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PMID: 6253400 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Interaction of streptolysin O from Streptococcus pyogenes and theta-toxin from Clostridium perfringens with human fibroblasts.

Infection and immunity ·Vol. 29 ·No. 3 ·1980-09-00 ·Pages 863-72

Thelestam M, Möllby R

Abstract

The membrane-damaging properties on human diploid embryonic lung fibroblasts of streptolysin O (from Streptococcus pyogenes) and theta-toxin (from Clostridium perfringens) were compared. The results are consistent with the suggested mechanism for hemolysis by streptolysin O involving one fixation site and one lytic site of this cytolysin. However, the membrane-damaging activity of the two toxins differed with respect to (i) relative cytolytic activity on human diploid lung fibroblasts compared with that on sheep erythrocytes, (ii) binding to the fibroblast membrane, (iii) activity at 0 degrees C, (iv) membrane repair after more than 30 min, and (v) effect on influx of amino acids. It is concluded that the mechanism of membrane damage caused by theta-toxin differs from that of cytoplasmic membrane. These results question the current concept that all thiol-activated, cholesterol-inactivated bacterial toxins are similar both structurally and functionally.

MeSH Terms
Binding Sites Biological Transport Cations, Divalent Cell Survival Clostridium perfringens Dose-Response Relationship, Immunologic Fibroblasts/microbiology Humans Streptococcus pyogenes Streptolysins Temperature Time Factors Toxins, Biological
Chemicals
Cations, Divalent Streptolysins Toxins, Biological
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Thelestam M
Möllby R
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32 references, click to expand
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Article Info
Journal
Infection and immunity
Abbr.
Infect Immun
ISSN
0019-9567
DOI
10.1128/iai.29.3.863-872.1980
Published
1980-09-00
Pages
863-72
Language
English
Region
United States
NLM ID
0246127
PMCID
PMC551210
Subset
IM
External Links
PubMed source DOI: 10.1128/iai.29.3.863-872.1980 PMC Full Text View journal details
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