Autophagy is the main cellular pathway for degradation of long-lived proteins and organelles and regulates cell fate in response to stress. Beclin 1 is a key regulator of this process. In some settings autophagy and apoptosis seem to be interconnected. Recent reports indicate that fibroblasts in idiopathic pulmonary fibrosis (IPF) acquire resistance to apoptosis. Here, we examined the expression of beclin 1, and of the anti apoptotic protein Bcl-2 in human IPF fibroblasts using immunohistochemistry and molecular biology in bioptic sections, in primary cultures of fibroblasts taken from patients with IPF and in fibroblast cell lines. Expression of beclin 1 in fibroblasts from IPF was down-regulated in comparison with fibroblasts from normal lungs while the anti-apoptotic protein Bcl-2 expression was over-expressed. Treatment of fibroblast cell cultures with cisplatin induced a significant increase in beclin 1 and caspase 3 protein levels but a reduction in Bcl-2 expression. These observations were confirmed by the analysis of acid compartments and transmission electron microscopy. Our results demonstrate a modified expression of the apoptotic beclin 1 Bcl-2 proteins in human IPF fibroblasts suggesting the existence of an autophagy/apoptosis system dysfunction.

Introduction. Sarcoidosis is a multisystemic granulomatous disorder characterized by multiple noncaseating granulomas involving intrathoracic lymph nodes and lung parenchyma. Recently, the use of anti-tumor necrosis factor alpha (anti-TNFα) agents has been introduced for therapy of chronic and refractory sarcoidosis with controversial results. Infliximab (Remicade) is a chimeric monoclonal antibody (mAb) that recognizes and binds TNFα, neutralizing its biological effects. In the present study,   99mTc labelled infliximab was used to study the expression of TNFα in sarcoid lesions and to evaluate its role as a predictive marker in response to therapy with Remicade. Material and Methods. A total of 10 patients with newly diagnosed sarcoidosis were enrolled together with 10 control patients affected by rheumatoid arthritis. All patients were studied by planar imaging of the chest with   99mTc-infliximab at 6 h and 24 h and total body [18F]-FDG PET/CT. Regions of interest were drawn over the lungs and the right arm and target-to-background ratios were analysed for   99mTc-infliximab. SUVmean and SUVmax were calculated over lungs for FDG. Results and Discussion. Image analysis showed low correlation between T/B ratios and BAL results in patients despite positivity at [18F]-FDG PET. Conclusion. In conclusion, patients with newly diagnosed pulmonary sarcoidosis, with FDG-PET and BAL positivity, showed a negative   99mTc-infliximab scintigraphy.

A 74-year-old non-smoker female presented to our attention with a history of dyspnea and cough. CT scan revealed multiple areas of patchy ground glass attenuation associated to a diffuse mosaic oligoemia. Scattered bilateral subcentimetric pulmonary nodules were also present. Patient underwent a surgical lung biopsy. Specimens showed features of diffuse neuroendocrine hyperplasia, microhoneycombing, fibroblast foci. A final diagnosis of diffuse neuroendocrine hyperplasia with obliterative bronchiolitis and UIP was rendered.

Background and Objectives:Tobacco smoke contains many substances that are harmful and induce cancerogenesis. Carbon monoxide (CO) is the parameter commonly monitored by smoking cessation centres. The purpose of this study was to analyse other parameters and risk factors, including respiratory function and CEA (serum carcinoembryonic antigen) levels, in patients undergoing smoking cessation. Methods:One hundred and eighty current smoking patients current smokers were recruited from the outpatients for smoking cessation. Sociodemographic and lifestyle analyses were performed on them. They were also studied for respiratory function parameters and CEA (serum carcinoembryonic antigen) levels. A control group of 171 former smoking patients were also studied for functional and clinical parameters. Current smokers were also monitored for several parameters in the first 3 months after starting therapy with nicotine inhaler and varenicline, in addition to the behaviour therapy. Results:Some functional and clinical differences were found between the smokers and the former smokers groups. In the smokers' group we found no significant differences in sociodemographic and lifestyle between females and males. Regarding the response to varenicline-nicotine treatment combined with minimal advice, 56% of patients stopped smoking after 3 months of therapy; 30% of these had a level of severe bronchial obstruction. Operating parameters and the level of CEA at the beginning of the therapy were evaluated after 3 months, showing significant differences. Carboxyhemoglobin was reduced by 1.06%, oxyhemoglobin increased by 2.94%, FEF 25/75% increased by 16%. Conclusions:We can say that smoking cessation leads quickly to the improvement of clinical, functional and laboratory parameters. Patients with severe obstruction are more motivated to stop smoking.