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- 저자 : Jiu-Yao Wang (검색결과 3 건)
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The Innate Immune Response in House Dust Mite-Induced Allergic Inflammation
Jiu-Yao Wang 대한천식알레르기학회 2013 Allergy, Asthma & Immunology Research Vol.5 No.2
Hypersensitivity to house dust mite (HDM; Dermatophagoides sp.) allergens is one of the most common allergic responses, affecting up to 85% ofasthmatics. Sensitization to indoor allergens is the strongest independent risk factor associated with asthma. Additionally, >50% of children andadolescents with asthma are sensitized to HDM. Although allergen-specific CD4+ Th2 cells orchestrate the HDM allergic response through inductionof IgE directed toward mite allergens, activation of innate immunity also plays a critical role in HDM-induced allergic inflammation. This review highlightsthe HDM components that lead to activation of the innate immune response. Activation may due to HDM proteases. Proteases may be recognizedby protease-activation receptors (PARs), Toll-like receptors (TLRs), or C-type lectin receptors (CTRs), or act as a molecular mimic for PAMP activationsignaling pathways. Understanding the role of mite allergen-induced innate immunity will facilitate the development of therapeutic strategiesthat exploit innate immunity receptors and associated signaling pathways for the treatment of allergic asthma.
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Yuan, Jiu,Yao, Junhu,Yang, Fengxia,Yang, Xiaodan,Wan, Xinjie,Han, Jincheng,Wang, Yaojie,Chen, Xinke,Liu, Yurui,Zhou, Zhenfeng,Zhou, Ningbo,Feng, Xinyu Asian Australasian Association of Animal Productio 2008 Animal Bioscience Vol.21 No.5
A trial was conducted to study the influence of different levels of a commercial enzyme complex on performance, nutrient availability, blood parameters, digestive tract measurements, amylase and trypsin activity of the digestive tract and gut morphology in broilers fed the typical diets in north China. There were four treatments: the control diet and the other three enzyme complex supplemented diets which were 180 mg/kg, 360 mg/kg and 720 mg/kg enzyme complex supplemented to the control diet, respectively. The birds fed the diets supplemented with 180 mg/kg and 360 mg/kg enzyme complex had better performance and nutrient availability, the activities of amylase and trypsin in the digestive tract in the two treatments were improved, the villus height and surface area of villus in the small intestine increased and the crypt depth and epithelial thickness of small intestine decreased. Relative weights of pancreas and relative weights and lengths of small intestine decreased. However, the addition of 720 mg/kg enzyme complex had no effects on these parameters and increased crypt depth and epithelial thickness of the small intestine. The data suggested that suitable supplementation of enzyme complex was beneficial for the birds, while excess enzyme complex inhibited secretion of endogenous enzyme and destroyed the structure of the small intestine.
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Cui, Jiu-Wei,Li, Yan,Wang, Chang,Yao, Cheng,Li, Wei Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.2
Purpose: PRIL (proliferation-inducing ligand) is a newly identified member of the tumor necrosis factor (TNF) family and modulates death ligand-induced apoptosis. Here, we investigated the effect of PRIL on cellular characteristics relating to tumor progression in human gastric cancer. Method: Recombinant lentivirus containing PRIL siRNA was constructed and then infected MGC803 and SGC7901 gastric cancer cells. MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] colony formation and cell cycle analysis were used to study the effect of PRIL knockdown on gastric cancer cell proliferation. Results: PRIL expression in lentivirus infected cells was significantly reduced as evidenced by quantitative real-time PCR. Cell viability and colony formation of MGC803 and SGC7901 cells were significantly hampered in PRIL knock-down cells. Moreover, the cell cycle was arrested at G2/M phase, elucidating the mechanism underlying the inhibitory effect of siRNA on cell proliferation. Conclusions: Our study indicated that PRIL functions in promoting cell growth, and lentivirus-mediated PRIL gene knockdown might be a promising strategy in the treatment of gastric cancer.
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