机构地区:[1]Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, China [2]Department of Pulmonary Medicine, Huadong Hospital, Fudan University, Shanghai 200040, China [3]Key Laboratory of Medical Molecular Virology, Shanghai Medical College, Fudan University, Shanghai 200032, China
出 处:《Acta Pharmacologica Sinica》2008年第10期1202-1208,共7页中国药理学报(英文版)
基 金:Project supported by the National Natural Science Foundation of China (No 30571542) and Shanghai Leading Academic Discipline Project (Project Number: B 115) Author contribution Jie-ming QU, Hui-jun ZHANG, Chang-zhou SHAO, Jing ZHANG, and Li-xian HE designed research; Hui-jun ZHANG performed research; Zheng-hong YUAN contributed new analytical tools and reagents; Hui-jun ZHANG analyzed data; Hui-jun ZHANG wrote the paper.
摘 要:Aim: To determine if NOD2 is involved in host recognition of Aspergillus fumigatus (Af) conidia. Methods: An Af conidia pulmonary infection murine model was established by intranasal inoculation of Af conidia suspensions. Protein levels of NOD2 in lung tissue were determined by immunohistochemistry. A549 and phorbol-12-myristate 13-acetate (PMA)-activated THP-1 cell lines were treated with heat-killed Af conidia, then the presence of NOD2 protein in these cell lines was detected by Western blotting. The ability of muramyl dipeptide (MDP) to induce the secretion of TNF-α after incubation with heat- killed Afconidia was measured by enzyme-linked immunosorbent assay. Results: The expression of NOD2 protein in lung tissue increased after Af conidia infection. Heat-killed Afconidia significantly upregulated NOD2 protein expression in A549 cells and PMA-activated THP-1 cells. Additionally, Af conidia in conjuction with MDP, significantly increased the secretion of TNF-α in A549 cells and PMA-activated THP-1 cells. Conclusion: Afconidia upregulates NOD2 protein expression in vitro and in vivo. These findings indicate that NOD2 protein may respond to Afconidia.Aim: To determine if NOD2 is involved in host recognition of Aspergillus fumigatus (Af) conidia. Methods: An Af conidia pulmonary infection murine model was established by intranasal inoculation of Af conidia suspensions. Protein levels of NOD2 in lung tissue were determined by immunohistochemistry. A549 and phorbol-12-myristate 13-acetate (PMA)-activated THP-1 cell lines were treated with heat-killed Af conidia, then the presence of NOD2 protein in these cell lines was detected by Western blotting. The ability of muramyl dipeptide (MDP) to induce the secretion of TNF-α after incubation with heat- killed Afconidia was measured by enzyme-linked immunosorbent assay. Results: The expression of NOD2 protein in lung tissue increased after Af conidia infection. Heat-killed Afconidia significantly upregulated NOD2 protein expression in A549 cells and PMA-activated THP-1 cells. Additionally, Af conidia in conjuction with MDP, significantly increased the secretion of TNF-α in A549 cells and PMA-activated THP-1 cells. Conclusion: Afconidia upregulates NOD2 protein expression in vitro and in vivo. These findings indicate that NOD2 protein may respond to Afconidia.
关 键 词:Aspergillus fumigatus NOD2 protein pattern recognition receptors
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