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 HighWire Citing Articles via Google Scholar Google Scholar Articles by Fierer, J. Articles by Braude, A. I. Search for Related Content PubMed Articles by Fierer, J. Articles by Braude, A. I.

Release of ⁵¹Cr-Endotoxin from Bacteria as an Assay of Serum Bactericidal Activity¹

Veterans Administration Hospital of San Diego, Department of Medicine and Departments of Medicine and Pathology, University of California, San Diego School of Medicine, San Diego, California 92161

Abstract

In order to facilitate the study of normal serum on Gram-negative bacteria we have developed a bactericidal assay based on the release of ⁵¹Cr from labeled bacteria. Release of radioactivity was shown to be mediated by complement and paralleled the bactericidal action of sera measured by change in colony-forming units. Serum from the C6 deficient rabbits and serum that had been treated to inactivate complement did not release ⁵¹Cr. The rate of release of ⁵¹ Cr was decreased by absorption of serum with Bentonite but the maximum percentage released was not decreased. ⁵¹Cr was not released from serum resistant bacteria.

The ⁵¹Cr appears to be associated with the lipopolysaccharide fraction of the bacteria. Since this structure is the target for the bactericidal reaction, the release of ⁵¹Cr is a direct measure of the effect of complement on the bacteria. Under most conditions this reaction leads to cell death so that the release of ⁵¹Cr can be used as an assay of bactericidal activity. It was shown that the assay was feasible with Escherichia coli, Salmonella and Hemophilus influenza B.

Footnotes

¹ This work was supported by Veterans Administration Grant MRIS 2815 and National Institute of Health Grant USPHS HE-12967-05.

This article has been cited by other articles:

				P. van Langevelde, K. M. C. Kwappenberg, P. H. P. Groeneveld, H. Mattie, and J. T. van Dissel Antibiotic-Induced Lipopolysaccharide (LPS) Release from Salmonella typhi: Delay between Killing by Ceftazidime and Imipenem and Release of LPS Antimicrob. Agents Chemother., April 1, 1998; 42(4): 739 - 743. [Abstract] [Full Text]