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Tuberc Respir Dis > Volume 43(6); 1996 > Article
Tuberculosis and Respiratory Diseases 1996;43(6):954-964.
DOI:    Published online September 4, 2015.
Chemokine Secretion From Alveolar Macrophages in Patientswith Diffuse Interstitial Lung Diseases(DILD)..
Dong Soon Kim, , Sang Hoon Paik, , Chae Man Lim, , Sang Do Lee, , Younsuck Koh, , Woo Sung Kim, , Won Dong Kim,
1Asan Medical Center, Ulsan University, Seoul, Korea.
2Asan Institute for Life Science, School of Medicine, Ulsan University, Seoul, Korea.
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.
Key Words: Interstitial lung disease (DILD), BAL, IL-8, MIP-1alpha

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