Why Do Intravascular Schistosomes Coat Themselves in Glycolytic Enzymes?. (29th October 2019)

• Record Type: Journal Article
• Authors: Pirovich, David; Da'dara, Akram A.; Skelly, Patrick J.
• Is Part Of: BioEssays. Volume 41:Number 12(2019:Dec.)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2019-10-29
• Subjects: host‐parasite interaction -- immunomodulation -- Schistosoma -- tegument -- thrombomodulation; Molecular biology -- Periodicals; Cytology -- Periodicals; Developmental biology -- Periodicals; 572.8
• DOI: 10.1002/bies.201900103
• Languages: English
• ISSNs: 0265-9247

Abstract

Abstract: Schistosomes are intravascular parasitic helminths (blood flukes) that infect more than 200 million people globally. Proteomic analysis of the tegument (skin) of these worms has revealed the surprising presence of glycolytic enzymes on the parasite's external surface. Immunolocalization data as well as enzyme activity displayed by live worms confirm that functional glycolytic enzymes are indeed expressed at the host–parasite interface. Since these enzymes are traditionally considered to function intracellularly to drive glycolysis, in an extracellular location they are hypothesized to engage in novel "moonlighting" functions such as immune modulation and blood clot dissolution that promote parasite survival. For instance, several glycolytic enzymes can interact with plasminogen and promote its activation to the thrombolytic plasmin; some can inhibit complement function; some induce B cell proliferation or macrophage apoptosis. Several pathogenic bacteria and protists also express glycolytic enzymes externally, suggesting that moonlighting functions of extracellular glycolytic enzymes can contribute broadly to pathogen virulence. Also see the video abstract here https://youtu.be/njtWZ2y3k_I Abstract : Intravascular parasitic flatworms called schistosomes express normally cytosolic, glycolytic enzymes on their external surface. Here, the enzymes are hypothesized to engage in novel (nonglycolytic) "moonlighting" functions such as immune modulation (e.g., by inducing B‐cell mitogenesis) and blood clot dissolution (e.g., by promoting plasmin activation) to promote parasite survival.