scholarly journals Induction of Maturation and Cytokine Release of Human Dendritic Cells by Helicobacter pylori

2004 ◽  
Vol 72 (8) ◽  
pp. 4416-4423 ◽  
Author(s):  
Katharina Kranzer ◽  
Alexander Eckhardt ◽  
Michael Aigner ◽  
Gertrud Knoll ◽  
Ludwig Deml ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Dendritic Cells ◽  
Immune System ◽  
Immune Escape ◽  
Cell Surface Expression ◽  
Cytokine Release ◽  
Proinflammatory Response ◽  
Ulcer Disease ◽  
H Pylori ◽  
Human Dendritic Cells

ABSTRACT Helicobacter pylori causes a persistent infection in the human stomach, which can result in chronic gastritis and peptic ulcer disease. Despite an intensive proinflammatory response, the immune system is not able to clear the organism. However, the immune escape mechanisms of this common bacterium are not well understood. We investigated the interaction between H. pylori and human dendritic cells. Dendritic cells (DCs) are potent antigen-presenting cells and important mediators between the innate and acquired immune system. Stimulation of DCs with different concentrations of H. pylori for 8, 24, 48, and 72 h resulted in dose-dependent interleukin-6 (IL-6), IL-8, IL-10 and IL-12 production. Lipopolysaccharide (LPS) from Escherichia coli, a known DC maturation agent, was used as a positive control. The cytokine release after stimulation with LPS was comparable to that induced by H. pylori except for IL-12. After LPS stimulation IL-12 was only moderately released compared to the large amounts of IL-12 induced by H. pylori. We further investigated the potential of H. pylori to induce maturation of DCs. Fluorescence-activated cell sorting analysis of cell surface expression of maturation marker molecules such as CD80, CD83, CD86, and HLA-DR revealed equal upregulation after stimulation with H. pylori or LPS. We found no significant differences between H. pylori seropositive and seronegative donors of DCs with regard to cytokine release and upregulation of surface molecules. These data clearly demonstrate that H. pylori induces a strong activation and maturation of human immature DCs.

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 Comparative Analysis of the Interaction of Helicobacter pylori with Human Dendritic Cells, Macrophages, and Monocytes

2012 ◽  
Vol 80 (8) ◽  
pp. 2724-2734 ◽  
Author(s):  
Michael Fehlings ◽  
Lea Drobbe ◽  
Verena Moos ◽  
Pablo Renner Viveros ◽  
Jana Hagen ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Dendritic Cells ◽  
Inflammatory Responses ◽  
M2 Macrophages ◽  
M1 Macrophages ◽  
Content Type ◽  
Immune Evasion Mechanism ◽  
Enhanced Expression ◽  
H Pylori ◽  
Human Dendritic Cells

ABSTRACTHelicobacter pylorimay cause chronic gastritis, gastric cancer, or lymphoma. Myeloid antigen-presenting cells (APCs) are most likely involved in the induction and expression of the underlying inflammatory responses. To study the interaction of human APC subsets withH. pylori, we infected monocytes, monocyte-derived dendritic cells (DCs), and monocyte-derived (classically activated; M1) macrophages withH. pyloriand analyzed phenotypic alterations, cytokine secretion, phagocytosis, and immunostimulation. Since we detected CD163+(alternatively activated; M2) macrophages in gastric biopsy specimens fromH. pylori-positive patients, we also included monocyte-derived M2 macrophages in the study. UponH. pyloriinfection, monocytes secreted interleukin-1β (IL-1β), IL-6, IL-10, and IL-12p40 (partially secreted as IL-23) but not IL-12p70. Infected DCs became activated, as shown by the enhanced expression of CD25, CD80, CD83, PDL-1, and CCR7, and secreted IL-1β, IL-6, IL-10, IL-12p40, IL-12p70, and IL-23. However, infection led to significantly downregulated CD209 and suppressed the constitutive secretion of macrophage migration inhibitory factor (MIF).H. pylori-infected M1 macrophages upregulated CD14 and CD32, downregulated CD11b and HLA-DR, and secreted mainly IL-1β, IL-6, IL-10, IL-12p40, and IL-23. Activation of DCs and M1 macrophages correlated with increased capacity to induce T-cell proliferation and decreased phagocytosis of dextran. M2 macrophages upregulated CD14 and CD206 and secreted IL-10 but produced less of the proinflammatory cytokines than M1 macrophages. Thus,H. pyloriaffects the functions of human APC subsets differently, which may influence the course and the outcome ofH. pyloriinfection. The suppression of MIF in DCs constitutes a novel immune evasion mechanism exploited byH. pylori.

scholarly journals Helicobacter pylori Preferentially Induces Interleukin 12 (IL-12) Rather than IL-6 or IL-10 in Human Dendritic Cells

2003 ◽  
Vol 71 (7) ◽  
pp. 4163-4166 ◽  
Author(s):  
Donald G. Guiney ◽  
Patty Hasegawa ◽  
Sheri P. Cole
Keyword(s):  
Helicobacter Pylori ◽  
Dendritic Cells ◽  
Type Iv Secretion ◽  
Interleukin 12 ◽  
Th1 Cell ◽  
Type Iv ◽  
Serovar Typhimurium ◽  
H Pylori ◽  
Human Dendritic Cells ◽  
Antigen Presenting

ABSTRACT Dendritic cells are potent antigen-presenting cells that are present in the gastrointestinal tract and are required for the induction of a Th1 T-cell acquired immune response. Since infection with the gastric pathogen Helicobacter pylori elicits a Th1 cell response, the interaction of these organisms with dendritic cells should reflect the Th1 bias. We incubated H. pylori with cultured human dendritic cells and measured the cytokine induction profile, comparing the response to that induced by Salmonella enterica serovar Typhimurium. We found that H. pylori induced little interleukin 6 (IL-6) and essentially no IL-10 in contrast to S. enterica. However, H. pylori induced levels of IL-12 that were 30% of those induced by S. enterica, indicating a Th1 response. An isogenic cagE mutant of H. pylori lost about 50% of its IL-12-inducing ability, suggesting a role for the cag type IV secretion system in the stimulation of dendritic cells.

scholarly journals Gastric Microenvironment—A Partnership between Innate Immunity and Gastric Microbiota Tricks Helicobacter pylori

2021 ◽  
Vol 10 (15) ◽  
pp. 3258
Author(s):  
Cristina Oana Mărginean ◽  
Lorena Elena Meliț ◽  
Maria Oana Săsăran
Keyword(s):  
Helicobacter Pylori ◽  
Immune System ◽  
Pathogenic Bacteria ◽  
T Regulatory Cells ◽  
Inflammatory Responses ◽  
Mucosal Barrier ◽  
Pathogen Recognition ◽  
Microenvironmental Factors ◽  
H Pylori ◽  
Major Factors

Helicobacter pylori (H. pylori) carcinogenicity depends on three major factors: bacterial virulence constituents, environmental factors and host’s genetic susceptibility. The relationship between microenvironmental factors and H. pylori virulence factors are incontestable. H. pylori infection has a major impact on both gastric and colonic microbiota. The presence of non-H. pylori bacteria within the gastric ecosystem is particularly important since they might persistently act as an antigenic stimulus or establish a partnership with H. pylori in order to augment the subsequent inflammatory responses. The gastric ecosystem, i.e., microbiota composition in children with H. pylori infection is dominated by Streptoccocus, Neisseria, Rothia and Staphylococcus. The impairment of this ecosystem enhances growth and invasion of different pathogenic bacteria, further impairing the balance between the immune system and mucosal barrier. Moreover, altered microbiota due to H. pylori infection is involved in increasing the gastric T regulatory cells response in children. Since gastric homeostasis is defined by the partnership between commensal bacteria and host’s immune system, this review is focused on how pathogen recognition through toll-like receptors (TLRs—an essential class of pathogen recognition receptors—PRRs) on the surface of macrophages and dendritic cells impact the immune response in the setting of H. pylori infection. Further studies are required for delineate precise role of bacterial community features and of immune system components.

scholarly journals Identification of Markers for Helicobacter pylori Strains Isolated from Children with Peptic Ulcer Disease by Suppressive Subtractive Hybridization

2006 ◽  
Vol 74 (7) ◽  
pp. 4064-4074 ◽  
Author(s):  
Mónica Oleastro ◽  
Lurdes Monteiro ◽  
Philippe Lehours ◽  
Francis Mégraud ◽  
Armelle Ménard
Keyword(s):  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Peptic Ulcer Disease ◽  
Subtractive Hybridization ◽  
Suppressive Subtractive Hybridization ◽  
Ulcer Disease ◽  
Lipopolysaccharide Biosynthesis ◽  
The Difference ◽  
H Pylori

ABSTRACT Peptic ulcer disease (PUD) occurs after a long-term Helicobacter pylori infection. However, the disease can develop earlier, and rare cases have been observed in children, suggesting that these H. pylori strains may be more virulent. We used suppressive subtractive hybridization for comparative genomics between H. pylori strains isolated from a 5-year-old child with duodenal ulcer and from a sex- and age-matched child with gastritis only. The prevalence of the 30 tester-specific subtracted sequences was determined on a collection of H. pylori strains from children (15 ulcers and 30 gastritis) and from adults (46 ulcers and 44 gastritis). Two of these sequences, jhp0562 (80.0% versus 33.3%, P = 0.008) and jhp0870 (80.0% versus 36.7%, P = 0.015), were highly associated with PUD in children and a third sequence, jhp0828, was less associated (40.0% versus 10.0%, P = 0.048). Among adult strains, none of the 30 sequences was associated with PUD. However, both jhp0562 and jhp0870 were less prevalent in adenocarcinoma strains than in PUD strains from children and adults, the difference being statistically significant for jhp0870. In conclusion, two H. pylori genes were identified as being strongly associated with PUD in children, and their putative roles as an outer membrane protein for jhp0870 and in lipopolysaccharide biosynthesis for jhp0562, suggest that they may be novel virulence factors of H. pylori.

scholarly journals Prevalence of Helicobacter pylori infection among patients undergoing upper gastrointestinal endoscopy

2015 ◽  
Vol 3 (1) ◽  
Author(s):  
Vudumula Vijaya Lakshmi
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Normal Population ◽  
Gastric Ulcers ◽  
Upper Gastrointestinal Endoscopy ◽  
Contributing Factors ◽  
Duodenal Ulcers ◽  
Female Ratio ◽  
Ulcer Disease ◽  
H Pylori

Helicobacter pylori (H. pylori) has a role in the multifactorial etiology of peptic ulcer disease. A link between H. pylori infection and duodenal ulcer disease is now established. Other contributing factors and their interaction with the organism may initiate the ulcerative process. The fact that eradication of H. pylori infection leads to a long-term cure in the majority of duodenal ulcer patients and the fact that the prevalence of infection is higher in ulcer patients than in the normal population are cogent arguments in favor of it being the primary cause of the ulceration. This study was under taken at the Department of surgery, Narayana medical college, Nellore from January 2007 to July 2008. A total of 150 patients with duodenal ulcers, gastric ulcers, antral gastritis, gastric carcinoma and dyspepsia of any kind were studied. Maximum number of cases were in the age group of 31 years to 50 years among both sexes and number of cases gradually decreased after 50 years of age in males and females. Males were more in number and male to female ratio is (2.75:1) approximately 3:1.

scholarly journals Features of the endoscopic picture in paediatric gastroduodenal diseases caused by Helicobacter pylori

2020 ◽  
Vol 10 (3) ◽  
pp. 543-550
Author(s):  
Sh. T. Turdieva ◽  
E. A. Shamansurova
Keyword(s):  
Helicobacter Pylori ◽  
Inflammatory Diseases ◽  
Gastric Wall ◽  
Duodenogastric Reflux ◽  
Chronic Atrophic Gastritis ◽  
Endoscopic Examination ◽  
Ulcer Disease ◽  
Functional Studies ◽  
H Pylori ◽  
Endoscopic Picture

The aim of the study was to examine the features of the endoscopic picture in the upper digestive tract mucosa in paediatric chronic gastroduodenal pathology (CGDP) associated with Helicobacter pylori. Materials and methods. There were examined 286 patients, aged 6–15 years. Diagnostic criteria for chronic gastroduodenal pathology were anamnestic as well as instrumental and functional studies data: gastric fractional intubation, esophagogastroduodenoscopy (EPGDS) with endoscopic pH-metry without biopsy, and ultrasound examination of abdominal organs. H. pylori testing was carried out by two unrelated methods such as respiratory test and a immunochromatographic fecal test. Results. Detection of H. pylori in children with CGDP peaked in patients with peptic gastric and duodenal ulcer (up to 87.5%, p < 0.05). The main endoscopic signs were edema, hyperaemia and contact bleeding, as well as local haemorrhage were the major endoscopic signs of inflammation in the stomach and duodenum mucosa. Atrophic mucosal lesions were characterized by thinning, pale colour together with transilluminated submucosal vessels. Non-atrophic antral gastritis was featured with delayed gastric emptying, antral stasis and pyloric spasm. In contrast, hypotension of the gastric wall, duodenogastric reflux and decreased motility were more typical to chronic atrophic gastritis. Major endoscopic feature in patients with H. pylori infection was presented by dominant atrophic changes combined with gastroduodenal reflux (77.6%, p < 0.05) compared to patients without H. pylori infection. Conclusion. Detection of HP infection was peaked in children with CGDP coupled to peptic ulcer disease compared to patients with inflammatory diseases (p < 0.05). Endoscopic examination in HP-positive patients showed that atrophic changes were found by 4-fold more frequently together with gastroduodenal reflux compared to patients without HP infection (p < 0.05).

Atypical presentation at acute gastritis: significant gastric wall thickening as a presentation of a primary Helicobacter pylori infection in children

2021 ◽  
Vol 14 (7) ◽  
pp. e243912
Author(s):  
Kiyokuni Nakamura ◽  
Ryo Tamura ◽  
Yoshitomi Yasui ◽  
Hideaki Okajima
Keyword(s):  
Helicobacter Pylori ◽  
Epigastric Pain ◽  
Gastric Wall ◽  
Malignant Tumour ◽  
Wall Thickening ◽  
Atypical Presentation ◽  
Negative Consequences ◽  
Ulcer Disease ◽  
Acute Gastritis ◽  
H Pylori

Helicobacter pylori infection could cause chronic inflammation in the stomach and induce peptic ulcer disease or even malignant tumour. The initial infection of the organism happens in childhood but most of cases are latent. We had a case of 10-year-old girl who presented with acute epigastric pain and significant thickening of the stomach wall on CT. The finding seemed atypical for acute gastritis so oesophagogastroduodenoscopy and serology examination were added and the primary infection of H. pylori was confirmed with the exclusion of other possible diagnoses like eosinophilic gastritis and IgA vasculitis. Acute gastritis is one of the most common sickness in children, however, it would be worthwhile considering further investigation including H. pylori infection in a case of atypical presentation to prevent negative consequences derived from chronic H. pylori infection.

Pattern recognition receptors and their roles in the host response to Helicobacter pylori infection

2021 ◽  
Author(s):  
Ileana Gonzalez ◽  
Paulina Araya ◽  
Ivan Schneider ◽  
Cristian Lindner ◽  
Armando Rojas
Keyword(s):  
Pattern Recognition ◽  
Helicobacter Pylori ◽  
Host Response ◽  
Pattern Recognition Receptors ◽  
Innate Immune ◽  
Host Cells ◽  
Proinflammatory Response ◽  
H Pylori ◽  
Cancer Pattern ◽  
Main Pattern

Helicobacter pylori ( H. pylori) infection is highly prevalent, affecting 4.4 billion people globally. This pathogen is a risk factor in the pathogenesis of more than 75% of worldwide cases of gastric cancer. Pattern recognition receptors are essential in the innate immune response to H. pylori infection. They recognize conserved pathogen structures and myriad alarmins released by host cells in response to microbial components, cytokines or cellular stress, thus triggering a robust proinflammatory response, which is crucial in H. pylori-induced gastric carcinogenesis. In this review, we intend to highlight the main pattern recognition receptors involved in the recognition and host response to H. pylori, as well as the main structures recognized and the subsequent inflammatory response.

Helicobacter pylori causes gastrointestinal hemorrhage in patients with congenital bleeding disorders

2003 ◽  
Vol 89 (04) ◽  
pp. 741-746 ◽  
Author(s):  
Ann-Sofie Rehnberg ◽  
Marju Hein ◽  
Olga Hegedus ◽  
Per Lindmarker ◽  
Per Hellström ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastrointestinal Hemorrhage ◽  
Breath Test ◽  
Eradication Therapy ◽  
Urea Breath Test ◽  
Von Willebrand Disease ◽  
Bleeding Disorders ◽  
Ulcer Disease ◽  
H Pylori ◽  
One Year

Summary Helicobacter pylori (H. pylori) infection is associated with peptic ulcer disease and gastric cancer. The eradication of H. pylori is of special interest in patients with congenital bleeding disorders, for whom treatment of gastrointestinal hemorrhage with factor concentrates is costly. The prevalence of H. pylori varies between different populations and identification of high-risk subgroups may allow for more targeted screening and eradication of the infection. We performed a 5-year retrospective study of gastrointestinal bleeding, combined with screening and treatment for H. pylori and a long-term prospective follow-up in 168 Swedish and 23 Estonian patients with hemophilia or von Willebrand disease. The prevalence of seropositivity was lower in Sweden than in Estonia (28 versus 48%, p = 0.03), lower in native Swedes than in non-Nordic immigrants to Sweden (20 versus 76%, p = 0.0001) and lower in patients less than 40 years of age than older patients (16 versus 38%, p = 0.002). The incidence of gastrointestinal hemorrhages among the 35 Swedish patients with active H. pylori infection, confirmed by a urea breath test, was 6.0 per 100 patient-years before eradication therapy versus 1.7 during the prospective followup. A negative urea breath test one month after therapy always remained negative after one year. Screening, followed by treatment of all infected patients, yielded a reduction of direct costs over a 5-year period of 130 US-$ per screened patient. We conclude that screening and eradication therapy for infection with H. pylori in patients with congenital bleeding disorders is an effective and economic strategy.

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