PMID: 46449Feb 8, 1975

Functional role of cholesterol in infection and autoimmunity

Lancet
K C Watson, E J Kerr

Abstract

Cholesterol binds to streptolysin O and related bacterial toxins. In normal serum, only a fraction of the cholesterol attached to lipoprotein is available for binding, probably as a cholesterol-peptide complex formed during catabolic breakdown of the lipoprotein. Cholesterol esterase produced by certain organisms--e.g., Staphylococcus pyogenes and Pseudomonas oeruginosa--augments this fraction both in vitro and in vivo. Endogenous esterase similarly increases the amount of cholesterol-peptide complex, a mechanism which may be activated as a feedback process following binding of toxin to the cholesterol component of the complex. These complexes will thus supply a readily available means of binding bacterial toxins before antibody formation begins; Cholesterol-peptide complexes, either alone or modified by binding to toxin, may function as autoantigens. It is postulated that immune complexes so formed may be involved in atherosclerosis either by directly damaging vessels walls or by cross-reaction of antibody with cell-membrane-bound lipoproteins which equilibrate with plasma-lipoproteins.

References

Dec 1, 1976·Australian and New Zealand Journal of Medicine·B S Andrews, R Penny
Mar 1, 1978·Journal of Clinical Pathology·K C Watson, E J Kerr
Jan 1, 1983·Critical Reviews in Toxicology·D M Klurfeld

Related Concepts

Epicholesterol
Toxin
Antistreptolysin O
LDL-1
Genus staphylococcus
Feedback - System Communication
Staphylococcal Infections
Antibody Formation
Pseudomonas aeruginosa
Antigens

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