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Activation of granulocytes with vero toxins: A possible role of activation for the pathogenesis of hemolytic uremic syndrome caused by enterohemorrhagic E. coli.

Research Project

Project/Area Number10670268
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Bacteriology (including Mycology)
Research InstitutionIwate Medical University

Principal Investigator

INADA Katsuya  Iwate Medical Inversity, School of Medicine, Lecturer, 医学部, 講師 (80048446)

Project Period (FY) 1998 – 1999
Project Status Completed(Fiscal Year 1999)
Budget Amount *help
¥900,000 (Direct Cost : ¥900,000)
Fiscal Year 1999 : ¥900,000 (Direct Cost : ¥900,000)
Keywordsentrohemorrhagic E. coli / hemolytic uremic syndrome / vero toxins / granulocytes / Gb3 / interleukin 8 / multiple organ failure / PMN-alastase / サイトカイン / 接着分子
Research Abstract

Leukocytosis (mostly neutrophils) is thought to be one prognostic factor for the pathogenesis of hemolytic uremic syndrome (HUS) due to entrohemorrhagic E. coli.
The author speculated that neutrophils are activated and cells play a role for the pathogenesis of HUS due to entrohemorrhagic E. coli.
Thus, the author investigated 1) the increased levels of proinflammatory cytokines, which are especially involved in the activation of PMN, in plasmas from patients, and 2) the possibility of the activation of granulocytes by vero toxins.
The results are as follows:
1) Plasma levels of cytokines and other mediators: The levels of three groups; Group A (patients with HUS), Group B (patients hospitalized with diarrhea but not HUS), and Group C (outpatients with diarrhea), were compared. High levels of IL-8 and PMN-elastase were found in Group A and B, but the levels were higher in Group A. Other proinflammatory cytokines were also found especially in Group A. Endotoxin levels were within cut-off value, even insevere cases. Procalcitonin, as an indictor of severe bacterial infection, was found in Group A.
2) Activation of granulocytes with vero toxins: Vcro toxin (VT 1) activated granulocytes to produce proinflammatory cytokines (IL-6, IL-8, TNF-α, and IL-8) and to express the adhesion molecules (CD11b and CD18; Mac-I). VT2 also activated granulocytes to produce cytokines and to express the adhesion molecules. The potency of VT2 was superior to VT1. CD77 (Gb3) antigen was found to be expressed on granulocytes.
These results suggest that the activation of granulocytes plays a role in the pathogenesis of HUS and is a vehicle to deliver vero toxins to organs.

Report

(3results)
  • 1999 Annual Research Report   Final Research Report Summary
  • 1998 Annual Research Report

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Published : 1999-04-01   Modified : 2016-04-21  

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