2011 Fiscal Year Final Research Report
Analyzing the relationship between programmed cell death of Helicobacter pylori(apoptosis), persistence and host immunity
Project/Area Number |
21590631
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Laboratory medicine
|
Research Institution | Kochi University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
SUGIURA Teturou 高知大学, 教育研究部・医療学系, 教授 (50171145)
KUMON Yoshitaka 高知大学, 教育研究部・医療学系, 准教授 (40215033)
MORIMOTO Norihito 高知大学, 医学部附属病院, 主任臨床検査技師 (60398055)
|
Co-Investigator(Renkei-kenkyūsha) |
NAKAZAWA Teruko 山口大学, 医歯学系, 名誉教授 (40053053)
|
Project Period (FY) |
2009 – 2011
|
Keywords | ヘリコバクター・ピロリ / 細胞分裂 / 宿主免疫応答 / IL-8 / 細胞死 / 形態 / cdrA / FtsZ |
Research Abstract |
The H. pylori cdrA has a repressive role on cell division. Loss of cdrA was found during persistent infection in animal model and patients. Thus we investigated whether the cdrA affects on the host immune response in vitro and vivo. The IL-8 level was compared in AGS cells co-cultured with wild-type or cdrA-disruptant strains and in biopsy specimens from patients infected by cdrA-positive or cdrA-negative strains. IL-8 level induced in AGS by a cdrA-disruptant strain was significantly lower(P<0. 01) compared to wild-type : corresponding to 50%-60% of those of wild-type, which coincided with in vivo data using biopsy specimens from cdrA-positive and cdrA-negative groups. Therefore, colonization by a cdrA-negative or cdrA-dysfunctional strain resulted in decreased IL-8 production and repression of NF-κB, and hence, attenuate the host immunity leading to persistent infection.
|
Research Products
(16 results)