			Home About us Contact

Emphysematous Changes (emphysematous + change)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Altered expression of antimicrobial molecules in cigarette smoke-exposed emphysematous mice lungs

RESPIROLOGY, Issue 7 2008
Yoko SHIBATA
Background and objective: The natural history of COPD, a disease usually caused by cigarette smoking, is associated with frequent respiratory infections. Consistent with human COPD, bacterial clearance in the lungs has been reported to be impaired in mice exposed to cigarette smoke. In the airways, several antimicrobial molecules such as surfactant proteins (SP), beta-defensins (BD), secretory leucocyte protease inhibitor (SLPI) and lysozyme play important roles in the defence against invading pathogens. This study evaluated the expression of antimicrobial molecules in mice lungs with cigarette smoke-induced emphysematous changes. Methods: Six B6C3F1 mice were exposed to cigarette smoke (2 cigarettes/day/mouse for 6 months) or room air. Gene expression within the lungs of mice in both groups was assessed by RT-PCR. Results: The expression of SP-A, BD2, BD3 and SLPI was significantly elevated in the lungs of cigarette smoke-exposed mice compared with air-exposed mice. BD1 expression decreased in the smoke-exposed mice and lysozyme expression was unchanged. Conclusions: Chronic cigarette smoke exposure did not suppress the expression of antimicrobial molecules in the lung. Altered expression of antimicrobial molecules in this mouse model does not explain the impaired host defence against respiratory microbes seen in patients with COPD. [source]

Effects of melatonin on the oxidant/antioxidant status and lung histopathology in rabbits exposed to cigarette smoke

RESPIROLOGY, Issue 4 2006
Mehmet UNLU
Objectives and background: To evaluate the effects of cigarette smoking on the histopathology and the oxidant/antioxidant status of the lungs and to test the potential antioxidant benefits of melatonin on these induced changes. Methodology: Rabbits were exposed to cigarette smoke in a glass chamber for 1 h daily for 1 month with or without intraperitoneal melatonin injection. A melatonin control group was given intraperitoneal melatonin only. A control group was exposed to clean air only. At the end of 1 month, animals were sacrificed and lung tissues were examined histopathologically. Blood levels of protein sulphydryls, carbonyls, prostaglandin F2, (PGF2,), malondialdehyde (MDA), glutathione peroxidase and superoxide dismutase (SOD) were measured. Results: Intraparenchymal vascular congestion and thrombosis, intraparenchymal haemorrhage, respiratory epithelial proliferation, number of macrophages in the alveolar and bronchial lumen, alveolar destruction, emphysematous changes and bronchoalveolar haemorrhage scores were significantly increased in rabbits exposed to cigarette smoke compared with the control group. Protein sulphydryls and SOD levels were significantly decreased; carbonyls, PGF2, and MDA levels were significantly increased in the smoke exposed rabbits. Administration of melatonin to rabbits exposed to cigarette smoke caused a reduction in the bronchoalveolar haemorrhage score and blood carbonyls levels. Other parameters were unaffected by melatonin. Conclusion: Exposure to cigarette smoke causes severe histopathological changes and negatively affects the oxidant/antioxidant status in the lungs of rabbits. A low daily dose of melatonin has some protective effects on histopathological changes and oxidant/antioxidant status of the lungs in smoke exposed rabbits. [source]

Influence of long-term cigarette smoking on immunoglobulin E-mediated allergy, pulmonary function, and high-resolution computed tomography lung densitometry in elderly patients with asthma

CLINICAL & EXPERIMENTAL ALLERGY, Issue 1 2004
F. Mitsunobu
Summary Background Smoking is the most important cause of chronic obstructive pulmonary disease (COPD). However, the influence of cigarette smoking on the pathogenesis of asthma in the elderly remains controversial. This study attempted to clarify the influence of cigarette smoking on elderly asthmatics. Methods Forty-eight asthmatics over 70 years old (25 ex-smokers and 23 never-smokers) and 20 patients with COPD over 70 years old (all ex-smokers) were studied to determine the influence of cigarette smoking on IgE-mediated allergy (total IgE, IgE antibodies against inhalant allergens, bronchial hyper-responsiveness (BHR), generation of leukotriene (LT) B4 and C4), pulmonary function, and the relative area of lung showing attenuation values less than ,950 Hounsfield units (RA950) on high-resolution computed tomography scans. Results The incidence of positive IgE antibodies against inhalant allergens, BHR, and the generation of leukotriene B4 (LTB4) by leucocytes were significantly increased in patients with a history of smoking compared with those without. Residual volume (%RV) was significantly increased, and diffusing capacity for carbon monoxide was significantly decreased in ex-smokers with asthma and COPD compared with never-smokers with asthma. Inspiratory RA950 and ratio of expiratory RA950 to inspiratory RA950 were significantly larger in asthmatics with a smoking history than in those without, and in COPD patients than in asthmatics. Conclusion Cigarette smoking enhances the production of IgE antibodies, BHR, and generation of LTB4 by leucocytes in elderly asthmatics. Increased hyper-inflation or emphysematous changes of the lungs expressed by increased RA950, closely related to %RV, was more frequently observed in ex-smokers compared with never-smokers. [source]

IMPROVING THE CADMIUM-INDUCED CENTRIACINAR EMPHYSEMA MODEL IN RATS BY CONCOMITANT ANTI-OXIDANT TREATMENT

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2008
S Heili Frades
SUMMARY 1The aim of the present study was to perform an evolutionary analysis of the morphometrical, biochemical and functional parameters of centriacinar emphysema induced by cadmium chloride (CdCl2) in rats and to determine the effects of concomitant N -acetylcysteine (NAC) administration. 2Male Wistar rats were instilled orotracheally with either CdCl2 (n = 24) or saline (n = 24). One group of rats, consisting of both CdCl2 - and saline-treated rats, was fed a normal diet (n = 24), whereas the other group received NAC (n = 24). 3Changes in inspiratory capacity (IC), lung compliance (CL), expiratory flow at 75% (F75), forced vital capacity (FVC) and hydroxyproline content were assessed 2, 8, 21 and 45 days after instillation. Polymorphonuclear cells were evaluated 2 and 8 days after instillation and the mean linear intercept (Lm) was determined at 21 and 45 days. 4Over time, CdCl2 instillation causes several changes that are bound up with centriacinar emphysema. The concomitant administration of NAC to CdCl2 -treated rats partially reversed Lm at 21 days compared with CdCl2 alone (115 ± 2 vs 127 ± 2, respectively; P < 0.05). However, 45 days after instillation, NAC improved lung function in CdCl2 -treated rats compared with that in the saline-treated control group (IC 14.64 vs 15.25, respectively (P = 0.054); FVC 16.94 vs 16.28, respectively (P = 0.052), F75 31.41 vs 32.48, respectively (P = 0.062)). In addition, 45 days after instillation, NAC reduced lung collagen content in both the saline-treated control (100 vs 81% alone and in the presence of NAC, respectively) and CdCL2-treated groups (213 vs 161% alone and in the presence of NAC, respectively). In addition, although the results were not significant, NAC tended to reduce Lm and enhance CL in NAC + CdCl2 -treated rats. 5In conclusion, NAC partially improved emphysematous changes and reduced collagen deposition, which diminished the CdCl2 -induced fibrotic component of centriacinar emphysema. [source]