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Comparison between in vivo and in vitro chemokine production in Helicobacter pylori infection
Author(s) -
Ohsuga M.,
Kusugami K.,
Ina K.,
Ando T.,
Yamaguchi H.,
Imada A.,
Nishio Y.,
Shimada M.,
Tsuzuki T.,
Noshiro M.,
Konagaya T.,
Kaneko H.
Publication year - 2000
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.2000.014s1205.x
Subject(s) - caga , helicobacter pylori , chemokine , in vivo , gastritis , in vitro , immunology , gastric mucosa , biology , organ culture , antrum , microbiology and biotechnology , medicine , stomach , immune system , gastroenterology , gene , virulence , biochemistry
Summary Background : Enhanced gastric mucosal chemokine activity has been demonstrated in patients with Helicobacter pylori infection. However, little is known about the mechanisms involved in this phenomenon. Aim : To examine whether in vivo chemokine activity is similar to in vitro response of gastric epithelial cells infected by H. pylori . Patients and Methods : Antral biopsy specimens were obtained from patients with H. pylori infection for organ culture, isolation of H. pylori and histological examination. Results : In organ cultures of mucosal tissues, the levels of interleukin‐8 and growth‐related gene product α were elevated in patients with peptic ulcer disease compared with those with erosive gastritis or endoscopically normal mucosa. However, there were no significant differences in in vitro cultures of MKN45 or KATO III cells that were infected with H. pylori isolated from these same patients. These in vivo and in vitro α‐chemokine levels showed no significant association with the presence of cagA gene and CagA protein, ureB genotype, or binding capacity to MKN45 or KATO III cells in individual H. pylori isolates. In contrast, in vivo mucosal α‐chemokine activity correlated with H. pylori colonization density. Conclusion : Mucosal chemokine profiles and inflammatory responses in H. pylori infection may be associated more closely with host factors, including those determining bacterial adhesiveness, than with differences in H. pylori strains.