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A potential basis for suppressed inflammatory cell function in pediatric cholestatic hosts.

P T Roughneen1, A D Kulkarni, R J Andrassy

  • 1Department of Surgery, University of Texas Medical School, Houston 77030.

Journal of Pediatric Surgery
|February 1, 1990
PubMed
Summary

Experimental hepatic failure (EHF) in rats suppresses T cell function due to inhibitory macrophage activity. This finding may explain increased infection risk in children with liver disease.

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Area of Science:

  • Immunology
  • Hepatology
  • Pediatric Infectious Diseases

Background:

  • Infective mortality is a significant concern in pediatric hepatic failure.
  • Experimental hepatic failure (EHF) is known to suppress T cell function in vivo.
  • The precise mechanisms underlying this immune suppression require elucidation.

Purpose of the Study:

  • To investigate the basis of immune suppression in experimental hepatic failure (EHF).
  • To assess the roles of macrophage function, T cell subsets, IL-2 production, and serum inhibition.
  • To determine if splenic macrophages contribute to T cell dysfunction in EHF.

Main Methods:

  • Wistar Furth rats were allocated to EHF, sham, and normal control groups (n=23 each).
  • Immune assays were performed on splenocytes and sera harvested on day 21.

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  • Assays included assessment of macrophage function, T cell ratios, IL-2 production, and serum inhibitory activity.

    • Main Results:

    • EHF rats exhibited elevated serum bilirubin levels compared to controls.
    • EHF splenic macrophages significantly suppressed T cell proliferation (PHA response) in a dose-dependent manner in vitro.
    • T helper:suppressor cell ratios and IL-2 production did not significantly differ between EHF and control groups.
    • No T cell inhibitory activity was detected in EHF sera.

    Conclusions:

    • Splenic macrophages from rats with experimental hepatic failure exhibit potent inhibitory effects on T cell function in vitro.
    • This macrophage-mediated immune suppression may be a key factor predisposing children with liver disease to infections.
    • Further research is warranted to explore therapeutic strategies targeting macrophage function in hepatic failure.