2002Academic Journal of Second Military Medical UniversityRequires access

Difference of cag pathogenicity island splitand IS60 5 detected in Chinese Helicobacter pylori strains

Xu Guo

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Abstract

Objective:To investigate the role of IS6 0 5 in cag pathogenicity island split in Chinese H elicobacter pylori (Hp) strains.Methods:Cag A and conjunction of cag and cag in cag pathogenicity island and IS6 0 5 was amplified by polymerase chain reaction(PCR) in 10 7Hp strains isolated from Chinese patients. Results:The expected 2 98bp am plicom to cag A was identified in 99strains,while 2 2 8bp products to conjunction of cag and cag was in 5 strains,and 116 7bp fragm ent to IS6 0 5 was in 4 7strains. The rate of IS6 0 5 detected did not match that of split cag pathogenicity islands. Detectable rate of IS6 0 5 was lower in duodenal ulcer than in gastritis(P 0 ,0 5 ) ,and detectable rate of contiguous cag pathogenicity island was higher in duodenal ulcer than in gastritis (P0 .0 1) . Conclusion:The cag pathogenicity island split is not corresponding to detectable IS6 0 5 ,suggesting conjunction between cag and cag can be split by other genetic element besides IS6 0 5 ,cag pathogenicity island split and IS6 0 5 insertion m ay reduce the gradient virulence of Hp. [

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Objective:To investigate the role of IS6 0 5 in cag pathogenicity island split in Chinese H elicobacter pylori (Hp) strains.Methods:Cag A and conjunction of cag and cag in cag pathogenicity island and IS6 0 5 was amplified by polymerase chain reaction(PCR) in 10 7Hp strains isolated from Chinese patients. Results:The expected 2 98bp am plicom to cag A was identified in 99strains,while 2 2 8bp products to conjunction of cag and cag was in 5 strains,and 116 7bp fragm ent to IS6 0 5 was in 4 7strains. The rate of IS6 0 5 detected did not match that of split cag pathogenicity islands. Detectable rate of IS6 0 5 was lower in duodenal ulcer than in gastritis(P 0 ,0 5 ) ,and detectable rate of contiguous cag pathogenicity island was higher in duodenal ulcer than in gastritis (P0 .0 1) . Conclusion:The cag pathogenicity island split is not corresponding to detectable IS6 0 5 ,suggesting conjunction between cag and cag can be split by other genetic element besides IS6 0 5 ,cag pathogenicity island split and IS6 0 5 insertion m ay reduce the gradient virulence of Hp. [

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Available abstract

Objective:To investigate the role of IS6 0 5 in cag pathogenicity island split in Chinese H elicobacter pylori (Hp) strains.Methods:Cag A and conjunction of cag and cag in cag pathogenicity island and IS6 0 5 was amplified by polymerase chain reaction(PCR) in 10 7Hp strains isolated from Chinese patients. Results:The expected 2 98bp am plicom to cag A was identified in 99strains,while 2 2 8bp products to conjunction of cag and cag was in 5 strains,and 116 7bp fragm ent to IS6 0 5 was in 4 7strains. The rate of IS6 0 5 detected did not match that of split cag pathogenicity islands. Detectable rate of IS6 0 5 was lower in duodenal ulcer than in gastritis(P 0 ,0 5 ) ,and detectable rate of contiguous cag pathogenicity island was higher in duodenal ulcer than in gastritis (P0 .0 1) . Conclusion:The cag pathogenicity island split is not corresponding to detectable IS6 0 5 ,suggesting conjunction between cag and cag can be split by other genetic element besides IS6 0 5 ,cag pathogenicity island split and IS6 0 5 insertion m ay reduce the gradient virulence of Hp. [

Key concepts: Pathogenicity island, Pathogenicity, Virulence, Microbiology, Helicobacter pylori, Biology, Polymerase chain reaction, Gastritis

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