|
KMID : 0364820120480020109
|
|
Korean Journal of Microbiology
2012 Volume.48 No. 2 p.109 ~ p.115
|
|
|
Effect of Recombinant CagL Immunization on the Gastric Diseases Induced by Helicobacter pylori in Mongolian gerbils
|
|
Park Eun-Jung
Jang Sung-Il
Choi Yun-Hui
Kim Jin-Moon
Kim Ae-Ryun
Kim Ji-Hye
Woo Gye-Hyeong
Yu Yoon-Jeong
Lee Sung-Haeng
Cha Jeong-Heon
|
|
|
Abstract
|
|
|
Helicobacter pylori is an important factor of chronic gastritis, digestive ulcer, and stomach cancer. CagL, a virulence
factor of H. pylori, is well-known as a pilus protein which acts as adhesion to host cell and a component of Type 4
secretion system. In this study, we evaluated the protective response of recombinant CagL protein (rCagL) using
Mongolian gerbil animal model for H. pylori infection. The cagL gene was cloned from 26695 H. pylori followed by
over-expression and purification of the protein in E. coli. Mongolian gerbils were immunized with rCagL protein
mixed with aluminum adjuvant via intramuscular injections once a week during 4 weeks. At a week after the last
immunization, the Mongolian gerbils were administrated with H. pylori 7.13 strain into the stomach and sacrificed to
measure antibody titer on rCagL by ELISA and bacterial colonization in the stomach, and to examine the
histopathological changes and cytokine expression at 6 week after challenge. Antibody titers on recombinant protein
were significantly increased from a week after the first immunization. There was no significant change of the number
of bacterial colony between control group and immunized group. The relative stomach weight was significantly
decreased in immunized group, but the significant change of histopathological assessment was not observed in the
stomach. Cytokine expression such as IL-1β and KC also was not significantly different between control and
immunized groups. These results indicate that rCagL could effectively induce the formation of the specific IgG
antibodies. However, bacterial colonization and histopathological lesions could not be inhibited by the immunization
in the stomach, indicating not enough protection against H. pylori infection. We consider that along with CagL other
adequate antigens could be needed stimulating immune response and inducing protective effects against gastric
disease, and also a better adjuvant could be considered.
|
|
|
KEYWORD
|
|
|
Helicobacter pylori, CagL, IgG antibodies, immunization, Mongolian gerbils
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|
|