY). In the pig stomach, different proportions of CART-IR myenteric neurons were found in the antrum (42.3 ± 3.5%), corpus (18.0 ± 1.9%) and pylorus (33.2 ± 3.0%). CART-IR myeneric neurons were also found in the antrum, corpus and pylorus of the wild boar stomach (41.7 ± 3.2, 36.0 ± 2.2 and 35.8 ± 3.5%; respectively). In both species, none of gastric submucous neurons were CART-IR; however, CART-IR nerve fibres encircled submucous perikarya. In all portions of the pig and wild boar stomach, CART-IR nerve fibres were frequently found in the smooth muscle layer as well as in the lamina muscularis mucosae. In all regions of the pig and wild boar stomach, the expression of galanin and SP was found in CART-IR myenteric neurons and smooth muscle-supplying nerve fibres. CART/NPY coexpression was not found in the porcine stomach; however, in different regions of the wild boar stomach, subpopulations of CART-IR/NPY-IR myenteric neurons were noted. In conclusion, in this study, the existence and distribution patterns of CART in discrete regions of the pig and wild boar stomach were described in details. Colocalization studies revealed that in both animal species, a functional cooperation of CART with several neuropeptides is likely.

Synergistic effect of IL-1ß and TNF-α polymorphisms on the H. pylori-related gastric pre-malignant condition.

BACKGROUND/AIMS: We investigated the effect of IL-1ß and TNF-α polymorphisms, and its synergistic effect with age, gender and H. pylori status on the gastric pre-malignant condition. METHODOLOGY: IL-1ß-31(T>C) and -511(C>T) and TNF-α-857 (C>T) polymorphisms were genotyped in 123 cancer free subjects. Degree of histological gastritis in both antrum and corpus, and extension of endoscopic gastric atrophy were also evaluated. RESULTS: Significant associations were found between degrees of mononuclear cell infiltration (p=0.007) and atrophy (p=0.01) in the antrum with IL-1ß-31(T>C) polymorphism, and degree of endoscopic gastric atrophy with both IL-1ß-31(T>C), -511(C>T) polymorphisms (p=0.03, 0.04, respectively). When subjects were divided into the 3 groups according to the histological severity of gastric mucosal atrophy: the non-atrophic gastritis (NA) group (atrophy score=0 and metaplasia score=0), the severe atrophic gastritis (SA) group (atrophy score>=2 or metaplasia score>=2), and the mild atrophic gastritis (MA) group (all others), synergistic effect was found between numbers of IL-1ß-31C, IL-1ß-511T variant alleles with co-factors on the development of gastric atrophy in the antrum (gender + H. pylori + number of IL-1ß-31C allele: p=0.001, age + gender + H. pylori + number of IL-1ß-31C allele: p=0.0008, gender + H. pylori + number of IL-1ß-511T allele: p=0.016, age + gender + H. pylori + number of IL-1ß-511T allele: p=0.013), while such association was found for TNF-α-857 T allele in the antrum and all genotypes in the corpus. CONCLUSIONS: IL-1ß-31C, IL-1ß-511T variant alleles may accelerate gastric mucosal inflammation and atrophy, not only by themselves, but also through the interaction with co-factors.

Expression of melanoma differentiation associated gene 5 is increased in human gastric mucosa infected with Helicobacter pylori.

Helicobacter pylori infection is associated with gastroduodenal diseases. Melanoma differentiation associated gene 5 (MDA5) plays a role in antiviral host defense. We investigated the effect of H pylori infection on MDA5 expression in human gastric mucosa. Biopsy samples from the antrum and corpus were obtained from 33 patients. MDA5 mRNA and protein were examined by real-time PCR and immunohistochemical staining. Histological gastritis was graded according to updated Sydney System. MDA5 mRNA was significantly increased in the antrum infected with H pylori. MDA5 protein positively stained in infiltrating mononuclear cells. MDA5 mRNA expression was significantly correlated with the grade of glandular atrophy (rs = 0.767) and intestinal metaplasia (rs = 0.748) in the corpus with H pylori infection. These results indicate that MDA5 may be involved in innate immune reactions against H pylori and associate with glandular atrophy and intestinal metaplasia in patients with H pylori infection.

Blood and gastric FOXP3+ T cells are not decreased in human gastric graft-versus-host disease.

Previous studies suggest regulatory T cells (Tregs) inhibit graft-versus-host disease (GVHD) in mouse and human hematopoietic cell transplant (HCT) recipients. As the gastrointestinal tract represents one of the most common and severe sites of GVHD-related tissue damage, we sought to determine whether a deficit in circulating or gastric mucosal Treg numbers correlates with the clinical onset of gastric GVHD. We used the marker FOXP3 to quantify Tregs in blood and in gastric antral biopsies in a cohort of 60 allogeneic HCT recipients undergoing endoscopy at a single center to evaluate symptoms suspicious for gastrointestinal GVHD. We show for the first time in the gastric mucosa and, contrary to existing reports, in the blood, that the percent of T cells expressing FOXP3 is at least as high in the presence as in the absence of GVHD involving the upper gut. There was no correlation of Treg frequency with the histologic or clinical severity of gastrointestinal GVHD. We conclude that Treg depletion is not a central feature in the pathogenesis of gastric GVHD in humans.

Immune response to Helicobacter pylori and its association with the dynamics of chronic gastritis in the antrum and corpus.

The aim of the study was to establish possible factors which play a role in progression of gastritis to atrophic gastritis in long-term follow-up among the Estonian population, to assess the association between the host immune response and different Helicobacter pylori antigens and autoantigens in relation to the histological parameters of gastritis in the antrum and corpus. ELISA and immunoblot were used for detection of IgG to H. pylori acid glycine-extracted cell surface proteins, CagA protein, and H. pylori HSP60. Anticanalicular autoantibodies (ACAB) in the serum were evaluated according to Faller et al. (1996). Apoptosis was evaluated using the TUNEL method. Study subjects were 1958 persons from an unselected Estonian population, and 70 persons from a sample from Saaremaa Island, who had been investigated over a period of 18 years. Seropositivity for CagA was a sign of gastritis activity [OR=14.8 (4.5-50.3)] and atrophy [OR=7.0 (2.1-23.1)] and might predict development of atrophy, particularly in the corpus [OR=7.1 (1.8-27.7)]. The prevalence of ACAB increased significantly with duration of H. pylori gastritis from 22% in 1985 to 46% in 1997 (p=0.004). Immune response to H. pylori HSP60 indicates chronic inflammation in the antrum (p=0.003). Apoptosis of gastric epithelial cells is largely dependent on grade of activity of gastritis, and, particularly in the antrum, on grade of H. pylori colonization (p=0.01; p=0.02), but is not associated with development of atrophy. Seropositivity for different H. pylori antigens (CagA, HSP 60) serves as a marker of different histological manifestations in the antrum and corpus mucosa.

Prevalence and risk factors of atrophic gastritis and intestinal metaplasia in a Korean population without significant gastroduodenal disease.

BACKGROUND AND AIM: The prevalence of gastric cancer and Helicobacter pylori infection is unacceptably high in Korea. This study was performed to evaluate the prevalence of atrophic gastritis (AG) and intestinal metaplasia (IM) and to identify their risk factors with respect to H. pylori virulence factors, and environmental and host factors, in Korean population without significant gastroduodenal disease. METHODS: The study cohort consisted of 389 subjects (> or = 16 years). AG and IM were scored histologically using the Sydney classification in the antrum and body, respectively. Prevalences and bacterial factors (i.e. cagA, vacA m1, and oipA), environmental factors (i.e. smoking and alcohol), and host factors (i.e. genetic polymorphisms of IL-1B-511, IL-1RN, TNF-A-308, IL-10-592, IL-10-819, IL-10-1082, IL-8-251, IL-6-572, GSTP1, p53 codon 72, and ALDH2) were evaluated. RESULTS: Prevalences of AG in the antrum and body were 42.5% and 20.1%, and those of IM were 28.6% and 21.2%, respectively. The presences of AG and IM were significantly higher in H. pylori-positive than in the H. pylori-negative subjects. Multivariate analysis showed that the risk factors for AG were H. pylori infection, age > or = 61 years, and cagA and vacA m1 positivity. For IM the risk factors were H. pylori infection, age > or = 61 years, a smoking history (rather than current smoking), strong spicy food, occupation (unemployed or nonprofessional vs. professional), and the presence of IL10-592 C/A as opposed to A/A. In addition, IL6-572 G carrier was found to have a protective effect against IM development as compared with C/C. CONCLUSION: H. pylori infection was most important risk factor of AG and IM. Bacterial factors were found to be important risk factor for AG but environmental and host factors were more important for IM.

Naturally occurring regulatory T cells (CD4+, CD25high, FOXP3+) in the antrum and cardia are associated with higher H. pylori colonization and increased gene expression of TGF-beta1.

BACKGROUND: Helicobacter pylori causes gastric inflammation. Despite the induction of H. pylori-specific B- and T cells, the immune response is not sufficient to clear the infection. Regulatory T cells (Treg cells) suppress the activation and proliferation of antigen-specific T cells and mediate immunologic tolerance. FOXP3 was shown to be expressed in a subset of Treg cells known as 'naturally occurring Treg cells'. These cells have not been sufficiently studied in context to H. pylori-induced inflammation in human gastric mucosa. MATERIALS AND METHODS: The study included 76 patients stratified according to the presence of H. pylori. Gene expression levels of FOXP3, transforming growth factor (TGF)-beta1, and interleukin-10 were analyzed by quantitative real-time polymerase chain reaction in biopsies from gastric antrum, corpus, and cardia. FOXP3 expression was also analyzed by immunohistochemistry. Differences in expression levels were analyzed by comprehensive statistical analyses and correlated with clinical and histomorphologic parameters. RESULTS: H. pylori-positive patients revealed a 19- to 25-fold induction of FOXP3 transcript levels in antrum and cardia (p < .02). FOXP3 transcript levels correlated positively with inflammation (p < .04) and TGF-beta1 transcript levels (p < .001). Furthermore, a positive correlation between FOXP3(+) Treg cells and H. pylori colonization was demonstrated. CONCLUSION: This study demonstrates that H. pylori-induced gastritis is associated with a recruitment of naturally occurring FOXP3(+) Treg cells that correlates with the degree of bacterial colonization and mucosal TGF-beta1 expression. Together, these data support the hypothesis that naturally FOXP3(+) Treg cells play a role in the lifelong persistence of H. pylori infection in humans.

Comparison of mucosal B- and T-cell responses in Helicobacter pylori-infected subjects in a developing and a developed country.

Helicobacter pylori is highly endemic in developing countries, but comparatively little is known about mucosal immune responses to H. pylori in these settings. Therefore, we have compared B- and T-cell responses, with a focus on the gastrointestinal mucosa, in H. pylori-infected adults in a developing (Bangladesh) and a developed (Sweden) country. We found comparable numbers of CD19(+) B cells and CD4 (+)T cells and similar levels of H. pylori-specific IgA antibodies in gastric mucosa from Bangladeshi and Swedish volunteers. However, about threefold higher numbers of CD19(+) B cells and 12-fold increased levels of H. pylori-specific IgA antibodies were found in the duodenum of Bangladeshi subjects. The gastric and duodenal immune responses in Bangladeshi asymptomatic carriers and duodenal ulcer patients were comparable. Bangladeshi subjects had about twofold lower titers of H. pylori-specific IgA and IgG antibodies in the circulation compared with Swedish volunteers. In conclusion, our findings suggest that Bangladeshi individuals have comparable gastric immune responses, but lower systemic antibody responses to H. pylori, compared with Swedish volunteers. Increased inflammation is present in the duodenum of Bangladeshi volunteers, maybe as a result of frequent exposure to enteric infections in these individuals.

Immunoreactivity against Goblet cells in patients with inflammatory bowel disease.

BACKGROUND: A number of autoantibodies have been reported in inflammatory bowel disease (IBD). The aim of this study was to investigate to what extent sera from patients with IBD contain autoantibodies directed against normal human gastrointestinal mucosa. METHODS: Samples of sera from 50 patients with IBD and 50 healthy subjects were used for immunostaining of normal and affected human gastrointestinal tissues. RESULTS: Eighty-four percent of the sera from IBD patients showed immunoreactivity against goblet cells in the appendix compared with 8% of the sera from healthy subjects. Goblet cell reactivity of IBD patient sera varied between regions in the gastrointestinal tract. Sera from healthy subjects only reacted with goblet cells in the appendix. In the colon and the appendix, goblet cell reactivity of IBD sera was generally weak at the base of the crypts and gradually increased toward the lumen. Three IBD sera samples reacted with gastrin cells in the antrum. In colon biopsies from patients with ulcerative colitis, immunoreactivity against the remaining goblet cells showed an inverse correlation with inflammatory activity. CONCLUSIONS: These findings suggest that immunoreactivity against goblet cells may be of central importance in the pathogenesis of IBD. Identification of goblet cell antigens could lead to a better understanding of IBD and provide a new diagnostic tool.

Alterations in antral cytokine gene expression in peptic ulcer patients during ulcer healing and after Helicobacter pylori eradication.

Earlier studies have shown that the antral immune response in Helicobacter pylori infection has a mixed Th1-Th2-T-regulatory profile. After eradication, a chronic inflammation remains in some patients, but a follow-up study with a comprehensive cytokine profile in has not previously been published. Twelve patients with H. pylori positive peptic ulcer disease (five antral and seven duodenal) were enrolled and cytokine gene expressions in antral biopsies were determined (1) at entry, (2) after resolving the ulcer with proton pump inhibitor (PPI) treatment and (3) after eradication. The second endoscopy was performed 4 weeks after ending the PPI treatment, and the third endoscopy was performed after a mean of 10 months after eradication. Inflammation was graded according to the updated Sydney system. Interleukin (IL)1beta, IL8, IL12A, IL18, TNFalpha, IFNgamma, IL4, IL6 and IL10 expression levels were analysed by real-time RT-PCR. Mixed mononuclear and neutrophil infiltrates were seen at entry and after ulcer healing. After eradication, low-grade mononuclear infiltrates were found. The cytokine expression levels after ulcer healing (H. pylori positive gastritis) were not significantly different from the levels at entry (ulcer). After eradication, attenuation of the Th1 cytokines except for TNFalpha and a persisting increase of IL4 levels were observed, whereas the IL10 expression was markedly reduced. The present data did not indicate a specific ulcer promoting cytokine gene regulation profile. However, after eradication a chronic low-grade inflammation was seen with reduced Th1, prolonged Th2 and disappearance of the T-regulatory response.

Small bowel gastric metaplasia: a report of three cases in children.

AIMS: To report three children displaying gastric metaplasia antral pyloric type of the small bowel mucosa. METHODS: Analysis of clinical, histopathological and immunohistochemical data. RESULTS: The first patient was a 14-year-old girl with history of chronic intestinal pseudo-obstruction and chronic jejunitis; the second patient was a 6-year-old girl with a long-lasting jejunostomy; and the third patient was a 5-year-old girl with ileal-rectal anastomosis. The foci of gastric metaplasia were obvious with H&E-stained sections. The cells at the gastric metaplasia mucosa proved to be MUC-1 and sialyl-Tn positive by immunohistochemistry and they were in a pattern that was different from that of the adjacent mucosa; the cells were autofluorescent in H&E-stained sections. CONCLUSIONS: Gastric metaplasia of the small bowel mucosa in these cases seems to have resulted from chronic inflammation and persistent regenerative activity. This has rarely been reported outside Crohn disease, and if ever in children.

[The participation of some innate immunological defense components in children with chronic gastritis associated H. pylori infection in ultrastructure and function of the mast cells aspects]. / Udzial niektórych elementów odpornosci wrodzonej w zapaleniu blony sluzowej zoladka z zakaieniem H. pylori u dzieci w aspekcie ultrastruktury i funkcji komórki tucznej.

UNLABELLED: It has been clearly established that Helicobacter pyloni (H. pylori) play an important role in the pathogenesis of some chronic diseases of upper gastrointestinal tract. A lot of attention to the complicated immunological processes induced by the infection was paid. The clinical outcome of the damage of gastric mucosa by H. pylori depends on the type and the intensification of these processes. During many years the acquired (specific) immunological response on the infection was analyzed by scientists, but much more researches on innate defense was done lately The mast cells constitute some important parts of the immunological innate defense. H. pylori colonization of gastric mucosal surface elicits a conspicuous infiltration comprising of lymphocytes, and plasma cells as well as neutrophils, eosinophils, macrophages and the granule cells of connective fissue. Some difficulties with the mastocytes visualization in conventional histological slides in light microscope caused so far the little attention of their participation in chronic gastritis. The aim of the study was the assessment of the mastocytes participation in the infiltration of immunological cells induced by H. pylonri in chronic gastritis. MATERIAL AND METHODS: The subjects were twenty dyspeptic children aged 9-17 years underwent upper GI endoscopy procedure. Twelve children were H. pylori positive. Remaining eight children H. pylori negative composed a control group. Gastric antrum and corpus tissue specimens in the conventional (light) and electron microscopy were examined. The specimens intended for electron microscope assessment were fixed in the solution of 1% glutaraldehyde and 2.5% paraformaldehyde at 40 C (pH 7.4) for 24 hours, and postfixed in 2% osmium tetroxide at the same conditions. Ultrathin sections were contrasted with uranyl acetate and lead citrate. Results. Ultrastructural analysis revealed two distinct, morphological forms of mast cells in gastric mucosa. All mast cells contained multiple granules with fine-grained material but their appearance was distinct in both types of these cells. Statistical analysis revealed that the count of mast cells in gastric mucosa was increased in H. pylori positive when compared with H. pylori negative children. It was also affirmed that in specimens from H. pylori infected children mast cells more frequently were seen in the gastric epithelium.

Russell body gastritis: expanding the spectrum of Helicobacter pylori - related diseases?

We report a new case of Helicobacter pylori gastritis showing plasma cell infiltrates with extensive formation of Russell bodies (Mott cells) within the lamina propria of the antral mucosa. The patient was a 60-year-old woman with a history of epigastric pain. Endoscopy revealed non-specific congestion of the mucosa. Microscopically, the intracytoplasmic inclusions were homogeneous, mainly round to oval, and pushed the nucleus toward the periphery. They were intensely PAS-positive and reacted to antibodies against polytypic light chains, CD79a, and anti-plasma cell antibody. Because of the accumulation of intracytoplasmic inclusions, Russell body gastritis is a potential source of diagnostic difficulties in endoscopic biopsy specimens that can be confused with immunocytic neoplasms, such as lymphoplasmacytic lymphoma or plasmocytoma, or signet-ring cell carcinoma. In the light of similar cases published previously, it seems as if the association between Russell body gastritis and Helicobacter pylori infection is not merely coincidental.

Atrophic autoimmune pangastritis: A distinctive form of antral and fundic gastritis associated with systemic autoimmune disease.

The 2 major recognized forms of atrophic gastritis are autoimmune and environmental atrophic gastritis. These differ in their topographical distribution in the stomach, histologic features, and etiology. Autoimmune atrophic gastritis results from immune-mediated destruction of specialized oxyntic glands, is restricted to the body and fundus, and shows characteristic neuroendocrine hyperplasia. Environmental atrophic gastritis is associated with long-standing Helicobacter pylori infection and preferentially involves antrum and transition zone mucosa. In this study, we describe a distinctive form of atrophic gastritis that differs markedly from both of these classic variants. This gastritis is characterized by: (1) intense mucosal inflammatory infiltrates, persisting even into the phase of severe glandular atrophy, (2) pangastric distribution with diffuse involvement of both body and antrum, (3) lack of association with H. pylori, and (4) lack of neuroendocrine hyperplasia. The 8 patients presented ranged from 1 to 75 years and showed a slight female predominance (5F:3M). All had systemic autoimmune and/or connective tissue diseases including autoimmune enterocolitis (4 cases), systemic lupus erythematosus, refractory sprue, autoimmune hemolytic anemia, and disabling fibromyalgia. Positive serum autoimmune markers were documented in 7 of 8 (87%) patients, but serologies for antiparietal cell and anti-intrinsic factor antibodies were undertaken in only 1 patient each and were negative. We propose that the distinctive histology of this form of atrophic pangastritis and its association with systemic autoimmune disease suggests an autoimmune process directed against multiple cell lineages in the stomach. The development of multifocal low-grade dysplasia in 1 patient, a 19-year-old woman, suggests that this condition might have neoplastic potential.