Wei Lei1, Da-Xiong Zeng1, Can-Hong Zhu1, Gao-Qin Liu1, Xiu-Qin Zhang1, Chang-Guo Wang1, Qin Wang1, Jian-An Huang1. 1. 1 Department of Respiratory Medicine, The First Affiliated Hospital of Soochow University, Suzhou 215006, China ; 2 Department of Respiratory Medicine, Children's Hospital of Soochow University, Suzhou 215003, China ; 3 Institute of Medical Biotechnology of Soochow University, Suzhou 215007, China.
Abstract
OBJECTIVE: To investigate whether the expression of OX40/OX40 ligand (OX40L) was upregulated in a murine model of asthma and their significance in the pathogenesis of asthma. METHODS: After an ovalbumin-sensitized/challenged murine model of asthma was established, the expressions of OX40, OX40L in peripheral blood mononuclear cells (PBMCs) and bronchoalveolar lavage fluid (BALF) cell pellets were measured. Then T cell proliferation was analyzed by cell counting kit-8 (CCK8), and the protein levels of OX40 and OX40L in the lungs were determined by immunohistochemistry. The concentrations of IL-4 and IFN-γ in BALF and T cell culture supernatant were evaluated by ELISA. RESULTS: The percentages of CD4(+)OX40(+), CD19(+)OX40L(+), F4/80(+)OX40L(+) in PBMCs and BALF cell pellets were higher in asthma group than in control group (all P<0.01). The proliferation capacity of T cells in asthma group was higher than that in control group (P<0.05). In asthma group, stimulation of OX40 by anti-OX40 mAb obviously promoted T cell proliferation and secretion of IL-4 and IFN-γ. Immunohistochemistry assay showed that OX40 and OX40L protein levels were higher in asthma group than those in control group (all P<0.05). CONCLUSIONS: The expressions of OX40 and OX40L were upregulated in the murine asthmatic model. The upregulation of OX40/OX40L signals could induce the proliferation and cytokines secretion of T cells in asthmatic mice, indicating that OX40/OX40L signal was involved in the pathogenesis of asthma.
OBJECTIVE: To investigate whether the expression of OX40/OX40 ligand (OX40L) was upregulated in a murine model of asthma and their significance in the pathogenesis of asthma. METHODS: After an ovalbumin-sensitized/challenged murine model of asthma was established, the expressions of OX40, OX40L in peripheral blood mononuclear cells (PBMCs) and bronchoalveolar lavage fluid (BALF) cell pellets were measured. Then T cell proliferation was analyzed by cell counting kit-8 (CCK8), and the protein levels of OX40 and OX40L in the lungs were determined by immunohistochemistry. The concentrations of IL-4 and IFN-γ in BALF and T cell culture supernatant were evaluated by ELISA. RESULTS: The percentages of CD4(+)OX40(+), CD19(+)OX40L(+), F4/80(+)OX40L(+) in PBMCs and BALF cell pellets were higher in asthma group than in control group (all P<0.01). The proliferation capacity of T cells in asthma group was higher than that in control group (P<0.05). In asthma group, stimulation of OX40 by anti-OX40 mAb obviously promoted T cell proliferation and secretion of IL-4 and IFN-γ. Immunohistochemistry assay showed that OX40 and OX40L protein levels were higher in asthma group than those in control group (all P<0.05). CONCLUSIONS: The expressions of OX40 and OX40L were upregulated in the murine asthmatic model. The upregulation of OX40/OX40L signals could induce the proliferation and cytokines secretion of T cells in asthmatic mice, indicating that OX40/OX40L signal was involved in the pathogenesis of asthma.
Authors: Fabrina M C Gaspal; Mi-Yeon Kim; Fiona M McConnell; Chandra Raykundalia; Vasilios Bekiaris; Peter J L Lane Journal: J Immunol Date: 2005-04-01 Impact factor: 5.422