Elevated chemokine levels in bronchoalveolar lavage fluid of patients with eosinophilic pneumonia

被引:44
作者
Katoh, S
Matsumoto, N
Fukushima, K
Mukae, H
Kadota, J
Kohno, S
Matsukura, S
机构
[1] Miyazaki Med Coll, Dept Internal Med 3, Kiyotake, Miyazaki 8891692, Japan
[2] Nagasaki Perfecture Tarami Hosp, Nagasaki, Japan
[3] Nagasaki Univ, Sch Med, Dept Internal Med 2, Nagasaki 852, Japan
关键词
eosinophilic pneumonia; eotaxin; RANTES; monocyte chemotactic protein 1; macrophage inflammatory protein 1 beta; IL-8; bronchoalveolar lavage fluid; eosinophil;
D O I
10.1067/mai.2000.109827
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Background: Allergic lung inflammation is caused by accumulation and activation of different leukocyte subsets, such as eosinophils and T lymphocytes, in the lung, The chemokines are a large group of chemotactic cytokines that regulate leukocyte trafficking and may play an important role in allergic lung inflammation. Objective: The purpose of this study was to evaluate the role of various chemokines, including eotaxin, RANTES, monocyte chemotactic protein (MCP)-1, macrophage inflammatory protein (MIP)-1 beta, and IL-8 in the pathogenesis of eosinophilic pneumonia (EP). Methods: The concentrations of eotaxin, RANTES, MCP-1, MIP-1 beta, and IL-8 in bronchoalveolar lavage fluid (BALF) were measured by using ELISA in 15 patients with EP, 10 with idiopathic pulmonary fibrosis, 10 with sarcoidosis, and 11 healthy volunteers. Results: Eotaxin in BALF was high only in patients with EP, and its level correlated significantly with the number of eosinophils in BALF of patients with EP and healthy volunteers. MCP-1 and MIP-1 beta in BALF were preferentially increased in patients with EP. There was a significant correlation between MCP-1 levels and the number of macrophages in BALF of patients with EP and healthy volunteers. Conclusion: Our findings suggest that these CC chemokines contribute to the pathogenesis of EP through the specific recruitment of leukocyte subsets in the lung.
引用
收藏
页码:730 / 736
页数:7
相关论文
共 29 条
[1]   Chemokines in allergic inflammation [J].
Alam, R .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1997, 99 (03) :273-277
[2]   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
[3]   EOSINOPHILIC LUNG-DISEASES [J].
ALLEN, JN ;
DAVIS, WB .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1994, 150 (05) :1423-1438
[4]   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
[5]   Detection of IL-5 and IL-1 receptor antagonist in bronchoalveolar lavage fluid in acute eosinophilic pneumonia [J].
Allen, JN ;
Liao, ZM ;
Wewers, MD ;
Altenberger, EA ;
Moore, SA ;
Allen, ED .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1996, 97 (06) :1366-1374
[6]   MONOCYTE CHEMOATTRACTANT PROTEIN-1 ACTS AS A T-LYMPHOCYTE CHEMOATTRACTANT [J].
CARR, MW ;
ROTH, SJ ;
LUTHER, E ;
ROSE, SS ;
SPRINGER, TA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (09) :3652-3656
[7]   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-&
[8]  
Chensue SW, 1996, J IMMUNOL, V157, P4602
[9]   COOPERATION BETWEEN INTERLEUKIN-5 AND THE CHEMOKINE EOTAXIN TO INDUCE EOSINOPHIL ACCUMULATION IN-VIVO [J].
COLLINS, PD ;
MARLEAU, S ;
GRIFFITHSJOHNSON, DA ;
JOSE, PJ ;
WILLIAMS, TJ .
JOURNAL OF EXPERIMENTAL MEDICINE, 1995, 182 (04) :1169-1174
[10]  
GILAT D, 1994, J IMMUNOL, V153, P4899