NATURAL IMMUNITY TO BACTERIAL INFECTIONS: THE RELATION OF COMPLEMENT TO HEAT-LABILE OPSONINS*

  1. Mary Ruth Smith,
  2. Hyun S. Shin, and
  3. W. Barry Wood, Jr.
  1. DEPARTMENT OF MICROBIOLOGY, THE JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE

Abstract

Heat-labile opsonins to pneumococci in normal mammalian sera, unlike antibodies, fail to interact with the bacteria at 0°C and require Ca++ and/or Mg++. They are readily removed from serum by antigen-antibody complexes that fix complement (C) and are inhibited by reagents that inactivate various C components. The principal heat-labile opsonin to pneumococci is activated C3 (C3b), but a slight enhancing effect is exerted by one or more of the late-reacting components of the hemolytic complement system (C5-C9). Since heat-labile opsonins are immunologically polyspecific, they presumably play a broad protective role in the early (preantibody) phase of acute bacterial infections.

Footnotes

  • ↵ * These studies were supported from 1964 to 1966 by the Commission on Streptococcal and Staphylococcal Diseases of the Armed Forces Epidemiological Board (contract DA 49-193 MD 2313). Since August 1966 they have been supported by the National Science Foundation (grant GB 5387) and also, during the past year, by the National Science Foundation (grant GB 2597), the Office of Naval Research (contract 248-60), and the U.S. Public Health Service (grants AI-02566 and 5 TI-AI 282).

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  1. PNAS 1969-08 vol. 63 no. 4 1151-1156
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