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Recently, the incidence of infectious diseases continues to decline in many developed countries; however, the incidence of autoimmune diseases and allergic asthma appears a tendency towards a rise over years. “Hygiene hypothesis” provides new insights into the treatment of autoimmune disorders and allergic diseases based on parasitic infections. Increasing evidence shows that parasitic infections may effectively inhibit the development of diabetes, multiple sclerosis, inflammatory bowel disease, rheumatoid arthritis and allergic asthma. There are complex mechanisms underlying the relationship between parasitic infections and “hygiene hypothesis”, among which regulatory T (Treg) cells and Th17 cells are becoming a hot topic of research. This paper reviews the progresses in the research on the relationship between parasitic infections and “hygiene hypothesis”, and summarizes the roles of Treg cells and Th17 cells in the interplay between parasitic infections and “hygiene hypothesis”.

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OBJECTIVE: To investigate the dynamic expression of transforming growth factor-ß1 (TGF-ß1) and heat shock protein 47 (HSP47) and explore their roles in the progression of hepatic fibrosis induced by Schistosoma japonicum infection. METHODS: Fifty female mice of the ICR strain were randomly divided into the infection group and the normal control group, of 25 mice in each group. Each mouse in the infection group was infected with 20 ± 1 cercariae of S. japonicum via the abdominal skin, while uninfected animals served as normal control. Five mice were sacrificed 4, 6, 8, 10 and 12 weeks post-infection and liver tissues were sampled. Serum HSP47 and TGF-ß1 was determined using enzyme-linked immunosorbent assay (ELISA), and the pathological changes of liver specimens were observed with hematoxylin & eosin (HE) staining. In addition, the synthesis of alpha 1 chain of type I collagen (COL1A1) was measured using Masson staining, and the mRNA expression of TGF-ß1, HSP47 and COL1A1 was determined using real-time fluorescent quantitative PCR (qPCR) assay. RESULTS: During the period of S. japonicum-induced hepatic fibrosis, the serum HSP47 and TGF-ß1 levels and the mRNA expression of TGF - ß1, HSP47 and COL1A1 gradually increased with the progression of hepatic fibrosis. The serum levels of HSP47 and TGF-ß1 were (179.26 ± 29.87) pg/mL and (22.37 ± 5.21) ng/mL 6 weeks post-infection, respectively, which were significantly greater than those [(150.29 ± 34.91) pg/mL and (18.54 ± 7.78) ng/mL, respectively] in the normal control group (both P values < 0.05). In addition, the mRNA expression of HSP47, COL1A1 and TGF-ß1 was (0.86 ± 0.04), (1.17 ± 0.06) and (0.64 ± 0.13) in mouse liver specimens, which was significantly higher than that (0.23 ± 0.03, 0.20 ± 0.02 and 0.38 ± 0.02) in the normal control group (all P values < 0.01). CONCLUSIONS: The expression of TGF-ß1 and HSP47 during the period of S. japonicum-induced hepatic fibrosis is consistent with the progression of the hepatic fibrosis, and exhibits the same tendency with type I collagen expression. HSP47 is a novel promising diagnosis marker and therapeutic target for S. japonicum-induced hepatic fibrosis.

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Objective To investigate the dynamic expression of transforming growth factor-β1 (TGF-β1) and heat shock protein 47 (HSP47) and explore their roles in the progression of hepatic fibrosis induced by Schistosoma japonicum infection. Methods Fifty female mice of the ICR strain were randomly divided into the infection group and the normal control group, of 25 mice in each group. Each mouse in the infection group was infected with 20 ± 1 cercariae of S. japonicum via the abdominal skin, while uninfected animals served as normal control. Five mice were sacrificed 4, 6, 8, 10 and 12 weeks post-infection and liver tissues were sampled. Serum HSP47 and TGF-β1 was determined using enzyme-linked immunosorbent assay (ELISA), and the pathological changes of liver specimens were observed with hematoxylin & eosin (HE) staining. In addition, the synthesis of alpha 1 chain of type I collagen (COL1A1) was measured using Masson staining, and the mRNA expression of TGF-β1, HSP47 and COL1A1 was determined using real-time fluorescent quantitative PCR (qPCR) assay. Results During the period of S. japonicum-induced hepatic fibrosis, the serum HSP47 and TGF-β1 levels and the mRNA expression of TGF - β1, HSP47 and COL1A1 gradually increased with the progression of hepatic fibrosis. The serum levels of HSP47 and TGF-β1 were (179.26 ± 29.87) pg/mL and (22.37 ± 5.21) ng/mL 6 weeks post-infection, respectively, which were significantly greater than those [(150.29 ± 34.91) pg/mL and (18.54 ± 7.78) ng/mL, respectively] in the normal control group (both P values < 0.05). In addition, the mRNA expression of HSP47, COL1A1 and TGF-β1 was (0.86 ± 0.04), (1.17 ± 0.06) and (0.64 ± 0.13) in mouse liver specimens, which was significantly higher than that (0.23 ± 0.03, 0.20 ± 0.02 and 0.38 ± 0.02) in the normal control group (all P values < 0.01). Conclusions The expression of TGF-β1 and HSP47 during the period of S. japonicum-induced hepatic fibrosis is consistent with the progression of the hepatic fibrosis, and exhibits the same tendency with type I collagen expression. HSP47 is a novel promising diagnosis marker and therapeutic target for S. japonicum-induced hepatic fibrosis.

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Objective To investigate the dynamic expression of transforming growth factor-β1 (TGF-β1) and heat shock protein 47 (HSP47) and explore their roles in the progression of hepatic fibrosis induced by Schistosoma japonicum infection. Methods Fifty female mice of the ICR strain were randomly divided into the infection group and the normal control group, of 25 mice in each group. Each mouse in the infection group was infected with 20 ± 1 cercariae of S. japonicum via the abdominal skin, while uninfected animals served as normal control. Five mice were sacrificed 4, 6, 8, 10 and 12 weeks post-infection and liver tissues were sampled. Serum HSP47 and TGF-β1 was determined using enzyme-linked immunosorbent assay (ELISA), and the pathological changes of liver specimens were observed with hematoxylin & eosin (HE) staining. In addition, the synthesis of alpha 1 chain of type I collagen (COL1A1) was measured using Masson staining, and the mRNA expression of TGF-β1, HSP47 and COL1A1 was determined using real-time fluorescent quantitative PCR (qPCR) assay. Results During the period of S. japonicum-induced hepatic fibrosis, the serum HSP47 and TGF-β1 levels and the mRNA expression of TGF - β1, HSP47 and COL1A1 gradually increased with the progression of hepatic fibrosis. The serum levels of HSP47 and TGF-β1 were (179.26 ± 29.87) pg/mL and (22.37 ± 5.21) ng/mL 6 weeks post-infection, respectively, which were significantly greater than those [(150.29 ± 34.91) pg/mL and (18.54 ± 7.78) ng/mL, respectively] in the normal control group (both P values < 0.05). In addition, the mRNA expression of HSP47, COL1A1 and TGF-β1 was (0.86 ± 0.04), (1.17 ± 0.06) and (0.64 ± 0.13) in mouse liver specimens, which was significantly higher than that (0.23 ± 0.03, 0.20 ± 0.02 and 0.38 ± 0.02) in the normal control group (all P values < 0.01). Conclusions The expression of TGF-β1 and HSP47 during the period of S. japonicum-induced hepatic fibrosis is consistent with the progression of the hepatic fibrosis, and exhibits the same tendency with type I collagen expression. HSP47 is a novel promising diagnosis marker and therapeutic target for S. japonicum-induced hepatic fibrosis.

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Exosomes are a group of membraneous vesicles generated and released by multi-vesicular bodies or cell membranes in a variety of cell types. Acting as important messages between cells, they participate in almost every physiological and pathological process of living organisms. Exosomes contain specific proteins, mRNA, miRNAs, etc. and mediate intercellular communications, signal transductions and gene expressions effectively. Exosomes are involved in the formation of hepatic fibrosis, which is the typical liver pathological change in the progression of schistosomiasis and is caused by the liver repair and (or) regeneration involving inflammation stimulated by exosomes, activated hepatic stellate cells and other related pathways in reaction to the parasite infection. Exosomes could serve as new markers for schistosomiasis hepatic fibrosis diagnosis and potential targets for its treatment. This paper briefly reviews the latest development of studies on the regulatory roles of exosomes in schistosomiasis hepatic fibrosis, so as to provide ideas for searching new treatment targets of the disease.

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Exosomes are a group of membraneous vesicles generated and released by multi-vesicular bodies or cell membranes in a variety of cell types. Acting as important messages between cells, they participate in almost every physiological and pathological process of living organisms. Exosomes contain specific proteins, mRNA, miRNAs, etc. and mediate intercellular communications, signal transductions and gene expressions effectively. Exosomes are involved in the formation of hepatic fibrosis, which is the typical liver pathological change in the progression of schistosomiasis and is caused by the liver repair and (or) regeneration involving inflammation stimulated by exosomes, activated hepatic stellate cells and other related pathways in reaction to the parasite infection. Exosomes could serve as new markers for schistosomiasis hepatic fibrosis diagnosis and potential targets for its treatment. This paper briefly reviews the latest development of studies on the regulatory roles of exosomes in schistosomiasis hepatic fibrosis, so as to provide ideas for searching new treatment targets of the disease.

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Exosomes are a group of membraneous vesicles generated and released by multi-vesicular bodies or cell membranes in a variety of cell types. Acting as important messages between cells, they participate in almost every physiological and pathological process of living organisms. Exosomes contain specific proteins, mRNA, miRNAs, etc. and mediate intercellular communications, signal transductions and gene expressions effectively. Exosomes are involved in the formation of hepatic fibrosis, which is the typical liver pathological change in the progression of schistosomiasis and is caused by the liver repair and (or) regeneration involving inflammation stimulated by exosomes, activated hepatic stellate cells and other related pathways in reaction to the parasite infection. Exosomes could serve as new markers for schistosomiasis hepatic fibrosis diagnosis and potential targets for its treatment. This paper briefly reviews the latest development of studies on the regulatory roles of exosomes in schistosomiasis hepatic fibrosis, so as to provide ideas for searching new treatment targets of the disease.

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The parasitic infection is still a severe public health problem in developing countries, which threatens people's health and social development. With the advances of molecular biology and immunology, more and more insights have been reached on the immunity and immunopathogenesis to parasitic infections. CD4+ T cells play a central role in the host's immunosurveillance and immunoregulation. Traditionally, naive CD4+ T cells are considered to be able to differentiate into Th1 and Th2 cell subsets both in vivo and in vitro. These Th1 and Th2 cells secret diverse cytokine profiles to exert different functions. Later, two new subsets of CD4+ T cells, Th17 and Treg cells, have been discovered. They are completely different from traditional Th1 and Th2 cells with independent differentiation and regulation mechanism. Ample studies suggest that Treg and Th17 cells play a key role in a variety of parasitic diseases. Furthermore, Treg and Th17 cells have been got increasing attention for their involvement in the hygiene hypothesis. Based on the current advances of researches of Treg and Th17 cells, we make a brief review about immunomodulatory effects of these two subsets in parasitic infections as well as the hygiene hypothesis.

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The Rho subfamily of GTPase belongs to the Ras superfamily of small GTP binding protein, it is a nucleotide dependent protein, which plays a "molecular switch" function in the signal transduction process and control of numerous signaling pathways. Rho protein has many biological effects on cytoskeleton or target proteins as a signal converter in signal transduction, such as the regulation of membrane transport function, cell migration, cell adhesion, and cell proliferation. It also plays a very important role in the infection and immune inflammation of the body. Rho protein is widely distributed in related immune cells, such as T cells, B cells, NK cells and so on. When the body is infected by microorganism, the immune inflammatory reaction will be regulated through a series of signal transduction mechanism, and Rho GTPases signal transduction mechanism is one of the important signal pathways. In this paper, we conclude that Rho GTPases how to regulate the body's immune response through its signal pathway, and ultimately affect the body's immune response.

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