2009 Fiscal Year Final Research Report
Acute encephalopathy associated with hemolytic uremic syndrome : Chemokines expressions exposed shiga toxin in normal human astrocytes
| Project/Area Number |
19591218
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Pediatrics
|
|---|
| Research Institution | Wakayama Medical University |
|---|
Principal Investigator |
MINAMI Koichi Wakayama Medical University, 医学部, 講師 (60301438)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Hiroyuki 和歌山県立医科大学, 医学部, 准教授 (80196865)
YOSHIKAWA Norishige 和歌山県立医科大学, 医学部, 教授 (10158412)
|
|---|
| Project Period (FY) |
2007 – 2009
|
| Keywords | 小児神経学 |
|---|
| Research Abstract |
Infection with Shiga toxin (Stx)-producing Escherichia coli can lead to development of hemolytic uremic syndrome (HUS). HUS is the most frequent cause of acute renal failure in children. Approximately 30% of patients with HUS suffer from central nervous system (CNS) complications and these patients have the poorest prognosis. It has been suggested that vascular endothelial injuries caused by Stxs play a crucial role in the development of the disease. However, the relationship of glial cell damage and Stxs are still unclear.
In this study, we investigated that immune response of chemokines expressions exposed Stx in cultured normal human astroctes (NHA). Stx-receptor Gb3 was expressed on the NHA, and Gb3 expression was elevated by IL-1β. IL-8 and MCP-1 mRNA expressions in Stx-stimulated NHAs were elevated than controlled cells. This study indicates that Stx-inducible immune responses of chemokines expression on NHAs may play a critical role in the pathogenesis of HUS encephalopathy.
|
