title: [Dynamic expressions of IL-22 and hepatic stellate cells senescence in mice infected with Schistosoma japonicum].
abstract: OBJECTIVE
  To investigate the dynamic expressions of interleukin-22 (IL-22) , Interleukin-22 receptor 1 (IL-22R1), and hepatic stellate cells (HSC) senescence in mice with Schistosoma japonicum infection.
  
  
  METHODS
  A murine model of S. japonicum infection was established and the serum samples and liver tissues were collected 4, 6, 8, 12 weeks post-infection. The serum samples were detected for the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). The pathological changes and proliferation of hepatic collagen fibers in the liver tissue were observed after HE staining and Masson staining. The HSC senescence in fibrotic livers was determined by the detection of senescence-associated beta-galactosidase (SA-beta-Gal). Sandwich ELISA was used to measure the expressions of IL-22, and Real-time PCR was used to test the mRNA levels of IL-22 and IL-22R1. The control group without S. japonicum infection was set up.
  
  
  RESULTS
  The serum levels of ALT and AST significantly increased 8 weeks and 12 weeks after the infection (vs. 0 week, all P < 0.05). The level of IL-22 increased 4 weeks and 6 weeks after the infection (vs. 0 week, both P < 0.05), but reduced 8 weeks post-infection, and was even lower 12 weeks post-infection (vs. 4 weeks and 6 weeks, both P < 0.01). Being consistent with the dynamic expression of IL-22 protein, the mRNA expression of IL-22 began to increase 4 weeks and reached the peak 6 weeks after the infection (vs. 0 week, both P < 0.05), and continuously declined 8 weeks and 12 weeks post-infections (vs. 6 weeks, both P< 0.05). The increase of the expression of IL-22R1 mRNA was correlated with the progression of fibrosis, and the peak was in 12 weeks post-infections (vs. 0 week and 6 weeks, both P < 0.05). The number of senescence-associated beta-galactosidase-positive HSCs was reduced with the decreasing expression of IL-22 in the advanced liver fibrosis.
  
  
  CONCLUSIONS
  IL-22 and IL-22R1 are involved in the pathogenesis of schistosomiasis liver fibrosis. As an inflammation factor, IL-22 significantly increases in the early stage of fibrosis. The expression of IL-22 decreases in the late stage of fibrosis, which may contribute to HSC senescence and restrict liver fibrosis.
authors: Lan
authors: L
authors: Li
authors: Ying
authors: Y
authors: Sun
authors: Hong-wu
authors: HW
authors: Wang
authors: Yu
authors: Y
authors: Huang
authors: Jia-quan
authors: JQ
authors: Huang
authors: Qin
authors: Q
authors: Ning
mesh_terms: D000818:Animals; D016922:Cellular Senescence; D005355:Fibrosis; D005786:Gene Expression Regulation; D055166:Hepatic Stellate Cells / Q000378:metabolism* / Q000469:parasitology / Q000473:pathology*; D007378:Interleukins / Q000235:genetics* / Q000378:metabolism*; D008099:Liver / Q000469:parasitology / Q000473:pathology; D008297:Male; D051379:Mice; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D018123:Receptors, Interleukin / Q000235:genetics; D012549:Schistosoma japonicum / Q000502:physiology*; D000097043:Interleukin-22
chemical_list: D007378:Interleukins; D012333:RNA, Messenger; D018123:Receptors, Interleukin; D000097043:Interleukin-22; C415369:interleukin-22 receptor