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Hepato-gastroenterology

Infection of sabA-positive H. pylori does not induce anti-Lewis X antibody in host.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala
Ingia / Ingia
Kiungo kimehifadhiwa kwenye clipboard
Fumika Nakasato
Tadashi Shimoyama
Tetsuro Yoshimura
Tatsuya Mikami
Akihiro Munakata
Shinsaku Fukuda

Maneno muhimu

Kikemikali

OBJECTIVE

H. pylori uses the sialic acid-binding adhesin (SabA) to recognize Lewis X (LeX) antigen of gastric epithelial cells. SabA is associated with nonopsonic activation of human neutrophils. The aims of this study were to examine the association of bacterial sabA status to the presence of anti-LeX antibody in host and the grade of gastritis.

METHODS

44 H. pylori strains cultured from gastric biopsies were examined by PCR for presence of 23SrRNA, cagA, and sabA. Serum samples were obtained from all the patients to measure the level of anti-LeX antibody. Histological grade of gastritis was graded according to the updated Sydney System.

RESULTS

23SrRNA gene and the cagA gene were seen in all the samples while 21 strains were sabA positive. The mean titer of anti-LeX antibody was 0.09 and 0.18 in patients infected with sabA-positive and -negative strain, respectively (NS). The grade of inflammatory infiltration was not significantly different between groups in both the corpus and the antral mucosa.

CONCLUSIONS

Possession of the sabA gene by infected H. pylori strain might not associate with the presence of anti-LeX antibody in the host. Possession of sabA gene by infected H. pylori might not associate with severity of gastric mucosal inflammation.

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