Sialic acid: a sweet swing between mammalian host and Trypanosoma cruzi

Abstract

Commonly found at the outermost ends of complex carbohydrates in extracellular medium or on outer cell membranes, sialic acids play important roles in a myriad of biological processes. Mammals synthesize sialic acid through a complex pathway, but Trypanosoma cruzi, the agent of Chagas’ disease, evolved to obtain sialic acid from its host through a trans-sialidase (TcTS) reaction. Studies of the parasite cell surface architecture and biochemistry indicate that a unique system comprising sialoglycoproteins and sialyl-binding proteins assists the parasite in several functions including parasite survival, infectivity, and host–cell recognition. Additionally, TcTS activity is capable of extensively remodeling host cell glycomolecules, playing a role as virulence factor. This review presents the state of the art of parasite sialobiology, highlighting how the interplay between host and parasite sialic acid helps the pathogen to evade host defense mechanisms and ensure lifetime host parasitism.

Bacterial periplasmic sialic acid-binding proteins exhibit a conserved binding site

“…Many Gram-negative bacteria mask their alien identity by decorating their outer layer with various forms of a linear monosaccharide that is also found on the surface of most animal cells: sialic acid (SA). By adding this nine-carbon sugar acid to the outermost end of certain glycolipids that coat the bacterial surface, the pathogen can primarily derail the activation of the host's most primitive immune response: the complement system (Hood et al, 1999;Harvey et al, 2001;Severi et al, 2007;Johnston et al, 2008;Freire-de-Lima et al, 2012).…”

Role of Small RNAs in Trypanosomatid Infections

“…The T. cruzi trans-sialidase transfers host sialic acid to parasite surface glycoconjugates, a process that supports host–cell recognition, infectivity, and parasite survival. Indeed, this trans-sialidase activity can remodel parasite glycomolecules, altering host immune responses against the parasite and playing a role as a virulence factor (Freire-de-Lima et al, 2012 ).…”

Alpha-Gal and Cross-Reactive Carbohydrate Determinants in the N-Glycans of Salivary Glands in the Lone Star Tick, Amblyomma americanum

“…This interaction causes the neutrophil to recognize the bacteria as 'self' which dampens the neutrophil reactivity [12]. Molecular mimicry of host glycans is also known in Trypanosoma cruzi, which utilizes host sialic acid transferred to the terminus of mucin-like O-glycan on the surface of the parasite [13,14]. Further, molecular mimicry has been identified as one of the mechanisms by which infections can initiate or exacerbate autoimmune diseases [15].…”