Schistosomiasis is an infectious disease caused by parasitic worms that affects more than 210-million people, predominantly in developing countries. Its main pathological feature is a pro-inflammatory reaction to the parasite eggs that are trapped in tissues or organs, with subsequent formation of hepatic granulomas (nodules of immune cells) and fibrosis, processes against which current treatments are often inefficacious. Recent data showed that the chemokine Cx3cr1, expressed by macrophages, promotes fibrotic processes. Thus, Cong-Yi Wang and colleagues sought to investigate whether reducing Cx3cr1 signalling in infiltrating macrophages can prevent hepatic granulomas in Schistosoma japonicum-infected mice – a well-established model of human schistosomiasis. The group found that S. japonicum infection increased the expression of Cx3cr1 in infiltrating macrophages, whereas lack of the Cx3cr1 gene prevented egg-induced granuloma formation and hepatic injury in the animals. Interestingly, loss of Cx3cr1 induced M2 polarisation of macrophages, a process that enhances the helper-T-cell-2 (Th2) response, a key T-cell-mediated pro-inflammatory reaction against intracellular parasites. These results suggest CX3CR1 as a viable therapeutic target for the treatment of human schistosomiasis. Page
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July 2015
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High-dose vitamin B1 therapy prevents the development of experimental fatty liver driven by overnutrition
Vitamin B1 is shown to prevent nutrition-induced fatty liver in our current Editor’s choice by Hay Davir and his colleagues, when they use sheep as a large-animal model for studying the disease.
Find out more in an interview with the paper's first authors, Mugagga Kalyesubula and Ramgopal Mopuri.
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Our upcoming special issue is welcoming submissions until 3 May 2021. Guest-edited by Donita Brady (Perelman School of Medicine at the University of Pennsylvania, USA) and Arvin Dar (Icahn School of Medicine at Mount Sinai, USA), the issue will focus on targeting the RAS pathway.
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