To evaluate findings of active pulmonary tuberculosis on computed tomographic (CT) scans and their sequential changes before and after antituberculous chemotherapy, 29 patients with newly diagnosed pulmonary tuberculosis and 12 patients with recent reactivation were studied prospectively. The diagnosis of active pulmonary tuberculosis was based on positive acid-fast bacilli in sputum (n = 29) and changes on serial radiographs obtained during treatment (n = 12). Twenty-six patients were followed up with CT during treatment for 1-20 months. Lungs from the cadavers of nine other patients, who died of pulmonary tuberculosis, were studied to provide a pathologic basis for diagnosis. At examination with CT, centrilobular lesions (nodules or branching linear structures 2-4 mm in diameter) were most commonly seen (n = 39 [95%]); in the 26 patients with follow-up, most of these lesions disappeared within 5 months after the start of treatment. In 11 of 12 patients with recent reactivation, CT clearly differentiated old fibrotic lesions from new active lesions. Lesions in and around the small airways appear to be the most characteristic CT feature of early active tuberculosis and may be a reliable criterion for disease activity.

Heat shock protein (HSP) induction confers protection against diverse forms of cellular and tissue injury. However, the mechanism by which HSP exerts cytoprotective effects is unclear. Because HSP induction inhibits genetic expression of pro-inflammatory cytokines, the transcription of which is dependent on NF-κB activation, we explored the relationship between the anti-inflammatory effect of HSP induction and the NF-κB/IκBα pathway. Both HS and sodium arsenite treatment increased HSP70 expression time dependently at mRNA and protein levels. Prior induction of HSP suppressed cytokine-induced IL-8 and TNF-α expression at both mRNA and protein levels. Although HSP induction did not affect total cellular expression of NF-κB, TNF-α-induced increase in NF-κB-DNA binding activity and nuclear translocation of the p65 subunit of NF-κB were inhibited by prior HSP induction, suggesting that activation of NF-κB was blocked. Cytokine-induced IκBα phosphorylation and its degradation were blocked in HSP-induced cells. Immune complex kinase assays demonstrated that TNF-α induced increase in IκB kinase activity was suppressed by prior HSP induction. These results suggest that the anti-inflammatory effect of HSP induction in respiratory epithelial cells is related to stabilization of IκBα, possibly through the prevention of IκB kinase activation, which thereby inhibits activation of NF-κB.

Background-Although smoking is the major causal factor in the development of chronic obstructive pulmonary disease (COPD), only 10-20% of chronic heavy cigarette smokers develop symptomatic COPD which suggests the presence of genetic susceptibility. This genetic susceptibility to COPD might depend on variations in enzyme activities that detoxify cigarette smoke products such as microsomal epoxide hydrolase (mEPHX) and glutathione-S transferase (GST). As there is increasing evidence that several genes influence the development of COPD, multiple gene polymorphisms should be investigated to find out the genetic susceptibility to COPD. Methods-The genotypes of 83 patients with COPD and 76 healthy smoking control subjects were determined by polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (PCR-RFLP) for the mEPHX gene, and multiplex PCR for GST M1 and GST T1 genes. The frequencies of polymorphic genotypes of mEPHX, GST M1, and GST T1 genes were compared both individually and in combination in patients with COPD and healthy smokers. Results-No diVerences were observed in the frequency of polymorphic genotypes in exons 3 and 4 of mEPHX, GST M1, and GST T1 genes between patients with COPD and healthy smokers. The frequencies of any combination of these genotypes also showed no diVerences between the COPD group and the control group. Conclusions-Genetic polymorphisms in mEPHX, GST M1, and GST T1 genes are not associated with the development of COPD in Koreans. (Thorax 2000;55:121-125)

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