We evaluated the effect of chronic tobacco smoke exposure on the function of the alveolar macrophage (AM) in mice. Tumor necrosis factor-α production of the AM triggered by lipopolysaccharides was smaller in smoke-exposed mice as compared to control mice but did not reach statistical significance (27.3 ± 4.0 vs. 34.8 ± 4.9 U/ml). The percentage of AM which did not phago-cytize latex particles in the smoke-exposed mice was significantly larger than that in control mice (33.9 ± 2.3 vs. 20.8 ± 2.1%; p < 0.05). la antigen expression of the AM was significantly larger in smoke-exposed mice (cytotoxicity index: 0.180 ± 0.033 vs. 0.038 ± 0.0118; p < O.Ol). The asialo-GMl antigen expression was similar in both groups (0.949 ± 0.007 vs. 0.961 ± 0.011). Although the precise mechanisms of these functional changes of the AM by tobacco smoke exposure are not clear, they may have some immunological effects on the alveolar space.

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1α,25-Dihydroxyvitamin D₃ [1α,25(OH)₂D₃, calcitriol] has been shown to modulate the immune function of peripheral monocytes and peritoneal macrophages. However, its effect on alveolar macrophage (AM) cytokine secretion has not been reported. We therefore investigated the influence of calcitriol on tumor necrosis factor (TNF-α) production by murine AMs and attempted to elucidate changes in the signal transduction system involved in such effects. Calcitriol significantly enhanced TNF-α secretion by AM stimulated with either lipopolysaccharide (LPS; 10 µg/ml; p < 0.005) or phorbol 12-myristate 13-acetate (PMA; 100ng/ml; p < 0.05) at low doses (between 10^-11 and 10^-9M). However the protein kinase C (PKC) inhibitor, H7 (10 µM), and the Ca²⁺/calmodulin inhibitor, W7 (25 µM), reversed such calcitriol effects. Calcitriol increased the total PKC activity of AMs. These findings indicate that calcitriol enhances both LPS- and PMA-stimulated TNF-α secretion through PKC- or Ca²⁺/calmodulin-dependent pathways.

A previously healthy young man presented with acute respiratory distress, high fever and bilateral ground-glass appearance on chest radiograph. Bronchoalveolar lavage analysis demonstrated significant eosinophilia (72%) with no evidence of infection. The transbronchial lung biopsy showed that the walls of bronchioli and alveolar septa were markedly infiltrated with eosinophils. The patient rapidly improved with corticosteroid therapy. This case exemplifies the recently described idiopathic acute eosinophilic pneumonia. Similar cases published in the Japanese literature were reviewed and discussed.

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