구형 Helicobacter pylori의 중성구 매개 산화활성
Neutrophil-Mediated Oxidative Activity of Coccoid Forms of Helicobacter pylori
홍원선, 김혜원, 이학성, 명승재, 정훈용, 양석균, 김진호, 민영열, 정명희,
소속 상세정보
홍원선 ( Hong Weon-Seon )
울산대학교 의과대학 내과학교실
김혜원 ( Kim Hea-Won )
울산대학교 의과대학 약리학교실
이학성 ( Lee Hak-Sung )
울산대학교 의과대학 약리학교실
명승재 ( Myung Seung-Jae )
울산대학교 의과대학 내과학교실
정훈용 ( Jung Hwoon-Yong )
울산대학교 의과대학 내과학교실
양석균 ( Yang Seok-Kyun )
울산대학교 의과대학 내과학교실
김진호 ( Kim Jin-Ho )
울산대학교 의과대학 내과학교실
민영열 ( Min Young-Il )
울산대학교 의과대학 내과학교실
정명희 ( Chung Myung-Hee )
서울대학교 의과대학 약리학교실
KMID : 0603520000050030154
Abstract
Helicobacter pylori (H. pylori) is now recognized as the major etiologic agent of chronic gastritis and plays an active role in the pathogenesis of peptic ulcer and gastric cancer. One of the characteristic features of H. pylori infection is the infiltration of neutrophils and their production of oxygen-derived free radicals (OFRs) in gastric epithelium.
H. pylori exists in two forms, spiral and coccoid form. Although spiral form is known to cause the mucosal injury by increased OFRs, it is still unclear whether coccoid form causes the OFR-mediated mucosal injury. Coccoid forms were induced by incubating spiral forms of two strains of H. pylori, ATCC 43504 (NCTC 11637) and DU-3, a clinical
isolate from a patient with duodenal ulcer, in Brucella broth media for 84 hr. Spiral forms were obtained after 36 hr incubation. The levels of OFRs were determined by luminol-dependent chemiluminescence (ChL). There was no significant difference in the production of ChL between spiral and coccoid forms of ATCC 43504 and DU-3. On the
other hand, the heat-killed H. pylori did not activate neutrophils to produce OFRs. These results suggest that not only spiral form but also coccoid form may contribute to OFR-mediated gastric mucosal injury.
키워드
pylori;Spiral form;Coccoid form;Oxygen-derived free radicals
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