The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article
Right arrow Full Text (PDF, 7082K)
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nogueira, N.
Right arrow Articles by Cohn, Z.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nogueira, N.
Right arrow Articles by Cohn, Z.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

Journal of Experimental Medicine, Vol 143, 1402-1420, Copyright © 1976 by Rockefeller University Press


ARTICLES

Trypanosoma cruzi: mechanism of entry and intracellular fate in mammalian cells

N Nogueira and Z Cohn

The mode of entry and intracellular fate of epimastigotes and trypomastigotes of Trypanosoma cruzi in cultured cells was studied. Electron microscopic observations indicated the uptake by phagocytosis of both forms into mouse peritoneal macrophages and of trypomastigotes and transition forms into other cultured cell types. In each instance the organisms were initially surrounded by a plasma membrane-derived phagosome. Trypsin and chymotrypsin treatment of the macrophages completely abolished attachment and ingestion of both forms, indicating that protease-sensitive structures on the macrophage plasma membrane mediate ingestion. The macrophage Fc or C3b receptors were not essential for uptake of T. cruzi in the conditions used. Cytochalasin B inhibited ingestion but not the attachment of both forms by macrophages. Epimastigotes were not taken up by HeLa, L cells, and calf embryo fibroblasts. In macrophages, epimastigotes were killed and digested within phagolysosomes. In contrast, trypomastigotes and transition forms escaped from the phagocytic vacuole and then multiplied in the cytoplasmic matrix. Amastigotes released from infected cells exhibited properties similar to those of trypomastigotes and were able to enter all cell types studied and multiply intracellularly.
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS