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Epidemiological and experimental studies suggest that diesel exhaust particles (DEP) may play an active role in the increased respiratory mortality and morbidity. We have shown that DEP augmented the production of inflammatory cytokines by human airway epithelial cells in vitro. ICAM-1 has been shown to play an important role in the local accumulation of inflammatory cells. We studied the effect of DEP on ICAM-1 gene expression and surface expression in human bronchial epithelial cell line BEAS-2B. DEP (5–50 μg/ml) showed a stimulatory effect on ICAM-1 mRNA levels as evaluated by reverse transcription-polymerase chain reaction (RT-PCR). Flow cytometric analysis demonstrated an increased ICAM-1 expression on the epithelial cell surfaces. The soluble form of ICAM-1 molecules was also increased by the stimulation of DEP. In vitro neutrophil attachment onto DEP-stimulated epithelial cells was augmented, which was partially blocked by anti-ICAM-1 neutralizing antibody. Finally, these events were significantly inhibited by pretreatment with anti-oxidants pyrrolidine dithiocarbamate and N-acetyl cysteine, and p38 mitogen activated protein kinase (MAPK) inhibitor SB203580. These findings suggested that DEP induced up-regulation of ICAM-1 gene, and this process might be largely dependent on oxidant-mediated NF-κB activation and p38-MAPK pathways. [ABSTRACT FROM AUTHOR]

ICAM-l plays an important role in inflammatory diseases. We analysed ICAM-l expression on BAL fluid cells and measured soluble ICAM-l (sICAM-I) concentrations in sent and BAL fluids from patients with extrinsic allergic alveolitis (EAA). We found significantly increased cellular ICAM-1 expression on BAL fluid lymphocytes and alveolar marcrophages, and significantly increased values of circulating and BAL fluid sICAM-l in EAA patients compared with controls. Successive measurement shows prompt decrease of both sICAM-l values in EAA patients during periods when antigen exposure was prevented. In BAL fluids from EAA patients sICAM-l values significantly correlated to neutrophil and ICAM-1+ lymphocyte counts. In EAA patients, circulating and BAL fluid sICAM-1 values has significant negative correlations to values of carbon monoxide diffusing capacity and to time intervals between last episode and sample collection. However, these values had significant positive correlation to values of alveolar arterial oxygen pressure difference. In EAA, antigen exposure appears to induce cellular ICAM-l expression on BAL fluid cells, and also appears to up-regulate shedding of ICAM-l in the alveolar lining fluid and in the circulation. The sICAM values appear to reflect disease activity of EAA. [ABSTRACT FROM AUTHOR]