LOCAL CYTOKINE AND THE CD74 EXPRESSION IN THE HELICOBACTER PYLORI ASSOCIATED GASTRITIS (original) (raw)
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Helicobacter pylori Binds to CD74 on Gastric Epithelial Cells and Stimulates Interleukin8 Production
Infection and Immunity, 2005
The pathogenesis associated with Helicobacter pylori infection requires consistent contact with the gastric epithelium. Although several cell surface receptors have been suggested to play a role in adhesion, the bacterium-host interactions that elicit host responses are not well defined. This study investigated the interaction of H. pylori with the class II major histocompatibility complex (MHC)-associated invariant chain (Ii; CD74), which was found to be highly expressed by gastric epithelial cells. Bacterial binding was increased when CD74 surface expression was increased by gamma interferon (IFN-␥) treatment or by fibroblast cells transfected with CD74, while binding was decreased by CD74 blocking antibodies, enzyme cleavage of CD74, and CD74-coated bacteria. H. pylori was also shown to bind directly to affinity-purified CD74 in the absence of class II MHC. Cross-linking of CD74 and the engagement of CD74 were verified to stimulate IL-8 production by unrelated cell lines expressing CD74 in the absence of class II MHC. Increased CD74 expression by cells increased IL-8 production in response to H. pylori, and agents that block CD74 decreased these responses. The binding of H. pylori to CD74 presents a novel insight into an initial interaction of H. pylori with the gastric epithelium that leads to upregulation of inflammatory responses.
Fems Immunology and Medical Microbiology, 2003
Helicobacter pylori is an important pathogen in gastroduodenal inflammation and ulceration. Several mechanisms have been proposed to explain its role. We studied the cytokine production patterns in situ in gastric mucosal biopsies from H. pylori-positive and H. pylorinegative patients with dyspepsia. Immunohistochemistry with monoclonal antibodies was used. The study showed enhanced expression of interleukin (IL) -8, IL-10 and interferon-Q (IFN-Q) in H. pylori infection and a significant association was found between these cytokines and the following parameters: bacteria load, chronic inflammation and activity. These parameters were significantly correlated with the cell markers CD19 and CD56. The study indicates a dual effect of H. pylori on the Th1 response, i.e. a stimulation of the response verified by increased IFN-Q and a feed-back verified by an increase of the counterinflammatory IL-10, which may dampen the inflammatory and cytotoxic effect of the Th1 response. Furthermore, the study confirms the connection between increase of IL-8 and inflammatory activity in gastric mucosa in H. pylori infection.
Gut, 1991
The production of tumour necrosis factor a (TNF a) and interleukin-6 by human antral mucosa during short term culture in vitro has been measured by enzyme linked immunosorbent assay. TNF a and interleukin-6 concentrations in culture supernatants were significantly greater (p<0001) in patients infected with Helicobacter pylon, all of whom had chronic gastritis, than in patients who were H pylori negative with histologically normal gastric mucosa. Among H pylon colonised patients, TNF a concentrations were significantly higher in those with active gastritis and neutrophil infiltration into the epithelium than in those with inactive gastritis. In contrast, interleukin-6 concentrations were raised in both active and inactive gastritis. This study shows that H pylon gastritis is associated with increased gastric mucosal production of TNF a and interleukin-6 and that the nature of the mucosal cytokine response varies with the immunohistology of the disease. Inflammatory cytokines generated locally within the gastric mucosa could be relevant to the gastric physiology of H pylon infection.
Comparison of IL-6, IL-8 Concentrations in H. pylori- and non-H. pylori-associated Gastritis
The Indonesian Biomedical Journal, 2014
BACKGROUND: Helicobacter pylori is a non-invasive microorganism causing intense gastric mucosal inflammatory and immune reaction. The gastric mucosal levels of the proinflammatory cytokines Interleukin 6 (IL-6) and IL-8 have been reported to be increased in H. pylori infection, but the serum levels in H. pylori infection is still controversial. The purpose of this study was to investigate the serum levels of IL-6 and IL-8 in H. pylori infection.METHODS: A cross sectional study was done on eighty consecutive gastritis patients admitted to endoscopy units at Adam Malik General Hospital and Permata Bunda Hospital, Medan, Indonesia from May-October 2014. Histopathology was performed for the diagnosis of gastritis. Rapid urease test for diagnosis of H. pylori infection. Serum samples were obtained to determine circulating IL-6 and IL-8. Univariate and bivariate analysis (independent t test) were done.RESULTS: There were 41.25% patients infected with H. pylori. Circulatory IL-6 levels wer...
Gastroenterology, 1995
Background~Aims: Helicobacter pylori is associated with neutrophil infiltrates, although the mechanism of their recruitment is only partially defined. The aim of the study was to determine if Kato III, a human gastric epithelial cell line, expressed cytokines and the intercellular adhesion molecule 1 (ICAM-1), which could contribute to the initiation of inflammation during infection with H. pylori. Methods: Kato III cells were stimulated with H. pylori and were examined for evidence of infection, cytokine production, and the expression of ICAM-I. Results: The expression of interleukin 8 messenger RNA and immunoreactive protein by Kato III cells was significantly increased over constitutive levels within 3 hours of infection with H. pylori. Infected
Helicobacter pylori cagA gene and expression of cytokine messenger RNA in gastric mucosa
Gastroenterology, 1996
Background & Aims: Helicobacter pylori strains posscription polymerase chain reaction (RT-PCR) method sessing the cagA gene are thought to be associated and found that the levels of expression of IL-7 and IL-8 with gastroduodenal diseases. Furthermore, some cy-mRNA were significantly higher in mucosa with H. pytokines are considered to play a role in gastric mucosal lori-positive gastritis than in H. pylori-negative normal inflammation. The aim of this study was to investigate mucosa. 9 IL-6 and IL-10 messenger RNA (mRNA) exthe relationship between cagA gene and cytokine mespression levels were also slightly higher in H. pylorisenger RNA (mRNA) expression in gastric mucosa.
Helicobacter pylori: Bacterial Factors and the Role of Cytokines in the Immune Response
Current Microbiology, 2010
Helicobacter pylori is a gram-negative microaerophilic bacterium that is widely distributed geographically and causes chronic gastritis, peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. Bacterial virulence factors play an important role, since the virulent strains are more aggressive and increase the risk of developing severe clinical manifestations; in addition, other determinant factors are the nutritional state and the immune response of the host. Studies on humans, non-human primates, and rodents have reported that regulating proteins of the Th1 phenotype predominate in the immune response to the bacterial infection. The cytokines produced by this phenotype, are not very effective in eradicating the microorganism and furthermore, contribute to gastro-duodenal pathogenesis. Gastric inflammation in patients infected with H. pylori has been characterized by increased production of IL-1, IL-6, IL-12, IL-18, TNF-a, and IFN-c. Many prophylactic and therapeutic strategies have been researched using experimental animals. The utilization and effectiveness of vaccination on humans requires more study.
International Journal of Clinical & Laboratory Research, 1996
It is thought thatHelicobacter pylori colonization of the gastric mucosa might stimulate the production of several cytokines, which might trigger and maintain the gastric inflammation associated withHelicobacter pylori infection. In the present study we evaluated interleukin-1β, interleukin-6, and the soluble receptor of interleukin-2 both in mucosal homogenates and in the sera ofHelicobacter pylori-infected (39 cases) and uninfected (40 cases) patients to investigate whether there was any relationship between variations in cytokines and (1) the severity ofHelicobacter pylori-associated gastritis or (2) CagA-positiveHelicobacter pylori strains. Mucosal, but not serum levels of interleukins-1 and-6 and interleukin-2 receptor were significantly higher in infected than uninfected patients, Serum levels ofHelicobacter pylori antibodies were significantly higher in infected than uninfected patients, These levels correlated with mucosal interleukin-1β. The degree of antral or body inflammatory grade was higher in infected than in uninfected patients; cytokines levels were higher in patients with high-grade gastritis, most of whom wereHelicobacter pylori positive. Patients infected with CagA-positive strains also had higher levels of interleukin-1β, but not of interleukin-2 receptor or interleukin-6. In conclusion,Helicobacter pylori infection results in a local increase in interleukins-1β and-6 and interleukin-2 receptor associated with high-grade mucosal inflammation. Interleukin-1β seems to favor anti-Helicobacter pylori antibody production, and mucosal levels are enhanced mainly in patients infected with cytotoxicHelicobacter pylori strains.