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In our study of 52 patients with idiopathic pulmonary fibrosis (IPF), we found that the incidence of clubbing of the fingers was significantly more frequent in male than in female [...]

The purpose of this study was to evaluate the role of high-resolution computed tomography (HRCT) in the clinical diagnosis of diffuse infiltrative lung disease (DILD). Diagnostic accuracy was compared using [...]

We compared the doubling time of fibroblasts derived from idiopathic pulmonary fibrosis (usual interstitial pneumonia) (IPF [UIP]) lung tissues and control fibroblasts, cultured in usual growth medium, and examined the [...]

The clinical features of 34 Japanese patients with bronchiolitis obliterans organizing pneumonia (BOOP) are discussed. Thirty-two patients (94 percent) had symptoms of cough, fever, or dyspnea. On chest roentgenograms, bilateral [...]

Bronchiolitis obliterans with organizing pneumonia (BOOP) is a clinicopathologic entity.[1] It is pathologically defined as granulation tissue plugs within lumens of small airways, sometimes with complete obstruction of small airways [...]

We report three cases of chronic hepatitis C (HC) with pneumonitis, suspected to be caused by natural and recombinant interferon (INF) alfa treatments. The patients were administered INF through intramuscular [...]

We investigated the effect of smoking on natural killer (NK) cell activity and distribution in bronchoalveolar lavage fluid (BALF) and blood. Initially, BALF NK cell activity was lower than the blood NK cell activity both in non-smokers (NS) and smokers (S). Following 24 hour culture, NK cell activity markedly increased in NS but not in S. Percentage distribution of Leu-7+cells and Leu-11+ cells in BALF was similar in NS and S. But the BALF NK cell activity was significantly augmented by IL-2 or OK-432 (a streptococcal preparation) in NS. It appears that smoking reduces NK cell activity in BALF. It is conceivable that the low NK cell activity in BALF in S might contribute to increased incidence of infection and malignancy in smokers. (Chest 1988; 94.-688-93)

To evaluate the activation of alveolar macrophages from smoking, we studied interleukin-1 (IL-1) activity released from alveolar macrophages in eight healthy smokers, compared to 12 healthy nonsmokers. We used 24-hour culture supernatants containing IL-1 of bronchoalveolar lavage fluid (BALF) macrophages/blood monocytes with or without LPS stimulation. Using C3H/HeJ thymocyte PHA costimulation assay, we found that IL-1 activity released from LPS stimulated BALF macrophages was significantly higher in smokers (2.39 ± 0.33 U/ml) than in nonsmokers (1.47 ± 0.19 U/ml, p<0.05). We also detected IL-1 inhibitory activity in supernatants by using IL-1 inhibitory assay. The inhibitory activity was higher in nonsmokers than in smokers especially under LPS stimulation. The presence of inhibitory (actors other than prostaglandin-E2, was suggested from the differential response to the addition of indomethacin into cultures from nonstimulated and LPS-stimulated supernatants of BALF macrophages. (Chest 1988; 94:694-700)

We investigated the mechanism of suppressive effect of alveolar macrophages (AM) on autologous blood NK cell activity in healthy nonsmokers (NS) and smokers (S). A 50 percent additional concentration of AM both in NS and S inhibited NK cell activity significantly (p<0.05). The degree of inhibition was not different in NS and S. Effects of prostaglandins (PG) and oxygen radicals were studied separately on the NK cell activity in the presence of AM. Indomethacin, catalase, or thiourea did not reverse inhibition of NK cell activity, but superoxide dismutase (SOD) prevented this phenomenon. These results suggest that the inhibition of NK cell activity by AM may be caused by O2release rather than PG, H2O2, and OH.