[Role of alveolar macrophages in the pathogenesis of idiopathic interstitial pneumonia].
To clarify role of alveolar macrophages in the pathogenesis of idiopathic interstitial pneumonia (IIP), we studied (1) the localization and expression of monocyte chemoattractant protein-1 (MCP-1) in IIP by immunohistochemistry and in situ hybridization. (2) the role of MCP-1 in macrophage recruitment to be lung, and (3) the clinical usefulness of measuring MCP-1. (1) In IIP, MCP-1 was observed in cuboidal and flattened metaplastic epithelial cells, alveolar macrophages, and vascular endothelial cells. In contrast, no epithelial cells from patients without IIP stained positive for MCP-1, although alveolar macrophages and vascular endothelial cells were labeled. MCP-1 production by epithelial cells in IIP may be caused by the metaplastic nature of the epithelial cells and may be a main cause of the irreversible progression of IIP. (2) MCP-1 levels in bronchoalveolar lavage fluid (BALF) were significantly higher in the IIP, the interstitial pneumonia due to collagen vascular disease (IP-CVD) and sarcoidosis groups than in normal controls. In the IIP group, the MCP-1 level was significantly higher than in any other patient groups. In all three groups of patients, the monocyte chemotactic activity in BALF correlated positively with the MCP-1 levels in BALF, and were neutralized by anti-MCP-1. (3) BALF MCP-1 levels were significantly higher than serum MCP-1 levels in the IIP group, and they were lower in the IP-CVD and non-specific interstitial pneumonia groups. Serum MCP-1 levels reflected the activity of interstitial lung diseases, especially during treatment with corticosteroids. These results indicate (1) that MCP-1 plays a significant role in the recruitment of monocytes into the lung in IIP, (2) that measuring MCP-1 levels both in BALF and in serum may help discriminate IIP from other types of interstitial lung diseases, and (3) that monitoring the serum MCP-1 level may be useful in estimating the activity of interstitial lung diseases.
Suga
M
M
First Department of Internal Medicine, Kumamoto University School of Medicine, Japan.
Iyonaga
K
K
Ando
M
M
D015415:Biomarkers / Q000032:analysis; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D018932:Chemokine CCL2 / Q000502:physiology*; D004730:Endothelium, Vascular / Q000378:metabolism; D006801:Humans; D017563:Lung Diseases, Interstitial / Q000209:etiology*; D016676:Macrophages, Alveolar / Q000502:physiology*
D015415:Biomarkers; D018932:Chemokine CCL2