透過您的圖書館登入
IP:13.58.244.216
  • 學位論文

血漿溶解性尿激酶型纖溶酶原活化因子受體與社區型肺炎嚴重程度的探討

Study of the Plasma Soluble Urokinase-Type Plasminogen Activator Receptor Levels and Severity in Patients with Community-Acquired Pneumonia

指導教授 : 楊順發
共同指導教授 : 葉兆斌(Chao-Bin Yeh)

摘要


尿激酶型血纖維蛋白溶解酶原活化因子受體 (urokinase-type plasminogen activator receptor, uPAR) 可調解各種細胞活性,並參與蛋白水解、血管生成和發炎。在這項研究中其目的為探討溶解性uPAR  (soluble PAR, suPAR)程度與社區型肺炎 (community-acquired pneumonia, CAP) 嚴重程度之間的關聯性。我們首先利用酵素免疫分析法 (Enzyme-linked immunosorbent assay; ELISA) 進行測量67位健康對照組和75位CAP患者其血漿中suPAR的濃度。我們的結果顯示,與對照組相比,CAP患者血漿中suPAR濃度有顯著升高,而抗生素治療可有效降低suPAR的濃度。基於肺炎嚴重程度指數 (pneumonia severity index, PSI)評分,血漿suPAR濃度與CAP嚴重程度具關聯性。此外,我們利用細胞實驗觀察到,在脂多醣 (lipopolysaccharide, LPS)的刺激下會顯著增加uPAR在RAW 264.7巨噬細胞中的表現。總結以上,血漿中的suPAR濃度可能在CAP嚴重程度的臨床評估扮演重要的角色。而這些發現對於CAP治療可能會提供更多新資訊。

並列摘要


The urokinase-type plasminogen activator receptor (uPAR) mediates various cellular activities and is involved in proteolysis, angiogenesis, and inflammation. The objective of this study was to investigate the association between soluble uPAR (suPAR) levels and community-acquired pneumonia (CAP) severity. A commercial enzyme-linked immunosorbent assay (ELISA) was performed to measure the plasma suPAR levels in 67 healthy controls and 75 patients with CAP. Our results revealed that plasma suPAR levels were significantly elevated in patients with CAP compared with the controls, and antibiotic treatment was effective in reducing suPAR levels. The plasma suPAR levels were correlated with the severity of CAP based on the pneumonia severity index (PSI) scores. Furthermore, in cell lines model, lipopolysaccharide (LPS)-stimulation significantly increased uPAR expression in RAW264.7 macrophages. In conclusion, plasma suPAR levels may play a role in the clinical assessment of CAP severity; these findings may provide information on new targets for treatment of CAP.

參考文獻


Andersen, E.S., Ruhwald, M., Moessner, B., Christensen, P.B., Andersen, O., Eugen-Olsen, J., Weis, N., 2011. Twelve potential fibrosis markers to differentiate mild liver fibrosis from cirrhosis in patients infected with chronic hepatitis C genotype 1. Eur J Clin Microbiol Infect Dis 30, 761-766.
Annane, D., Renault, A., Brun-Buisson, C., Megarbane, B., Quenot, J.P., Siami, S., Cariou, A., Forceville, X., Schwebel, C., Martin, C., Timsit, J.F., Misset, B., Ali Benali, M., Colin, G., Souweine, B., Asehnoune, K., Mercier, E., Chimot, L., Charpentier, C., Francois, B., Boulain, T., Petitpas, F., Constantin, J.M., Dhonneur, G., Baudin, F., Combes, A., Bohe, J., Loriferne, J.F., Amathieu, R., Cook, F., Slama, M., Leroy, O., Capellier, G., Dargent, A., Hissem, T., Maxime, V., Bellissant, E., Network, C.-T., 2018. Hydrocortisone plus Fludrocortisone for Adults with Septic Shock. N Engl J Med 378, 809-818.
Bajou, K., Herkenne, S., Thijssen, V.L., D'Amico, S., Nguyen, N.Q., Bouche, A., Tabruyn, S., Srahna, M., Carabin, J.Y., Nivelles, O., Paques, C., Cornelissen, I., Lion, M., Noel, A., Gils, A., Vinckier, S., Declerck, P.J., Griffioen, A.W., Dewerchin, M., Martial, J.A., Carmeliet, P., Struman, I., 2014. PAI-1 mediates the antiangiogenic and profibrinolytic effects of 16K prolactin. Nat Med 20, 741-747.
Balsara, R.D., Ploplis, V.A., 2008. Plasminogen activator inhibitor-1: the double-edged sword in apoptosis. Thromb Haemost 100, 1029-1036.
Barille, S., Akhoundi, C., Collette, M., Mellerin, M.P., Rapp, M.J., Harousseau, J.L., Bataille, R., Amiot, M., 1997. Metalloproteinases in multiple myeloma: production of matrix metalloproteinase-9 (MMP-9), activation of proMMP-2, and induction of MMP-1 by myeloma cells. Blood 90, 1649-1655.

延伸閱讀