Lectin receptors as markers for Trypanosoma cruzi. Developmental stages and a study of the interaction of wheat germ agglutinin with sialic acid residues on epimastigote cells.

Abstract

Chagas's disease is a chronic, debilitating, incurable disease affecting at least 12 million people in Central and South America (1, 2). TTypanosoma cruzi, the etiological agent, exists in three morphologically distinct forms related to different environments where it lives (1, 3): the amastigotes, which represent the multiplying stage found within the cells of mammalian hosts; the trypomastigotes, which are present in the bloodstream and in infected tissues of mammalian hosts, in the lumen of the rectum of the transmitting triatomid insect, and in culture; and the third form, epimastigotes, which are found intracellularly in mammalian hosts as a multiplying form in the vector's digestive tract, and in culture. Although bloodstream, insect, and culture trypomastigotes are highly infective, culture epimastigotes have very little, if any, capacity to initiate infection in the mammalian host (3). Although the morphologically defined forms of T. cruzi perform different functions in the life cycle of the parasite, the molecular mechanisms underlying the distinct behaviors remain unknown.The majority of exposed plasma membrane proteins are glycoproteins (4, 5), and there is increasing evidence that glycoproteins are of major importance in the maturation and regulation of functions displayed by cells such as those of the immune system (6, 7). On the other hand, much of the work concerning structure and function of cell surface carbohydrates is derived from studies with lectins, a class of sugarbinding proteins of nonimmune origin (8-10).In our study a systematic analysis of cell surface glyeoproteins and/or of glycolipids of T. cruzi developmental stages was undertaken, using ~30 highly purified, glycosidase-free lectins of various carbohydrate specificities as probes. The results showed that some lectins display unique selectivity in interacting with trypanosome forms as determined by agglutination and binding assays. It also showed that trypomastigotes obtained from blood of infected mice and from culture differed in their surface carbohydrates. Moreover, sialic acid residues detected and quantitated in epimasti-

Identification of carbohydrates on the surface membrane of pathogenic and nonpathogenic piscine haemoflagellates, Cryptobia salmositica, C. bullocki and C. catostomi (Kinetoplastida)

“…The terminal sugars of glycoproteins on the surface membrane were determined using digoxigenin labelled lectins and Biotin labelled lectins. Surface membrane protein from cryptobiids was separated using the discontinuous gel (Pereira et al 1980). Washed intact live parasites (1 X 10' ml-l) were mixed with an equal volume of trypsin in 50 mM Tris-HC1,…”

Lectins and their application to clinical microbiology

“…Cell surface carbohydrates of various T. cruzi stages were examined by agglutination and lectin-binding assays (118). Trypomastigotes obtained from the blood of infected mice and from culture differ in their surface carbohydrates.…”

Trypanosoma cruzi: cell charge distribution

“…There is no evidence of antigenic variation in T. cruzi, but there are some differences in cell surface properties between epimastigotes and trypomastigotes including lea tin-induced agglutination surface structures involved in macrophage attachment cell charge, and coat thickness (ALVES & COLLI 2; PE-REIRA et al 17 ; ZENIAN & KIERZENBAUM 24 ; DE SOUZA et al 3 ; Membrane components responsible for eliciting antibody response able to eliminate the entire T. cruzi population in the blood of infected animals have not been unequivocally demonstrated. Whether a population diversity with a sub-population showing distinct characteristics is important or not in the escape mechanism is not clear.…”