help button home button Am J Pathol International Conference on Pathology of Chest Diseases
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Chensue, S. W.
Right arrow Articles by Higashi, G. I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chensue, S. W.
Right arrow Articles by Higashi, G. I.

American Journal of Pathology, Vol 111, 78-87, Copyright © 1983 by American Society for Investigative Pathology

REGULAR ARTICLES

Exogenously administered prostaglandins modulate pulmonary granulomas induced by Schistosoma mansoni eggs

SW Chensue, SL Kunkel, PA Ward and GI Higashi

The inflammatory modulating activity of specific prostaglandins has been examined for both immune and foreign-body types of pulmonary granulomas. Lung granuloma formation generated in mice by embolization of Schistosoma mansoni eggs was markedly suppressed by treatment with the stable, functional analog of prostaglandin E, (PGE1), (15-(S)-15- methyl PGE1) while treatment with PGF2 alpha augmented the granulomatous response. Despite marked effects on egg-induced granuloma formation, PGs had no significant effect on the foreign body lesion induced by Sephadex beads. Likewise, PGs had no effect on the primary antibody response to schistosome egg antigens. However, notable derangements in splenic lymphoid populations occurred. While T-cell numbers appeared constant in face of PG treatment, B-cell populations were depressed by methyl-PGE1 and augmented by PGF2 alpha. Further analysis revealed that methyl-PGE1 appeared to suppress both the induction and elicitation phases of the cell-mediated response to schistosome eggs. Cyclophosphamide treatment could partially reverse this suppression, but the induction of suppressor cell activity was not solely responsible for this effect. The possible role and mechanism of PGs as modulators of chronic inflammation is discussed.


This article has been cited by other articles:


Home page
 Infect. Immun.Home page
A. B. Stavitsky
Regulation of Granulomatous Inflammation in Experimental Models of Schistosomiasis
Infect. Immun., January 1, 2004; 72(1): 1 - 12.
[Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
C. Jakubzick, S. L. Kunkel, B. H. Joshi, R. K. Puri, and C. M. Hogaboam
Interleukin-13 Fusion Cytotoxin Arrests Schistosoma mansoni Egg-Induced Pulmonary Granuloma Formation in Mice
Am. J. Pathol., October 1, 2002; 161(4): 1283 - 1297.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1983 by the American Society for Investigative Pathology.