The effect of surface membrane modifications of fibroblastic cells on the entry process of Trypanosoma cruzi trypomastigotes

• Published in: Molecular and biochemical parasitology Vol. 2; no. 5; pp. 359 - 366
• Main Authors: Henriquez, Diana, Piras, Romano, Piras, Marta M.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.01.1981
• Subjects: Agglutinins - pharmacology; Concanavalin A; Concanavalin A - metabolism; Cytoskeleton; Entry process; Fibroblastic cell infection; Fibroblasts - physiology; Glycoproteins - pharmacology; Host-Parasite Interactions - drug effects; Host-parasite interplay; Lectins; Phytohemagglutinins - pharmacology; Receptors, Concanavalin A - pharmacology; Ricin - pharmacology; Surface membrane modifications; Trypanosoma cruzi; Trypanosoma cruzi - growth & development; Trypanosoma cruzi - physiology; Con A, concavanalin A; WGA, wheat germ agglutinin; Entry process; Host-parasite interplay; PHA, phytohemagglutinin; Surface membrane modifications; Fibroblastic cell infection; Concanavalin A; Trypanosoma cruzi; αMM, methyl-α-D-mannopyranoside; MEM, Eagle's minimal essential medium; Succ-Con A, succinylated Con A; Lectins; Cytoskeleton; PBS, Dulbecco's phosphate-buffered saline; CEP cells, chick embryonic muscle cells
• ISSN: 0166-6851; 1872-9428
• DOI: 10.1016/0166-6851(81)90087-6

Treatment prior to infection with Trypanosoma cruzi trypomastigotes of Vero, MA-103, and chick muscle cells with concanavalin A, phytohemagglutinin, wheat germ agglutinin and ricin I results in a diminished parasite interiorization in these cells; succinylated concanavalin A is also inhibitory. The effect of these lectins is abolished by the corresponding sugar haptens. Trypsin and periodate treatment of the cells also inhibits infection, as well as calcium ionophore A23187 and drugs that disrupt microtubules and microfilaments directly, like colchicine, vinblastine and cytochalasin B. These results show that alteration(s) of a surface glycoprotein(s) and/or of the plasma membrane architecture of fibroblastic host cells inhibit infection, suggesting that the surface membrane of these cells does not play a passive role in the process of infection by T. cruzi.