Elevated levels of serum macrophage migration inhibitory factor in patients with pulmonary tuberculosis

被引:32
作者
Yamada, G
Shijubo, N
Takagi-Takahashi, Y
Nishihira, J
Mizue, Y
Kikuchi, K
Abe, S
机构
[1] Sapporo Med Univ, Sch Med, Dept Internal Med 3, Chuo Ku, Sapporo, Hokkaido 0608543, Japan
[2] Hokkaido Univ, Sch Med, Cent Res Inst, Sapporo, Hokkaido 060, Japan
[3] Sapporo Immunodiagnost Lab, Sapporo, Hokkaido, Japan
关键词
MIF; IFN-gamma; pulmonary tuberculosis;
D O I
10.1006/clim.2002.5255
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Macrophage migration inhibitory factor (MIF) was originally described as a T-cell-derived cytokine that inhibits the random migration of macrophages and promotes the delayed-type hypersensitivity reaction. MIF plays an important role in the regulation of the Th1/Th2 balance in inflammatory response. This study investigated serum levels of circulating MIF in patients with pulmonary tuberculosis. The levels of MIF in sera were measured by enzyme-linked immunosorbent assay in 34 patients with pulmonary tuberculosis (16 males and 18 females) and 30 healthy controls (15 males and 15 females). The mean levels of circulating MIF values were significantly higher in those with pulmonary tuberculosis (19.84 +/- 11.27 ng/ml; P < 0.0001) than in the healthy controls (4.38 +/- 1.34 ng/ml). Circulating MIF values significantly correlated with circulating interferon-gamma values (r = 0.537, P < 0.0001). Thus, MIF may play an important role in immune responses to human infection with Mycobacterium tuberculosis. (C) 2002 Elsevier Science (USA).
引用
收藏
页码:123 / 127
页数:5
相关论文
共 29 条
[1]  
ALBERTUS B, 2001, J CLIN ENDOCR METAB, V86, P2811
[2]   An essential regulatory role for macrophage migration inhibitory factor in T-cell activation [J].
Bacher, M ;
Metz, CN ;
Calandra, T ;
Mayer, K ;
Chesney, J ;
Lohoff, M ;
Gemsa, D ;
Donnelly, T ;
Bucala, R .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (15) :7849-7854
[3]   MIF IS A PITUITARY-DERIVED CYTOKINE THAT POTENTIATES LETHAL ENDOTOXEMIA [J].
BERNHAGEN, J ;
CALANDRA, T ;
MITCHELL, RA ;
MARTIN, SB ;
TRACEY, KJ ;
VOELTER, W ;
MANOGUE, KR ;
CERAMI, A ;
BUCALA, R .
NATURE, 1993, 365 (6448) :756-759
[4]   An essential role for macrophage migration inhibitory factor in the tuberculin delayed-type hypersensitivity reaction [J].
Bernhagen, J ;
Bacher, M ;
Calandra, T ;
Metz, CN ;
Doty, SB ;
Donnelly, T ;
Bucala, R .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 183 (01) :277-282
[5]   MECHANISM OF A REACTION IN VITRO ASSOCIATED WITH DELAYED-TYPE HYPERSENSITIVITY [J].
BLOOM, BR ;
BENNETT, B .
SCIENCE, 1966, 153 (3731) :80-&
[6]   Targeted disruption of migration inhibitory factor gene reveals its critical role in sepsis [J].
Bozza, M ;
Satoskar, AR ;
Lin, GS ;
Lu, B ;
Humbles, AA ;
Gerard, C ;
David, JR .
JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 189 (02) :341-346
[7]   MACROPHAGE IS AN IMPORTANT AND PREVIOUSLY UNRECOGNIZED SOURCE OF MACROPHAGE-MIGRATION INHIBITORY FACTOR [J].
CALANDRA, T ;
BERNHAGEN, J ;
MITCHELL, RA ;
BUCALA, R .
JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 179 (06) :1895-1902
[8]   Macrophage migration inhibitory factor is a critical mediator of the activation of immune cells by exotoxins of gram-positive bacteria [J].
Calandra, T ;
Spiegel, LA ;
Metz, CN ;
Bucala, R .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (19) :11383-11388
[9]   MIF AS A GLUCOCORTICOID-INDUCED MODULATOR OF CYTOKINE PRODUCTION [J].
CALANDRA, T ;
BERNHAGEN, J ;
METZ, CN ;
SPIEGEL, LA ;
BACHER, M ;
DONNELLY, T ;
CERAMI, A ;
BUCALA, R .
NATURE, 1995, 377 (6544) :68-71
[10]   Cytokine levels correlate with a radiologic score in active pulmonary tuberculosis [J].
Casarini, M ;
Ameglio, F ;
Alemanno, L ;
Zangrilli, P ;
Mattia, P ;
Paone, G ;
Bisetti, A ;
Giosuè, S .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1999, 159 (01) :143-148