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 Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Reiner, N. E. Articles by Malemud, C. J. Search for Related Content PubMed PubMed Citation Articles by Reiner, N. E. Articles by Malemud, C. J.

Eicosanoid Metabolism by Leishmania Donovani-Infected Macrophages: Mouse Strain Responses in Prostanoid Synthesis

Neil E. Reiner^*, Leslie A. Schultz AND Charles J. Malemud^,,

^* Departments of Medicine and Microbiology, Division of Infectious Diseases, The University of British Columbia School of Medicine and Vancouver General Hospital, Vancouver, British Columbia, Canada
Departments of Medicine
Developmental Genetics and Anatomy, Case-Western Reserve University School of Medicine and University Hospitals of Cleveland, Ohio

Arachidonic acid (20:4) conversion to prostanoids was examined in murine peritoneal macrophages infected in vitro with Leishmania donovani. Four strains of mice differing in resistance to in vivo L. donovani infection were studied. Normal macrophages from all strains converted 20:4 to prostanoids and this was augmented by L. donovani infection. Although cells from each strain synthesized elevated levels of prostaglandin-E₂ (PGE₂), there were differences with respect to relative increases of this product, with infected macrophages from the C3H/HeJ strain showing the smallest increase above basal levels.

These results indicate that macrophages from mouse strains with distinct levels of in vivo resistance to L. donovani all respond to infection with augmented prostanoid synthesis. Although some heterogeneity in strain-specific PGE₂ responses to in vitro infection were observed (with respect to increases in PGE₂ synthesis above basal levels), it is unlikely that differential resistance of these strains to in vivo infection is strictly related to these relative differences. It seems likely that other genetically controlled factors may have a major impact on disease expression.

Accepted for publication July 7, 1987.