Abstract
Cystic hydatid disease (CHD) is a worldwide neglected zoonotic disease caused by Echinococcus granulosus. The parasite is well adapted to its host by producing protective molecules that modulate host immune response. An unexplored issue associated with the parasite’s persistence in its host is how the organism can survive the oxidative stress resulting from parasite endogenous metabolism and host defenses. Here, we used hydrogen peroxide (H2O2) to induce oxidative stress in E. granulosus protoescoleces (PSCs) to identify molecular pathways and antioxidant responses during H2O2 exposure. Using proteomics, we identified 550 unique proteins; including 474 in H2O2-exposed PSCs (H-PSCs) samples and 515 in non-exposed PSCs (C-PSCs) samples. Larger amounts of antioxidant proteins, including GSTs and novel carbonyl detoxifying enzymes, such as aldo-keto reductase and carbonyl reductase, were detected after H2O2 exposure. Increased concentrations of caspase-3 and cathepsin-D proteases and components of the 26S proteasome were also detected in H-PSCs. Reduction of lamin-B and other caspase-substrate, such as filamin, in H-PSCs suggested that molecular events related to early apoptosis were also induced. We present data that describe proteins expressed in response to oxidative stress in a metazoan parasite, including novel antioxidant enzymes and targets with potential application to treatment and prevention of CHD.
Highlights
Echinococcus granulosus is the causative agent of cystic hydatid disease (CHD), a neglected zoonosis that harms human health and livestock farming worldwide[1,2,3]
After 2 and 4 h incubation, it was observed that PSCs adopted a rounded shape in the presence of different H2O2 concentrations, but no viability changes were noticed in comparison to the corresponding non-treated control cultures
Since previous data showed apoptosis induction in E. multilocularis vesicles treated with 5 mM H2O2 for 4 h, we chose a milder treatment with 2.5 mM H2O2 concentration for 2 h to allow the detection of proteins induced at earlier stages of the oxidative stress response
Summary
Echinococcus granulosus is the causative agent of cystic hydatid disease (CHD), a neglected zoonosis that harms human health and livestock farming worldwide[1,2,3]. ROS and RNS are harmful to tissue components because they can damage proteins, lipids, carbohydrates, and DNA, altering their functions[9]. For this reason, unicellular and multicellular organisms have developed non-enzymatic and enzymatic machineries, which include a repertoire of molecules to manage oxidative stress, such as glutathione and Cys-rich oligopeptides (for non-enzymatic mechanisms), and superoxide dismutases and peroxiredoxins (for enzymatic mechanisms)[10]. Other proteins that are targets of the proteolytic pathway of apoptotic cell death were down-regulated in H2O2-exposed PSCs. Overall, our results shed light on novel antioxidant mechanisms and cellular stress response in E. granulosus
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