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Helicobacter pylori cytotoxin-associated gene A impairs the filtration barrier function of podocytes via p38 MAPK signaling pathway

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Yang M., Wang L., Gu L.-j., Yuan W.-j.
Acta Biochimica Polonica
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2017
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vol. 64
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issue 3
471-475
EN
Helicobacter pylori (Hp) specific antigens were found deposited in the glomeruli in some kidney diseases. However, the underlying molecular mechanisms remain to be elucidated. The aim of this study was to investigate the effect of cytotoxin associated gene A protein (CagA), a key virulence factor of Hp, on mouse podocytes. Cells were cultured and treated with recombinant CagA protein. The expression of the tight junction protein ZO-1 and p38 MAPK signaling pathway activation were measured with real-time RT-PCR and western blotting. The filtration barrier function of podocytes was evaluated with albumin influx assay. CagA decreased the expression and membrane distribution of ZO-1, impaired the filtration barrier function of podocytes, while activating p38 MAPK signaling pathway in these cells. Selective p38 MAPK inhibition partly prevented CagA-induced filtration barrier dysfunction of podocytes through ameliorating ZO-1 downregulation. Taken together, the results suggested that CagA, at least via p38 MAPK signaling pathway, may induce podocyte injury. Anti-Hp therapy may be beneficial for the treatment of kidney diseases related to Hp antigen deposition.
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Helicobacter pylori isolation, serology and cagA, cagE and virB11 detection in patients with non-ulcer dyspepsia from Turkey: Correlation with histopathologic findings

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Ilga U., Ozyurt M., Yildirim S., Ergunay K., Ardic N., Demirturk L., Haznedaroglu T.
Open Medicine
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2008
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vol. 3
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issue 1
41-46
EN
Colonization with Helicobacter pylori (HP) may have major clinical consequences and HP virulence factors are associated with more severe gastroduodenal pathologies. In this study, prevalence of HP in patients with Non-Ulcer Dyspepsia (NUD) was determined by rapid urease test and culture and correlations of histopathologic changes with bacterial virulence factors and serologic profiles were investigated. Gastric biopsies from sixty-nine patients admitted to Haydarpasa Training Hospital Department of Gastroenterology were evaluated for rapid urease, HP isolation and examined histopathologically. PCR was employed for HP confirmation and detection of HP cagA, cagE and virB11 genes. For each patient, IgG and IgA antibodies and anti-cagA antibodies were also determined by ELISA tests. HP was isolated and confirmed by PCR in 74% (51/69) of the patients. Anti-HP IgG and IgA were detected in 96% (49/51) and 53% (27/51), respectively. Anti-cagA were present in 51% (26/51). cagA, cagE and virB11 were positive in 56.8% (29/51), 60.7% (31/51) and 58.8% (30/51) of the patients, respectively. Statistically significant correlation was observed between cagA PCR and inflammation/activity scores. Detection of cagA by molecular assays can be an alternative test that can be employed for individual patient assessment.
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