Elevated interleukin-18 levels in bronchoalveolar lavage fluid of patients with eosinophilic pneumonia

被引:39
作者
Katoh, S
Matsumoto, N
Matsumoto, K
Fukushima, K
Matsukura, S
机构
[1] Miyazaki Med Coll, Dept Internal Med 3, Miyazaki 8891692, Japan
[2] Nagasaki Prefecture Tarami Hosp, Nagasaki, Japan
关键词
bronchoalveolar lavage fluid; eosinophilic pneumonia; IL-2; interleukin (IL)-5; IL-10; IL-12; IL-13; IL-18;
D O I
10.1111/j.1398-9995.2004.00492.x
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Background: Interleukin (IL)-18 can induce Th2 cytokine production particularly in collaboration with IL-2. Accumulation of Th2 cells and increased levels of Th2 cytokines are found in bronchoalveolar lavage fluid (BALF) from patients with eosinophilic pneumonia (EP). To evaluate the role of IL-18 in the pathogenesis of EP, we measured the concentration of IL-2, IL-12, IL-18, and Th2 cytokines in BALF from patients with EP. Methods: The concentrations of interferon (IFN)-gamma, IL-2, IL-5, IL-10, IL-12, IL-13, and IL-18 in BALF were measured in patients with idiopathic acute eosinophilic pneumonia (AEP), with idiopathic chronic eosinophilicpneumonia (CEP), with sarcoidosis and healthy volunteers (HV). Results: The BALF concentrations of Th2 cytokines, IL-5, IL-10, and IL-13, were higher in patients with EP than in sarcoidosis and control. The IL-2 level in BALF was higher in EP than in sarcoidosis and control. The IL-18 and IL-12 (p40 + p70) levels were higher in patients with EP than sarcoidosis, while the level of IL-12 (p70) was below the detection limit in patients with EP. There was a significant correlation between IL-2 level and both IL-5 and IL-13 in BALF of patients with EP. Conclusions: Our findings suggest that IL-18 may contribute to Th2 cytokine-dominant responses in patients with EP in collaboration with IL-2.
引用
收藏
页码:850 / 856
页数:7
相关论文
共 35 条
[1]   ACTIVATED AND MEMORY ALVEOLAR T-LYMPHOCYTES IN IDIOPATHIC EOSINOPHILIC PNEUMONIA [J].
ALBERA, C ;
GHIO, P ;
SOLIDORO, P ;
MABRITTO, I ;
MARCHETTI, L ;
POZZI, E .
EUROPEAN RESPIRATORY JOURNAL, 1995, 8 (08) :1281-1285
[2]   EOSINOPHILIC LUNG-DISEASES [J].
ALLEN, JN ;
DAVIS, WB .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1994, 150 (05) :1423-1438
[3]   ACUTE EOSINOPHILIC PNEUMONIA AS A REVERSIBLE CAUSE OF NONINFECTIOUS RESPIRATORY-FAILURE [J].
ALLEN, JN ;
PACHT, ER ;
GADEK, JE ;
DAVIS, WB .
NEW ENGLAND JOURNAL OF MEDICINE, 1989, 321 (09) :569-574
[4]   CHRONIC EOSINOPHILIC PNEUMONIA [J].
CARRINGT.CB ;
ADDINGTO.WW ;
GOFF, AM ;
MADOFF, IM ;
MARKS, A ;
SCHWABER, JR ;
GAENSLER, EA .
NEW ENGLAND JOURNAL OF MEDICINE, 1969, 280 (15) :787-&
[5]  
ENOKIHARA H, 1989, BLOOD, V73, P1809
[6]   MOUSE INTERLEUKIN-12 (IL-12) P40 HOMODIMER - A POTENT IL-12 ANTAGONIST [J].
GILLESSEN, S ;
CARVAJAL, D ;
LING, P ;
PODLASKI, FJ ;
STREMLO, DL ;
FAMILLETTI, PC ;
GUBLER, U ;
PRESKY, DH ;
STERN, AS ;
GATELY, MK .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1995, 25 (01) :200-206
[7]   Reduced interleukin-18 levels in BAL specimens from patients with asthma compared to patients with sarcoidosis and healthy control subjects [J].
Ho, LP ;
Davis, M ;
Denison, A ;
Wood, FT ;
Greening, AP .
CHEST, 2002, 121 (05) :1421-1426
[8]  
Hoshino T, 1999, J IMMUNOL, V162, P5070
[9]   Cutting edge: IL-18-transgenic mice: In vivo evidence of a broad role for IL-18 in modulating immune function [J].
Hoshino, T ;
Kawase, Y ;
Okamoto, M ;
Yokota, K ;
Yoshino, K ;
Yamamura, K ;
Miyazaki, J ;
Young, HA ;
Oizumi, K .
JOURNAL OF IMMUNOLOGY, 2001, 166 (12) :7014-7018
[10]  
Kadota J, 1996, CLIN EXP IMMUNOL, V103, P461