1992 Fiscal Year Final Research Report Summary
Immunological assessment of the pathogenesis of septic-MOF
| Project/Area Number |
03454305
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General surgery
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
TORISU Motomichi Kyushu Univ. Faculty of Med., Lecture, 医学部, 講師 (90038810)
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| Co-Investigator(Kenkyū-buntansha) |
NOMOTO Kikuo Kyushu Univ. Med. Inst. of Bioregulation, Professor, 生医研, 教授 (50037355)
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| Project Period (FY) |
1991 – 1992
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| Keywords | Septic-MOF / Neutrophil / Adhesion molecule / Chemotaxis / Oxygen radicals / Lysosomal enzyme / Complement system |
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| Research Abstract |
This study was undertaken to clarify the pathogenesis of septic-MOF, measuring the functional changes in neutrophils and complement system.
Neutrophils isolated from 11 patients with septic-MOF exhibited cnhanced endothelial cell adhesion due to up-regulation of adhesion molecule such as CR3, increased oxgen radical generation, increased lysosomal enzymes release, and depressed chemotaxis.
As these changes in neutrophil function may have been influenced by complement activation, we performed complement assays in these patients. The activation of complement in these patients was demonstrated by decreases in serum concentrations of CH50 and C4 and increases in plasma concentrations of C3a and C4a. Furthermore, the incease in plasma concentrations of circulating IgG immune complex, and the decrease in neutrophil Fc gamma R expression, suggest that the classic pathway is the main pathway of complement activation in patients with septic-MOF.
The increase in serum concentrations of the membrane attack (SC5b-9) complex also suggested that activated complement is implicated in organ injury in patients with septic-MOF. Moreover, the neutrophil up-regulation of surface inhibitory factors of complement activation likely allows the neutrophils to survive and function.
In conclusion, the combination of changes in neutrophil function and complement activation appears to be intimately associated with the pathogenesis of septic-MOF.
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