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Research Article Free access | 10.1172/JCI109391

Deficient Serum Bactericidal Activity Against Escherichia Coli in Patients with Cirrhosis of the Liver

Joshua Fierer and Fred Finley

Department of Medicine, Veterans Administration Hospital, San Diego, California 92161

Department of Medicine, University of California, San Diego, California 92161

School of Medicine, San Diego, California 92161

Find articles by Fierer, J. in: PubMed | Google Scholar

Department of Medicine, Veterans Administration Hospital, San Diego, California 92161

Department of Medicine, University of California, San Diego, California 92161

School of Medicine, San Diego, California 92161

Find articles by Finley, F. in: PubMed | Google Scholar

Published May 1, 1979 - More info

Published in Volume 63, Issue 5 on May 1, 1979
J Clin Invest. 1979;63(5):912–921. https://doi.org/10.1172/JCI109391.
© 1979 The American Society for Clinical Investigation
Published May 1, 1979 - Version history
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Abstract

The serum bactericidal activity (SBA) of cirrhotic patients was compared with that of normal individuals using the release of 51Cr from radiolabeled Escherichia coli as the assay method. 80% (22/27) of patients were found to have deficient SBA against at least one of three smooth, serum-sensitive test strains of E. coli. Cirrhotic patients were found to have normal levels of serum lysozyme. Although some patients were mildly hypocomplementemic, this abnormality did not correlate with the presence of a bactericidal defect. Bactericidal antibody in normal and cirrhotics' sera was limited to the immunoglobulin (Ig)M class. Purified IgM from patients with deficient SBA against E. coli 0111 had lower concentrations of bactericidal antibody for that E. coli than did IgM from normal sera; the calculated bactericidal activity of total serum IgM was also lower. The bactericidal defect in cirrhotic serum could be completely corrected by either human antiserum to the homologous strain of E. coli or by purified, normal human IgM. However, because higher concentrations of IgM were required to restore normal SBA to a cirrhotic's serum than to agammaglobulinemic serum, there may be an inhibitor of bactericidal antibody in addition to a deficiency of bactericidal IgM antibody to E. coli in the serum of patients with cirrhosis. The bactericidal activity of the alternative complement pathway was also assessed. Sera from cirrhotic patients had no deficit in SBA attributable to the alternative complement pathway. In fact, in some, the activity of the alternative complement pathway was supernormal, compensating in part for the deficit in IgM-mediated SBA.

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