BackgroundVitamin D can translocate a vitamin D receptor (VDR) from the nucleus to the cell membranes. The meaning of this translocation is not elucidated in terms of a role in pathogenesis of chronic obstructive pulmonary disease (COPD) till now. VDR deficient mice are prone to develop emphysema, suggesting that abnormal function of VDR might influence a generation of COPD. The blood levels of vitamin D have known to be well correlated with that of lung function in patients with COPD, and smoking is the most important risk factor in development of COPD. This study was performed to investigate whether cigarette smoke extracts (CSE) can inhibit the translocation of VDR and whether mitogen activated protein kinases (MAPKs) are involved in this inhibition.MethodsHuman alveolar basal epithelial cell line (A549) was used in this study. 1,25-(OH2)D3 and/or MAPKs inhibitors and antioxidants were pre-incubated before stimulation with 10% CSE, and then nucleus and microsomal proteins were extracted for a Western blot of VDR.ResultsFive minutes treatment of 1,25-(OH2)D3 induced translocation of VDR from nucleus to microsomes by a dose-dependent manner. CSE inhibited 1,25-(OH2)D3-induced translocation of VDR in both concentrations of 10% and 20%. All MAPKs inhibitors did not suppress the inhibitory effects of CSE on the 1,25-(OH2)D3-induced translocation of VDR. Quercetin suppressed the inhibitory effects of CSE on the 1,25-(OH2)D3-induced translocation of VDR, but not in n-acetylcysteine.ConclusionCSE has an ability to inhibit vitamin D-induced VDR translocation, but MAPKs are not involved in this inhibition.

Tuberculosis (TB) is an infectious disease caused by mycobacterium, which most commonly affects the lungs. The adaptive immune response in Mycobacterium tuberculosis is predominantly mediated by the interferon-γ (IFN-γ) signaling pathway, which is regulated by IFN-γ receptors (IFNGR). IFN-γ activates the transcription of a number of genes that are important in immune responses, thus the appropriate function of IFNGR appears to be important in host defense against mycobacteria. In the present study, 22 genetic variants in IFNGR1 and IFNGR2 were genotyped in 673 patients and 592 normal controls to investigate the association between IFNGR1 and IFNGR2 polymorphisms and the risk of TB. Statistical analyses revealed that four genetic variants in IFNGR1, rs9376269, rs9376268, rs9376267 and rs56251346 were marginally associated with the risk of TB (P = 0.02-0.04), while other single nucleotide polymorphisms in IFNGR1 and IFNGR2 did not exhibit any associations. However, the significance of the four genetic variants rs9376269, rs9376268, rs9376267 and rs56251346 was eliminated following a multiple testing correction of the data (P>0.05). The present results revealed that certain genetic variants in IFNGR genes may be associated with TB development, which may be useful preliminary data for future investigation.

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BackgroundMost patients with influenza recover spontaneously or following treatment with an anti-viral agent, but some patients experience pneumonia requiring hospitalization. We conducted a retrospective review to determine the incidence and risk factors of pneumonia in hospitalized patients with influenza A or B.MethodsA total of 213 patients aged 18 years or older and hospitalized with influenza between January 2012 and January 2015 were included in this study. A reverse-transcriptase polymerase chain reaction assay was used to detect the influenza A or B virus in the patients' sputum samples. We collected demographic and laboratory data, combined coexisting diseases, and radiologic findings.ResultsThe incidence of pneumonia was higher in patients in the influenza A group compared to those in the influenza B group (68.6% vs. 56.9%), but this difference was not statistically significant. The presence of underlying respiratory disease was significantly associated with pneumonia in the influenza A group (adjusted odds ratio [OR], 3.975; 95% confidence interval [CI], 1.312–12.043; p=0.015). In the influenza B group, the white blood cell count (adjusted OR, 1.413; 95% CI, 1.053–1.896; p=0.021), platelet count (adjusted OR, 0.988; 95% CI, 0.978–0.999; p=0.027), and existence of an underlying medical disease (adjusted OR, 15.858; 95% CI, 1.757–143.088; p=0.014) were all significantly associated with pneumonia in multivariate analyses.ConclusionThe incidence of pneumonia was 65.7% in hospitalized patients with influenza A or B. The risk factors of pneumonia differed in hospitalized patients with influenza A or B.

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Cryptogenic organizing pneumonia (COP) is an idiopathic interstitial pneumonia characterized by a subacute course and favorable prognosis with corticosteroids. However, some patients show resistance to steroids. Macrolides have been used with success in those patients showing resistance to steroids. A few reports showed treatment failure with macrolides in patients with COP who were resistant to steroids. In this report, we described two cases of COP who showed different responses to clarithromycin. One recovered completely, but the other gradually showed lung fibrosis with clarithromycin.

Aspergillus fumigatus causes a variety clinical syndrome in lung including aspergilloma, chronic necrotizing aspergillosis, invasive pulmonary aspergillosis, and allergic bronchopulmonary aspergillosis. Aspergilloma develops by a colonization and growing of Aspergillus inside lung cavities with underlying lung disease. There is a few report of endobronchial aspergilloma without lung parenchymal lesion. We experienced a case of endobronchial aspergilloma did not fit any category of Aspergillus-induced lesion, who show minimal fibrostreaky denstities on chest PA and chest CT.

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