The evaluation of soluble Fas and soluble Fas ligand levels of bronchoalveolar lavage fluid in lung cancer patients

被引:0
作者
Erdogan, Beril [1 ]
Uzaslan, Esra [1 ]
Budak, Ferah [2 ]
Karadag, Mehmet [1 ]
Ediger, Dane [1 ]
Oral, Barbaros [2 ]
Goral, Gher [2 ]
Ege, Ercument [1 ]
Gozu, Oktay [1 ]
机构
[1] Uludag Univ, Tip Fak, Gogus Hastaliklari Anabilim Dali, TR-16059 Bursa, Turkey
[2] Uludag Univ, Tip Fak, Immunol Anabilim Dali, Bursa, Turkey
来源
TUBERKULOZ VE TORAK-TUBERCULOSIS AND THORAX | 2005年 / 53卷 / 02期
关键词
Lung cancer; bronchoalveolar lavage; sFas; sFasL;
D O I
暂无
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Fas-Fas Ligand (FasL) is one of the major mediator system that activates programmed cell death. Cleavage of membranebound FasL by a metalloproteinase-like enzyme resulted in the formation of soluble FasL (sFasL). sFasL as well as the transmembrane form of FasL binds to Fas and transduces apoptotic signal in Fas-expressing cells. It's suggested that soluble Fas (sFas) and sFasL has an impact on tumor progress and immune escape feature of tumor cells from the host immune system. Since Fas antigen expression in the lungs has been localized to alveolar and bronchial epithelial cells, in this study we aimed to investigate the sFas (pg/mL) and sFasL levels (pg/mL) of bronchoalveolar lavage (BAL) fluid in lung cancer patients. Study population was consisted of 27 patients with lung cancer (mean age 62.9 +/- 10.7 years, 25 control subjects (mean age 47.9 +/- 13.9 years). BAL was performed under local anesthesia, on the unaffected lung of patients; either subsegments of right middle or lingula. BAL sFas and sFasL were evaluated by using ELISA method. The mean levels of sFas was 60.8 +/- 56.8 in lung cancer patient and 39.5 +/- 25.9 in control subjects (p> 0.05). The mean levels of sFasL was 51.6 +/- 39.2 in cancer patient and 41.2 +/- 27.4 in control subjects (p> 0.05). In conclusion, although we did not observe any significant difference between two groups, higher BAL levels of sFas and sFasL levels in lung cancer patients than control subjects, made us thought that apoptosis might have a role development and progression of lung cancer.
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页码:127 / 131
页数:5
相关论文
共 37 条
[1]   FAS-MEDIATED CYTOTOXICITY BY FRESHLY ISOLATED NATURAL-KILLER-CELLS [J].
ARASE, H ;
ARASE, N ;
SAITO, T .
JOURNAL OF EXPERIMENTAL MEDICINE, 1995, 181 (03) :1235-1238
[2]   A ROLE FOR CD95 LIGAND IN PREVENTING GRAFT-REJECTION [J].
BELLGRAU, D ;
GOLD, D ;
SELAWRY, H ;
MOORE, J ;
FRANZUSOFF, A ;
DUKE, RC .
NATURE, 1995, 377 (6550) :630-632
[3]   Levels of soluble FasL and FasL gene expression during the development of graft-versus-host disease in DLT-treated patients [J].
Das, H ;
Imoto, S ;
Murayama, T ;
Kajimoto, K ;
Sugimoto, T ;
Isobe, T ;
Nakagawa, T ;
Nishimura, R ;
Koizumi, T .
BRITISH JOURNAL OF HAEMATOLOGY, 1999, 104 (04) :795-800
[4]   APOPTOSIS IN CANCER-THERAPY - CROSSING THE THRESHOLD [J].
FISHER, DE .
CELL, 1994, 78 (04) :539-542
[5]   Fas and Fas ligand in embryos and adult mice: Ligand expression in several immune-privileged tissues and coexpression in adult tissues characterized by apoptotic cell turnover [J].
French, LE ;
Hahne, M ;
Viard, I ;
Radlgruber, G ;
Zanone, R ;
Becker, K ;
Muller, C ;
Tschopp, J .
JOURNAL OF CELL BIOLOGY, 1996, 133 (02) :335-343
[6]   FAS LIGAND-INDUCED APOPTOSIS AS A MECHANISM OF IMMUNE PRIVILEGE [J].
GRIFFITH, TS ;
BRUNNER, T ;
FLETCHER, SM ;
GREEN, DR ;
FERGUSON, TA .
SCIENCE, 1995, 270 (5239) :1189-1192
[7]   Melanoma cell expression of Fas(Apo-1/CD95) ligand: Implications for tumor immune escape [J].
Hahne, M ;
Rimoldi, D ;
Schroter, M ;
Romero, P ;
Schreier, M ;
French, LE ;
Schneider, P ;
Bornand, T ;
Fontana, A ;
Lienard, D ;
Cerottini, JC ;
Tschopp, J .
SCIENCE, 1996, 274 (5291) :1363-1366
[8]   Elevated serum soluble Fas ligand in natural killer cell proliferative disorders [J].
Kato, K ;
Ohshima, K ;
Ishihara, S ;
Anzai, K ;
Suzumiya, J ;
Kikuchi, M .
BRITISH JOURNAL OF HAEMATOLOGY, 1998, 103 (04) :1164-1166
[9]   METALLOPROTEINASE-MEDIATED RELEASE OF HUMAN FAS LIGAND [J].
KAYAGAKI, N ;
KAWASAKI, A ;
EBATA, T ;
OHMOTO, H ;
IKEDA, S ;
INOUE, S ;
YOSHINO, K ;
OKUMURA, K ;
YAGITA, H .
JOURNAL OF EXPERIMENTAL MEDICINE, 1995, 182 (06) :1777-1783
[10]  
Koomagi R, 1999, INT J CANCER, V84, P239, DOI 10.1002/(SICI)1097-0215(19990621)84:3<239::AID-IJC7>3.0.CO