1. CC chemokine receptor 4 ligand production by bronchoalveolar lavage fluid cells in cigarette-smoke-associated acute eosinophilic pneumonia.
- Author
-
Nureki S, Miyazaki E, Ando M, Kumamoto T, and Tsuda T
- Subjects
- Adolescent, Adult, Chemokine CCL17, Chemokine CCL22, Chemokines, CC metabolism, Granulocyte-Macrophage Colony-Stimulating Factor metabolism, Humans, Immunohistochemistry, Interleukin-4 metabolism, Ligands, Pulmonary Eosinophilia etiology, Receptors, CCR4, Smoking metabolism, T-Lymphocyte Subsets metabolism, Th2 Cells metabolism, Bronchoalveolar Lavage Fluid immunology, Pulmonary Eosinophilia metabolism, Receptors, Chemokine metabolism, Smoking adverse effects
- Abstract
We examined the production of macrophage-derived chemokine (MDC/CCL22) and thymus- and activation-regulated chemokine (TARC/CCL17) by bronchoalveolar lavage fluid (BALF) cells in cigarette-smoke-associated acute eosinophilic pneumonia (CS-AEP). The CC Chemokine Receptor 4 (CCR4) ligand levels in BALF from patients with CS-AEP were considerably higher than those in healthy volunteers and correlated well with Th2 cytokine levels. Interleukin-4 enhanced CCR4 ligand production. MDC expression was observed in CD68-positive cells from patients with CS-AEP and in healthy control smokers. In contrast, TARC expression in CD68- or CD1a-positive cells was detected only in CS-AEP. An in vivo cigarette smoke challenge test induced increases in CCR4 ligands in the BALF and in the cultured supernatant of BALF adherent cells. These results suggest that alveolar macrophages and dendritic cells contribute to the pathogenesis of CS-AEP by generating CCR4 ligands, probably in response to cigarette smoke.
- Published
- 2005
- Full Text
- View/download PDF