Chemokine Secretion From Alveolar Macrophages in Patientswith Diffuse Interstitial Lung Diseases(DILD)..
10.4046/trd.1996.43.6.954
- Author:
Dong Soon KIM
1
;
Sang Hoon PAIK
;
Chae MAN LIM
;
Sang Do LEE
;
Younsuck KOH
;
Woo Sung KIM
;
Won Dong KIM
Author Information
1. Asan Medical Center, Ulsan University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Interstitial lung disease (DILD);
BAL;
IL-8;
MIP-1alpha
- MeSH:
Cell Count;
Chemokine CCL3;
Chemokines;
Collagen Diseases;
Humans;
Hypersensitivity;
Inflammation;
Interleukin-8;
Lung Diseases, Interstitial;
Lung*;
Lymphocytes;
Macrophages;
Macrophages, Alveolar*;
Neutrophils;
Sarcoidosis;
T-Lymphocytes
- From:Tuberculosis and Respiratory Diseases
1996;43(6):954-964
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: The type of the infiltrating cells in alveolitis may be determined by the chemokines in the lesion. MIP-1alpha, a C-C type chemokine, stimulates proliferation and cytokine secretion from macrophages and induces early neutrophilic and later monocytic inflammation in vivo. IL-8, a C-X-C type chemokine is known to attract neutrophils and T-lymphocytes. This study is performed to find out the relative role of two different chemokines in diffuse interstitial lung disease. SUBJECT AND METHOD: We measured the secretion of MIP-1alpha and IL-8 from alveolar macrophages(AM), and their level in BAL fluid of 26 patients with DILD (10 IPF, 4 collagen disease, 10 sarcoidosis, and 2 hypersensitivity pneumonitis) and 7 normal control. RESULT: IL-8 secretion was significantly increased in patients with DILD (8.15+/-4.58 ng/ml) than in normal (1.10+/-0.93 ng/ml, p=0.0003). Significant correlation was found between IL-8 secretion and total cell number in BAL fluid (r=0.484, p=0.0068), %(r=0.592, p=0.0004) and No. (r=0.516, p=0.0042) of lymphocyte, and % of AM (r=-0.505, 0.0032). MIP-1alpha secretion was also increased in DILD (2.41+/-1.45 ng/ml) compared to control (0.63+/-0.30 ng/ml, p=0.0031), and showed a tendency of correlation with total cell number (r=0.368, p=0.0456) and No. of alveolar macrophages (r=0.356, p=0.0579) in BAL fluid. The concentration of IL-8 in BAL fluid was significantly increased in the patients with DILD (40.4+/-34.5 pg/ml) compared to control (3.90 +/- 2.47 pg/ml, p=0.0094) and it showed a significant correlation with the total cell number(r=0.484, p=0.0068), %(r=-0.505, p=0.0032) of AM, and % (r=0.592, p=0.0004) and No. (r=0.516, p=0.0042) of lymphocyte in BAL fluid. But there was a no significant difference in MIP-1alpha concentration in BAL fluid between normal control group and the patients with DILD. Conclusion: From the above results, we concluded that AM of DILD releases increased amount of both IL-8 and MIP-1alpha but IL-8 has better correlation with the type of alveolitis.
