BH Kang, BD Manderschied, YC Huang, JD Crapo and LY Chang
Department of Cell Biology, Duke University Medical Center, Durham, North Carolina, USA.

Induction of intercellular adhesion molecule-1 (ICAM-1) by proinflammatory cytokines during inflammation plays an important role in regulating polymorphonuclear neutrophil (PMN) migration and localization. In this report, we examined the effects of tumor necrosis factor-alpha (TNF alpha) and interferon-gamma (IFN gamma) on specific lung cell expression of ICAM-1 in vivo and the accompanying morphological changes. Balb-c mice were treated with phosphate-buffered saline (PBS) alone or with PBS containing 5 micrograms TNF alpha or IFN gamma through intranasal instillation. Twenty-four hours after treatment, their lungs were processed for immunoblot analysis and electron microscope immunocytochemistry. In the normal lung, the ICAM-1 level is high on type I alveolar epithelial cells, medium on arterial and venous endothelial cells, low on type II epithelial cells and capillary endothelium, and not detectable on bronchial epithelium. Topical treatment of the lung with either TNF alpha or IFN gamma induced a 50-60% increase in total lung and alveolar ICAM-1. A dramatic increase of alveolar type II cell surface ICAM-1 was observed (> 20- fold). Both cytokines caused 2-3-fold higher ICAM-1 expression on capillary endothelial cells and a 40% increase of ICAM-1 on alveolar type I cells that was not uniform. However, due to the large total surface area of type I epithelium, type I cells contribute 70-86% of total alveolar septal ICAM-1 and > 90% of alveolar surface ICAM-1 in either treated or normal mouse lungs. Increased ICAM-1 expression was also observed on nonparenchymal endothelial and epithelial cells. Margination and sequestration of PMN in cytokine-treated lungs were observed by histologic examination, measurements of total lung myloperoxidase activity, and number of neutrophils recovered in bronchoalveolar lavage fluid. These results showed that TNF alpha and IFN gamma induce ICAM-1 expression and infiltration of neutrophils in the lung. The response of specific lung cells in terms of induction of ICAM-1 in response to cytokine stimulation varied significantly, particularly between type I and type II epithelial cells.

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