Complement activated granulocytes can cause autologous tissue destruction in man

Activation of polymorphonuclear granulocytes (PMNs) by C5a is thought to be important in the pathogenesis of multiple organ failure during sepsis and after trauma. In our experiment exposure of human PMNs to autologous zymosan activated plasma (ZAP) leads to a rapid increase in chemiluminescence. He...

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Main Authors: E. Löhde, H. Raude, M. Lück, E. Kraas, W. Lierse
Format: Article
Language:English
Published: Wiley 1992-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/S0962935192000279
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author E. Löhde
H. Raude
M. Lück
E. Kraas
W. Lierse
author_facet E. Löhde
H. Raude
M. Lück
E. Kraas
W. Lierse
author_sort E. Löhde
collection DOAJ
description Activation of polymorphonuclear granulocytes (PMNs) by C5a is thought to be important in the pathogenesis of multiple organ failure during sepsis and after trauma. In our experiment exposure of human PMNs to autologous zymosan activated plasma (ZAP) leads to a rapid increase in chemiluminescence. Heating the ZAP at 56°C for 30 min did not alter the changes, while untreated plasma induced only baseline activity. The respiratory burst could be completely abolished by decomplementation and preincubation with rabbit antihuman C5a antibodies. Observation of human omentum using electron microscopy showed intravascular aggregation of PMNs, with capillary thrombosis and diapedesis of the cells through endothelial junctions 90 s after exposure to ZAP. PMNs caused disruption of connections between the mesothelial cells. After 4 min the mesothelium was completely destroyed, and connective tissue and fat cells exposed. Native plasma and minimum essential medium did not induce any morphological changes. These data support the concept that C5a activated PMNs can cause endothelial and mesothelial damage in man. Even though a causal relationship between anaphylatoxins and organ failure cannot be proved by these experiments C5a seems to be an important mediator in the pathogenesis of changes induced by severe sepsis and trauma in man.
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spelling doaj-art-1144a265cb794fb6af9a40ae3df6a26e2025-02-03T01:27:52ZengWileyMediators of Inflammation0962-93511466-18611992-01-011317718110.1155/S0962935192000279Complement activated granulocytes can cause autologous tissue destruction in manE. Löhde0H. Raude1M. Lück2E. Kraas3W. Lierse4Surgical Department, Academic Hospital Moabit, Turmstr. 21, Berlin 21 D-1000, GermanySurgical Department, Academic Hospital Moabit, Turmstr. 21, Berlin 21 D-1000, GermanySurgical Department, Academic Hospital Moabit, Turmstr. 21, Berlin 21 D-1000, GermanySurgical Department, Academic Hospital Moabit, Turmstr. 21, Berlin 21 D-1000, GermanyInstitut of Neuroanatomy, Martinistr 52, University of Hamburg, Hamburg 20 2000, GermanyActivation of polymorphonuclear granulocytes (PMNs) by C5a is thought to be important in the pathogenesis of multiple organ failure during sepsis and after trauma. In our experiment exposure of human PMNs to autologous zymosan activated plasma (ZAP) leads to a rapid increase in chemiluminescence. Heating the ZAP at 56°C for 30 min did not alter the changes, while untreated plasma induced only baseline activity. The respiratory burst could be completely abolished by decomplementation and preincubation with rabbit antihuman C5a antibodies. Observation of human omentum using electron microscopy showed intravascular aggregation of PMNs, with capillary thrombosis and diapedesis of the cells through endothelial junctions 90 s after exposure to ZAP. PMNs caused disruption of connections between the mesothelial cells. After 4 min the mesothelium was completely destroyed, and connective tissue and fat cells exposed. Native plasma and minimum essential medium did not induce any morphological changes. These data support the concept that C5a activated PMNs can cause endothelial and mesothelial damage in man. Even though a causal relationship between anaphylatoxins and organ failure cannot be proved by these experiments C5a seems to be an important mediator in the pathogenesis of changes induced by severe sepsis and trauma in man.http://dx.doi.org/10.1155/S0962935192000279
spellingShingle E. Löhde
H. Raude
M. Lück
E. Kraas
W. Lierse
Complement activated granulocytes can cause autologous tissue destruction in man
Mediators of Inflammation
title Complement activated granulocytes can cause autologous tissue destruction in man
title_full Complement activated granulocytes can cause autologous tissue destruction in man
title_fullStr Complement activated granulocytes can cause autologous tissue destruction in man
title_full_unstemmed Complement activated granulocytes can cause autologous tissue destruction in man
title_short Complement activated granulocytes can cause autologous tissue destruction in man
title_sort complement activated granulocytes can cause autologous tissue destruction in man
url http://dx.doi.org/10.1155/S0962935192000279
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AT ekraas complementactivatedgranulocytescancauseautologoustissuedestructioninman
AT wlierse complementactivatedgranulocytescancauseautologoustissuedestructioninman