HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Fine, D. P. Search for Related Content PubMed Articles by Fine, D. P.

Activation of the Classic and Alternate Complement Pathways by Endotoxin

From the Bacteriology Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, Maryland 21701

Abstract

The ability of bacterial endotoxin (LPS) to activate the complement system was studied in guinea pig serum (GPS). In serum chelated with ethyleneglycol tetraacetic acid (EGTA) 10 mM, which permits alternate complement pathway activation but inhibits classic complement pathway activation, lysis of LPS-coated sheep erythrocytes (E-LPS) was inhibited. Furthermore, E-LPS could not decomplement GPS chelated with EGTA. GPS absorbed twice at 0°C with E-LPS retained normal levels of hemolytic complement (CH50) and reacted normally (as measured by CH50 depression) with both zymosan (which activates the alternate pathway) and LPS. The absorbed GPS did not react with E-LPS, whether measured by percentage of lysis of E-LPS or by CH50 depression after incubation with E-LPS. These results suggest that endotoxin is capable of activating both complement pathways but erythrocyte-associated endotoxin can activate only the classic patheay, requiring a serum factor absorbable by E-LPS at 0°C.