scholarly journals BACTERIAL SYMBIOSIS IN COMPLICATED ULCERS: THE PATHOGENETIC HYPOTHESIS

2021 ◽  
Vol 11 (2) ◽  
pp. 26-27
Author(s):  
Andrew Martusevich ◽  
Gulnar Orudzhova ◽  
Anastasia Romanova ◽  
Oksana Shubina
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Microbial Contamination ◽  
Mucosal Damage ◽  
Healthy Individuals ◽  
Ulcer Disease ◽  
Stomach Mucosa ◽  
Bacterial Symbiosis ◽  
Mucosal Layer ◽  
Dual Contamination

Aim of this paper is to estimate crystallogenic properties of gastric mucosa in connection with its microbial contamination. We investigated crystallogenic properties of some biological substrata (gastric mucosa, gastric mucosal layer homogenates) in 12 healthy individuals and 30 patients with ulcer disease complicated in 12 cases by perforation, bleeding or penetration. Biological substrata were received at fibrogastroduodenoscopy. Estimation of crystallogenic properties of biological material was accomplished by classic crystalloscopy. Biological substrata crystalloscopic investigation was accompanied by its traditional microbiological study for Helicobacter pylori and detection of other microorganisms. Our data allow to suppose dual contamination of stomach mucosa both by Helicobacter pylori and Providencia or Morganella. This combination caused elevation of gastric mucosa crystallogenic properties that provoked formation of ulcer. Procrystallogenic potential of this symbiosis may be an important link to the pathogenesis of ulcer disease which realized through microorganism-associated mucosal damage and the progression of complications.

scholarly journals Relationship Between Mucosal TNF-α Expression and Th1, Th17, Th22 and Treg Responses in Helicobacter Pylori Infection

2021 ◽  
Author(s):  
Ghorbanali Rahimian ◽  
Milad Shahini Shams Abadi ◽  
Reza Ahmadi ◽  
Mohammedhadi Shafigh ◽  
Fatemeh Azadegan-Dehkordi
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Treg Cells ◽  
Infected Group ◽  
Ulcer Disease ◽  
Tnf Α ◽  
H Pylori ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background: Helicobacter pylori (H. pylori) -induced gastric inflammation in the gastric mucosa and significantly increases the risk of developing gastritis and peptic ulcer disease (PUD). The objective of this research is to determine the role of tumor necrosis factor-α (TNF-α) expression in the gastric mucosa of patients with H. pylori –associated gastritis and PUD compared to uninfected patients, and we determined the relation between TNF-α expression and Th1/Th17/Th22, and Treg cells.Methods: Fifty-five patients with H. pylori –associated gastritis, 47 patients with H. pylori –associated PUD, and 48 uninfected patients were in this research. Antrum biopsy was used to detect H. pylori, virulence factors and histopathological assessments.Results: Expression of TNF-α in the infected group was significantly higher than the uninfected group. Also, cagA/oipA-positive infected patients induce significantly more TNF-α expression than do cagA/oipA-negative infected patients. Expression of TNF-α was significantly increased in the PUD group than the gastritis group. Notably, TNF-α expression had a significant positive correlation with the frequency of Th1/Th17/Th22 lymphocytes in the PUD group.Conclusion: These findings indicate the importance of increasing TNF-α with Th1, Th17, Th22 responses increase as an important risk factor for PUD in context of H. pylori infection.

scholarly journals Follow-up analysis and histopathological study of gastric mucosa in patients with Helicobacter pylori infection

2021 ◽  
Vol 49 (12) ◽  
pp. 030006052110553
Author(s):  
Guang Zhao ◽  
Zhishang Zhang ◽  
Baohui Li ◽  
Silin Huang ◽  
Wensi Li ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Intraepithelial Neoplasia ◽  
Mucosal Damage ◽  
Helicobacter Pylori Infection ◽  
Gastric Mucosal Damage ◽  
Histopathological Study ◽  
Significant Difference ◽  
H Pylori

Objective To investigate the histomorphological characteristics of the gastric mucosa and the prognosis in patients with Helicobacter pylori infection. Methods Progressive damage to the gastric mucosa was examined by immunohistochemistry in 2294 patients with H. pylori infection and follow-up information was analyzed. Results H. pylori initially colonized the mucus layer covered by the gastric mucosa epithelium, then selectively adhered to and destroyed the surface mucus cells causing intra-gastric and extra-gastric lesions. Gastric mucosal damage induced by H. pylori was divided into five stages according to the depth of H. pylori invasion and degree of lesion deterioration: mucilaginous, surface mucocellular, lamina propria lesion, mucosal atrophy, and intraepithelial neoplasia stages. Morphological follow-up analysis revealed no significant difference in 6-month curative effects between stage I and stage II, but significant differences were found between stages II and III, stages III and IV, and between stages IV and stage V, respectively. Conclusions This novel staging strategy may be a valuable tool for diagnosing and predicting the results of gastric mucosal damage induced by H. pylori infection.

scholarly journals Detection of Anti-CagA Antibodies in Sera of Helicobacter pylori-Infected Patients Using an Immunochromatographic Test Strip

2019 ◽  
Vol 58 (3) ◽  
pp. 217-222
Author(s):  
Cebrail Karakus ◽  
Zeynep Ulupinar ◽  
Fahri Akbas ◽  
Duygu Yazici
Keyword(s):  
Helicobacter Pylori ◽  
Test Strip ◽  
Mucosal Damage ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Line ◽  
Immunochromatographic Test ◽  
Caga Gene ◽  
Serum Samples ◽  
Ulcer Disease ◽  
H Pylori

Abstract The cagA gene of Helicobacter pylori that encodes an immunodominant CagA protein provokes severe mucosal damage and acts as a risk factor for the development of peptic ulcer disease and gastric cancer. Our aim is to develop an immunochromatographic test strip (ICTS) using our previously developed recombinant CagA (rCagA) protein and anti-rCagA monoclonal antibody (Mab) for the detection of anti-CagA antibodies in sera of infected patients. The rCagA was firstly conjugated to gold nanoparticle and placed into the conjugate pad. A nonconjugated rCagA and anti-rCagA Mab (CK-02) were immobilized on the test line and control line, respectively. Biopsy and serum samples from 30 H. pylori-infected patients were used. The presence of cagA gene in biopsy samples was first detected by PCR (Polymerase Chain Reaction), and 22 patients were found positive while 8 were negative. When serum samples were tested by our developed ICTS, 21 were positive for anti-CagA antibodies while 9 were negative. The serum samples were also tested by a commercial ELISA (Enzyme Linked Immunosorbent Assay), and when compared to the ICTS a sensitivity of 95% and a specificity of 100% were obtained. The ICTS can be used for rapid detection of CagA-positive H. pylori infection instead of expensive, time consuming and laborious invasive approaches.

scholarly journals DC-LAMP+Dendritic Cells Are Recruited to Gastric Lymphoid Follicles in Helicobacter pylori-Infected Individuals

2013 ◽  
Vol 81 (10) ◽  
pp. 3684-3692 ◽  
Author(s):  
Malin Hansson ◽  
Malin Sundquist ◽  
Susanne Hering ◽  
B. Samuel Lundin ◽  
Michael Hermansson ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Dendritic Cells ◽  
Gastric Mucosa ◽  
Human Gastric Mucosa ◽  
Lymphoid Follicles ◽  
Content Type ◽  
Ulcer Disease ◽  
Hla Dr ◽  
H Pylori ◽  
Antigen Presenting

ABSTRACTInfection withHelicobacter pyloriis associated with development of ulcer disease and gastrointestinal adenocarcinoma. The infection leads to a large infiltration of immune cells and the formation of organized lymphoid follicles in the human gastric mucosa. Still, the immune system fails to eradicate the bacteria, and the substantial regulatory T cell (Treg) response elicited is probably a major factor permitting bacterial persistence. Dendritic cells (DCs) are professional antigen-presenting cells that can activate naive T cells, and maturation of DCs is crucial for the initiation of primary immune responses. The aim of this study was to investigate the presence and localization of mature human DCs inH. pylori-infected gastric mucosa. Gastric antral biopsy specimens were collected from patients withH. pylori-associated gastritis and healthy volunteers, and antrum tissue was collected from patients undergoing gastric resection. Immunohistochemistry and flow cytometry showed that DCs expressing the maturation marker dendritic cell lysosome-associated membrane glycoprotein (DC-LAMP; CD208) are enriched in theH. pylori-infected gastric mucosa and that these DCs are specifically localized within or close to lymphoid follicles. Gastric DC-LAMP-positive (DC-LAMP+) DCs express CD11c and high levels of HLA-DR but little CD80, CD83, and CD86. Furthermore, immunofluorescence analyses demonstrated that DC-LAMP+DCs are in the same location as FoxP3-positive putative Tregs in the follicles. In conclusion, we show that DC-LAMP+DCs with low costimulatory capacity accumulate in the lymphoid follicles in humanH. pylori-infected gastric tissue, and our results suggest that Treg-DC interactions may promote chronic infection by rendering gastric DCs tolerogenic.

scholarly journals Detection of Helicobacter suis bacteria in pigs of different age groups

2021 ◽  
pp. 266-271
Author(s):  
F. M. Nurgaliev
Keyword(s):  
Gastric Ulcer ◽  
Gastric Mucosa ◽  
Age Groups ◽  
Biochemical Tests ◽  
Ulcer Disease ◽  
Stomach Mucosa ◽  
Suckling Piglets ◽  
Ulcerative Lesions ◽  
Fattening Pigs

Currently, the pathogenesis of gastric ulcer in pigs remains largely unexplored. The origin of this pathology is most often associated with the type and the technologies of feeding, stresses and disorders of homeostasis of the animal body. The possible involvement of bacteria of the genus Helicobacter in the development of chronic gastritis and gastric ulcer disease in pigs was suggested by the researchers relatively recently. The article comprises the results of investigations aimed at detection of Helicobacter suis bacteria and the contamination degree of porcine gastric mucosa in pigs of different age groups. The stomachs, obtained from suckling pigs, fattening pigs and sows in the slaughterhouse of the Mari El Republic, were examined. The study determined the dependence of pathomorphological changes in the gastric mucosa of pigs on the detection of H. suis in microscopic and biochemical tests as well as in PCR. Thus, no pathomorphological changes in the gastric mucosa of suckling pigs were detected. Severe hyperkeratosis, erosions, and ulcers were found on the stomach mucosa of fattening pigs and sows that were infected with H. suis bacteria. Sows also had ulcerative lesions in the non-glandular region of esophagus. In the biomaterial of suckling piglets the DNA of H. suis bacteria was found only in the pyloric region of the stomach, while in fattening pigs, the DNA of these bacteria was most often isolated from the fundal region, and in sows – from the fundal and cardial regions. This indicates a shift in colonization by helicobacters of the mucous membrane of the stomach from the pyloric to the cardiac sectionincreased with animal age. The obtained research data provide the additional evidence of the etiological role of H. suis in the pathogenesis of gastric ulcer in pigs.

scholarly journals Helicobacter pylori Induces Transendothelial Migration of Activated Memory T Cells

2005 ◽  
Vol 73 (2) ◽  
pp. 761-769 ◽  
Author(s):  
Karin Enarsson ◽  
Mikael Brisslert ◽  
Steffen Backert ◽  
Marianne Quiding-Järbrink
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
Helicobacter Pylori ◽  
T Cell ◽  
Gastric Mucosa ◽  
Memory T Cells ◽  
Umbilical Vein ◽  
Transendothelial Migration ◽  
Ulcer Disease ◽  
H Pylori

ABSTRACT Helicobacter pylori infection is associated with pronounced infiltration of granulocytes and lymphocytes into the gastric mucosa, resulting in active chronic gastritis that may develop into duodenal ulcer disease or gastric adenocarcinoma. Infiltrating T cells play a major role in the pathology of these diseases, but the signals involved in recruitment of T cells from blood to H. pylori-infected tissues are not well understood. We therefore examined H. pylori-induced T-cell transendothelial migration (TEM). The Transwell system, employing a monolayer of human umbilical vein endothelial cells, was used as a model to study TEM. H. pylori induced a significant T-cell migration, compared to spontaneous migration. CD4+ and CD8+ T cells migrated to the same extent in response to H. pylori, whereas there was significantly larger transmigration of memory T cells compared to naive T cells. Both H. pylori culture filtrate and urease induced migration, and the presence of the H. pylori cag pathogenicity island increased TEM. T-cell TEM was mediated by LFA-1-ICAM-1 interactions in accordance with an increased ICAM-1 expression on the endothelial cells after contact with H. pylori. Migrating T cells had increased expression of activation marker CD69 and chemokine receptors CXCR3, CCR4, and CCR9. Furthermore, T cells migrating in response to H. pylori secreted Th1 but not Th2 cytokines upon stimulation. In conclusion, our data indicate that live H. pylori and its secreted products contribute to T-cell recruitment to the gastric mucosa and that the responding T cells have an activated memory Th1 phenotype.

scholarly journals CCL28 Is Increased in Human Helicobacter pylori-Induced Gastritis and Mediates Recruitment of Gastric Immunoglobulin A-Secreting Cells

2008 ◽  
Vol 76 (7) ◽  
pp. 3304-3311 ◽  
Author(s):  
Malin Hansson ◽  
Michael Hermansson ◽  
Helena Svensson ◽  
Anders Elfvin ◽  
Lars-Erik Hansson ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
B Cell ◽  
Immunoglobulin A ◽  
Receptor Expression ◽  
Cell Populations ◽  
Ulcer Disease ◽  
Migratory Pattern ◽  
H Pylori ◽  
Transwell System

ABSTRACT Human Helicobacter pylori infection gives rise to an active chronic gastritis and is a major risk factor for the development of duodenal ulcer disease and gastric adenocarcinoma. The infection is accompanied by a large accumulation of immunoglobulin A (IgA)-secreting cells in the gastric mucosa, and following mucosal immunization only H. pylori-infected volunteers mounted a B-cell response in the gastric mucosa. To identify the signals for recruitment of gastric IgA-secreting cells, we investigated the gastric production of CCL28 (mucosa-associated epithelial chemokine) and CCL25 (thymus-expressed chemokine) in H. pylori-infected and uninfected individuals and the potential of gastric B-cell populations to migrate toward these chemokines. Gastric tissue from H. pylori-infected individuals contained significantly more CCL28 protein and mRNA than that from uninfected individuals, while CCL25 levels remained unchanged. Chemokine-induced migration of gastric lamina propria lymphocytes isolated from patients undergoing gastric resection was then assessed using the Transwell system. IgA-secreting cells and IgA+ memory B cells from H. pylori-infected tissues migrated toward CCL28 but not CCL25, while the corresponding cells from uninfected patients did not. Furthermore, IgG-secreting cells from H. pylori-infected patients did not migrate to CCL28 but instead to CXCL12 (SDF-1α). However, chemokine receptor expression did not correlate to the migratory pattern of the different B-cell populations. These studies are the first to show increased CCL28 production during gastrointestinal infection in humans and provide an explanation for the large influx of IgA-secreting cells to the gastric mucosa in H. pylori-infected individuals.

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