Abstract
Trapping of Schistosoma japonicum (S. japonicum) eggs in host tissue, mainly in the intestine and liver, causes severe gastrointestinal and hepatic granulomatous immune responses and irreversible fibrosis. Although the gut microbiota plays a central role in regulating pathological responses in several diseases, the effect of the gut microbiota on the pathologenesis progression of schistosomiasis remains largely unknown. In this study, we aimed to investigate the regulatory function of the gut microbiota in schistosomiasis japonica. We found that the depletion of the gut microbiota significantly ameliorated egg granulomas formation and fibrosis in the intestine of infected mice. This role of the gut microbiota in intestinal granuloma formation and fibrosis was reinforced when normal and infected mice were housed together in one cage. Notably, changes in the gut microbiota induced by S. japonicum infection were partly reversible with microbiota transfer in the cohousing experiment. Transfer of the gut microbiota from normal to infected mice attenuated the intestinal pathological responses. Depletion of the gut microbiota by antibiotics, or transfer of the gut microbiota from normal to infected mice decreased the levels of IL-4, IL-5, and IL-13 and promoted the production of cytokines and mRNA levels of IL-10 and TGF-β in infected mice. Our findings indicated a regulatory effect of the gut microbiota on intestinal pathological injury associated with schistosomiasis japonica in mice, and thus suggested a potential strategy for schistosomiasis treatment.
Highlights
Schistosomiasis japonica is a severe zoonotic disease that can lead to irreversible fibrosis and portal hypertension and eventually give rise to splenomegaly, ascites and, gastrointestinal varices [1]
To investigate whether gut microbiota homeostasis could be disturbed in mice with S. japonicum infection, mice were infected with 15 cercariae for 7 weeks
All the data indicated that the diversity of the gut microbiota was reduced in mice with S. japonicum infection compared to normal mice
Summary
Schistosomiasis japonica is a severe zoonotic disease that can lead to irreversible fibrosis and portal hypertension and eventually give rise to splenomegaly, ascites and, gastrointestinal varices [1]. Schistosoma japonicum (S. japonicum) infection remains one of the most important public health problems in tropical and subtropical areas; by 2018, there are still 29,214 advanced schistosomiasis cases were documented in China [2]. Immature male and female schistosomula, migrate downstream to the hepatic portal-mesenteric system via the circulatory system, in which females lay inside the groves of males, and release thousands of eggs. Some of the eggs are permanently intravenously trapped in the intestinal wall, or are deposited in the liver via the portal system [3]. Mounting evidence has indicated that deposited eggs, which are the major pathogenic factors of these parasites, induce granuloma formation by stimulating dominant CD4+ Th2 immune responses accompanied by eosinophil, macrophage, hepatic stellate cell and lymphocyte recruitment [4]. The exact immunopathological mechanisms that are involved in schistosomiasis japonica remain to be fully defined
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