Abstract
Schistosomiasis is a severe public health problem, which can cause tissue fibrosis and can even be fatal. Previous studies have proven that galectins and different kinds of cells involve in the regulation of tissue fibrosis process. In this study, outbred Kunming mice were infected with Schistosoma japonicum (S. japonicum). Our results showed that compared with uninfected mice, there were severe egg granulomatous inflammation and tissue fibrosis in the livers, spleens, and large intestines of S. japonicum-infected mice at 8 weeks post-infection (p.i.), and the number of eosinophils by hematoxylin and eosin staining and CD68 macrophage-positive area by immunohistochemical staining were significantly increased. Detected by using quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR), at 8 weeks after S. japonicum infection, the mRNA expression levels of galectin (Gal)-1, Gal-3, CD69, eosinophil protein X (EPX), and chitinase 3-like protein 3 (Ym1) were significantly increased in liver, spleen, and large intestine; eotaxin-1 (CCL11) and eosinophil cationic protein were significantly increased in both liver and spleen; eotaxin-2 (CCL24) and Arginase1 (Arg1) were significantly increased in both spleen and large intestine; and CD200R was significantly increased in both liver and large intestine. However, interleukin (IL)-1ß and inducible nitric oxide synthase (iNOS) were only significantly increased in liver. The M2/M1 ratio of CD200R/CD86 genes was significantly increased in liver, and ratios of Ym1/IL-1β and Ym1/iNOS were significantly increased in liver, spleen, and large intestine of S. japonicum-infected mice. Ex vivo study further confirmed that the levels of Gal-1, Gal-3, CD200R, Arg1, and Ym1 were significantly increased, and the ratios of CD200R/CD86 and Ym1/IL-1β were significantly increased in peritoneal macrophages isolated from S. japonicum-infected mice at 8 weeks p.i. In addition, correlation analysis showed that significant positive correlations existed between mRNA levels of Gal-1/Gal-3 and EPX in liver, between Gal-3 and Ym1 in both liver and large intestine, and between Gal-3 and CD200R in peritoneal macrophages of S. japonicum-infected mice. Our data suggested that Gal-1, Gal-3, eosinophils, and macrophages are likely involved in the development of egg granulomatous response and fibrosis induced by S. japonicum infection.
Highlights
Schistosomiasis is a zoonotic parasitic disease caused by Schistosoma spp. among human beings and animals, which affects nearly 250 million population worldwide [1]
The results showed that the sections of livers, spleens, and large intestines from uninfected control mice were negative for pathological changes and egg granulomas
The understanding of host responses during S. japonicum infection remains inadequate. To address this scientific question, we used outbred Kunming mice to develop a mouse model of schistosomiasis japonica, which could thereby allow us to investigate the immune response of tissue pathology and consequent fibrosis caused by S. japonicum egg deposition
Summary
Schistosomiasis is a zoonotic parasitic disease caused by Schistosoma spp. among human beings and animals, which affects nearly 250 million population worldwide [1]. The eggs of S. japonicum immigrate and deposit in liver and intestine tissues, which recruit macrophages, neutrophils, and eosinophils into the tissues during granulomatous reactions [3], and fibrotic deposits distributed around granulomas results in pipestem fibrosis [4]. It has been reported that granuloma eosinophils are highly activated and produce the majority of Th2 cytokines in granulomatous inflammation, which may be important determiners of immunopathology in murine schistosomiasis caused by S. mansoni [6]. In patients infected with S. haematobium, both ECP and EPX protein levels are higher in association with rubbery papules in genital lavage, which may serve as markers for a potential early-stage inflammatory lesion in female genital schistosomiasis [14]. Eosinophils play an essential role in granulomas and tissue fibrosis
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