An Anticomplementary Agent, K-76 Monocarboxylic Acid: Its Site and Mechanism of Inhibition of the Complement Activation Cascade

Open Access
Publisher Website
Google Scholar
Abstract
A monocarboxylic acid derivative (K-76 COOH) of K-76, purified from the culture filtrate of Stachybotrys complementi nov. sp. K-76, inhibits complement (C) activity. Its inhibitory action is mainly on C5 step. It strongly inhibits the generation of EAC1̄,4b,2a,3b,5b from C5 and EAC1̄,4b,2a,3b, and accelerates the decay of EAC1̄,4b,2,3b,5b. It also causes some inhibition of the reactions of C2, C3, C6, C7, and C9 with their respective preceding intermediate cells. It has no effect on the generation of EAC1̄,4b from C4 and EAC1̄, or of EAC-8 from C8 and EAC-7, and apparently increases the generation of EAC1̄,4b from C1 and EAC4b probably by inhibiting transfer or turnover of C1. It does not affect the rate of decay of EAC1̄,4b,2a or the T max of generation of EAC1̄,4b,2a, and it inhibits immune adherence only at high concentration. K-76 COOH also strongly inhibits hemolysis through the alternative pathway of C activation by cobra venom factor, but it does not seem to inhibit the early steps of the alternative pathway, because it has little affect on the consumption of C3 or the conversion of β1C to β1A on treatment of C serum with zymosan. K-76 COOH probably combines with C5 molecules, forming the inactive complexes, or it causes the structural alteration of C5.

This publication has 0 references indexed in Scilit: