Browsing by Subject "Cigarette smoke"

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    Effects of combustible cigarettes and electronic nicotine delivery systems on the regenerative properties of mesenchymal stem cells derived from periodontal ligament (PDL-MSCs)
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Kastratovic, Nikolina; Milosevic Djordjevic, Olivera; Harrell, Carl Randall; Djonov, Valentin; Volarevic, Vladislav; Biología Celular e Histología
    Introduction. Periodontal ligament-derived mesenchymal stem cells (PDL-MSCs) are promising cells with crucial roles in maintaining and repairing periodontal tissue. However, their regenerative capacity can be influenced by various factors, including cigarette smoke and electronic nicotine delivery system (ENDS) aerosols. Smoking and vaping can impair their regenerative potential, and even though ENDS are perceived as safer tobacco products, there is a lack of evidence to guarantee this assumption. Material and methods. Changes in the viability and proliferation of PDL-MSCs will be investigated after smoke and aerosol generation and cell exposure. In addition, the effects of smoke and aerosols on the immunomodulatory capacity of PDL-MSCs co-cultured with T lymphocytes will be further determined via the evaluation of cytokine profiles and flow cytometry analysis of T-cell phenotypes. Results. Combustible cigarettes (CCs) induced more severe impairment in the viability and proliferation of PDL-MSCs compared with ENDS. Also, CCs promoted a proinflammatory immune response that could cause tissue damage to progress. On the other hand, ENDS had the potential to generate an immunosuppressive response that would prevent further cell decay. Discussion. The regenerative capacity of PDL-MSCs decreased after treatment with both cigarette smoke and ENDS-aerosols. Even though the results demonstrate less severe effects with ENDS, further research is essential to evaluate their safety and impact on the capacity of PDL-MSCs to prevent and restore oral injuries caused by chronic exposure to aerosols
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    Lung CD57+ cell density is increased in very severe COPD
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2012) Olloquequi, Jordi; García Valero, José; Rodríguez, Esther; Montero, M. Ángeles; Ferrer, Jaume; Montes, Juan F.
    Among all inflammatory cells involved in COPD, those with a cytolytic or elastolytic activity are thought to play a key role in the pathogenesis of the disease. However, there is no data about the infiltration of cells expressing the CD57 marker in small airways and parenchyma of COPD patients. In this study, surgical specimens from 43 subjects undergoing lung resection due to lung cancer (9 non-smokers, 18 smokers without COPD and 16 smokers with moderate COPD) and 16 patients undergoing double lung transplantation for very severe COPD were examined. CD57+ cells, neutrophils, macrophages and mast cells infiltrating bronchioles (epithelium, smooth muscle and connective tissue) and parenchymal interstitium were localized and quantified by immunohistochemical analysis. Compared to the other groups, the small airways of very severe COPD patients showed a significantly higher density of CD57+ cells, mainly infiltrated in the connective tissue (p=0.001), and a significantly higher density of neutrophils located characteristically in the epithelium (p=0.037). Also, the density of neutrophils was significantly higher in parenchyma of very severe COPD patients compared with the rest of the groups (p=0.001). Finally, there were significant correlations between the bronchiolar density of CD57+ cells and the FEV1 values (R=-0.43, p=0.022), as well as between the parenchymal density of neutrophils and macroscopic emphysema degree (R=0.43, p=0.048) in COPD groups. These results show that CD57+ cells may be involved in COPD pathogenesis, especially in the most severe stages of the disease
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    The modifications produced in allergic alveolitis and in goodpasture's syndrome due to exposure to cigarette smoke
    (Murcia : F. Hernández, 1991) Escolar Castellón, J.de D.; Roche Roche, P.A.; Escolar castellón, A.; Miñana Amada, C.
    Two groups of rats with experimental alveolitis were exposed to cigarette smoke. After comparing the results, the possible muffling effect of the cigarette smoke related to interstitial lung disease was discussed. 180 rats were divided into 6 groups of 30 animals each: Group 1: untreated controls; Group 2: exposed to cigarette smoke for 2 months: Group 3: sensitized with bovine albumin (BA) and exposed to an atmosphere with this antigen for two months, to reproduce a type of extrinsic allergic alveolitis (EAA); Group 4: treated with a single daily dose of anti-lung serum for three days followed by two days without treatment, to reproduce a type of Goodpasture's syndrome; Group 5: exposed to cigarette smoke and to BA; Group 6: exposed to cigarette smoke and treated with anti-lung serum. The animals were sacrificed and their lungs were treated for: Bronchoalveolar lavage (BAL), percentage lymphocyte count, polymorphonuclear (PMN) and alveolar macrophages (AM); semiquantitative and morphometric histological study. The semiquantitative study determined the area of the studied lung incision, affected by granulomae, increased alveolar aerial spaces, thickened alveolar walls and haemosiderine lung area. The morphometric study, based on the linear integration method, evaluated: the distance between two alveolar walls, the amount of interstice per field; and the number of AM with haemosiderine per field was counted. From the results we point out that the treated animals had significantly higher lymphocyte and BAL PMN counts than the untreated ones; no significant differences were found between the singly and doubly treated animals. The animals exposed to cigarette smoke and treated with anti-lung serum were those that showed the least number of lymphocytes and PMN of all the treated animals. The semiquantitative variables studied were all increased in comparison to the control group, most of the increases being significant. The morphometric variables revealed significant differences with respect to the untreated group, except for the animals which were treated with anti-lung serum and cigarette smoke, which showed a minimum decrease in the alveolar size and a slight increase of the interstitial tissue. Only one morphometric variable showed a significant difference between the group treated with anti-lung serum and the one treated with anti-lung serum and cigarette smoke: the number of AM with haemosiderine in the lung. From the results we conclude that: 1) exposure to cigarette smoke causes alveolo-interstitial alterations which are detected by means of BAL and histology; 2) these alterations have no adjuvant effect when combined with the administration of BA; 3) the alveolo-interstitial affection found in the animals exposed to cigarette smoke and anti-lung serum is lower than in the animals which were only given anti-lung serum.
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    The tick-derived rBmTI-A protease inhibitor attenuates the histological and functional changes induced by cigarette smoke exposure
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Lourenço, Juliana D.; Ito, Juliana T.; Cervilha, Daniela A.B.; Sales, Davi S.; Riani, Alyne; Suehiro, Camila L.; Genaro, Isabella S.; Duran, Adriana; Puzer, Luciano; Martins, Milton A.; Sasaki, Sérgio D.; Lopes, Fernanda D.T.Q.S.
    Introduction. Smoking is the main risk factor for chronic obstructive pulmonary disease development and cigarette smoke (CS) exposure is considered an important approach to reproduce in rodents this human disease. We have previously shown that in an elastase-induced model of emphysema, the administration of a protease inhibitor (rBmTI-A) prevented and attenuated tissue destruction in mice. Thus, in this study we aimed to verify the effects of rBmTI-A administration on the physiopathological mechanisms of CS-induced emphysema. Methods. Mice (C57BL/6) were exposed to CS or room air for 12 weeks. In this period, 3 nasal instillations of rBmTI-A inhibitor or its vehicle were performed. After euthanasia, respiratory mechanics were evaluated and lungs removed for analysis of mean linear intercept, volume proportion of collagen and elastic fibers, density of polymorphonuclear cells, macrophages, and density of positive cells for MMP-12, MMP-9, TIMP-1 and gp91phox. Results. The rBmTI-A administration improved tissue elastance, decreased alveolar enlargement and collagen fibers accumulation to control levels and attenuated elastic fibers accumulation in animals exposed to CS. There was an increase of MMP12, MMP-9 and macrophages in CS groups and the rBmTIA only decreased the number of MMP-12 positive cells. Also, we demonstrated an increase in gp91phox in CS treated group and in TIMP-1 levels in both rBmTI-A treated groups. Conclusion. In summary, the rBmTI-A administration attenuated emphysema development by an increase of gp91phox and TIMP-1, accompanied by a decrease in MMP-12 levels.