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PubMed1999

Neutrophil granule proteins in bronchoalveolar lavage fluid from subjects with subclinical emphysema.

Evidence for the contribution of neutrophils to the pathogenesis of pulmonary emphysema is not convincing. We evaluated neutrophil involvement in subclinical pulmonary emphysema by measuring human neutrophil lipocalin (HNL) and two matrix metalloproteinases, gelatinase B (MMP-9) and neutrophil collagenase (MMP-8), in bronchoalveolar lavage fluid (BALF) from 65 community-based older volunteers. HNL is a recently isolated 24-kD protein secreted from secondary granules of activated neutrophils. Despite no appreciable increase in the number of neutrophils, the level of HNL was significantly increased in BALF from subjects with emphysema evidenced by computed tomography regardless of current smoking, as compared with smokers without emphysema. The levels of MMP-9 and MMP-8 were also significantly higher in current smokers with emphysema than in those without emphysema. The appearance of a 130-kD HNL/MMP-9 complex on gelatin zymography and HNL immunoblot indicated neutrophils to be a significant source of MMP-9 in the subjects' BALF. In a 24-h culture medium of alveolar macrophages, only a latent form of MMP-9 was detected, and there was no difference in the level of MMP-9 between the groups. These data provide further evidence for neutrophil involvement in subclinical pulmonary emphysema.

Acute-Phase Proteins↗
PubMed1999

Noninvasive diagnosis of emphysema. Aerosol morphometry and aerosol bolus dispersion in comparison to HRCT.

Aerosol-derived airway morphometry (ADAM) and aerosol bolus dispersion (ABD) test are altered in patients with emphysema. We examined the diagnostic power of these aerosol methods in comparison with the noninvasive "gold-standard" HRCT in 50 consecutive patients with various lung diseases. The severity of airflow limitation was mild to moderate in the group of patients without emphysema and moderate to severe in the group of patients with HRCT-confirmed emphysema (FEV(1), 78 +/- 23% pred versus 53 +/- 33% pred; p < 0. 001). Among all lung function parameters under consideration ADAM showed the highest sensitivity and specificity for separating patients with emphysema from those without emphysema (area under the operating characteristics curve: p(ROC), 0.92), followed by ABD (p(ROC), 0.90), a marker for ventilation inhomogeneities. In patients with HRCT-confirmed macroscopic emphysema, peripheral air-space dimensions (EAD) at a relative volumetric lung depth V(pr) of 0.20 measured by ADAM were 155% larger, and bolus dispersion (ABD) at a lung depth of V(p) 600 ml was 53% larger than those observed in patients with other lung diseases (EAD = 0.84 +/- 0.53 mm versus 0.33 +/- 0.10 mm, p < 0.0001; ABD = 706 +/- 154 cm(3) versus 462 +/- 109 cm(3); p < 0.0001). EAD showed a significant correlation with the HRCT visual score (r = 0.78, p = 0.01). ABD showed weak significant correlations with all HRCT parameters under consideration (visual score, pixel density, mean lung density) (r = 0.45 to 0.66; p < 0.05). ADAM and ABD are powerful tools for the noninvasive diagnosis of macroscopic emphysema.

Aerosols↗
PubMed2000

Computed tomographic measurements of airway dimensions and emphysema in smokers. Correlation with lung function.

Chronic obstructive pulmonary disease (COPD) is characterized by the presence of airflow obstruction caused by emphysema or airway narrowing, or both. Low attenuation areas (LAA) on computed tomography (CT) have been shown to represent macroscopic or microscopic emphysema, or both. However CT has not been used to quantify the airway abnormalities in smokers with or without airflow obstruction. In this study, we used CT to evaluate both emphysema and airway wall thickening in 114 smokers. The CT measurements revealed that a decreased FEV(1) (%predicted) is associated with an increase of airway wall area and an increase of emphysema. Although both airway wall thickening and emphysema (LAA) correlated with measurements of lung function, stepwise multiple regression analysis showed that the combination of airway and emphysema measurements improved the estimate of pulmonary function test abnormalities. We conclude that both CT measurements of airway dimensions and emphysema are useful and complementary in the evaluation of the lung of smokers.

Adult↗
PubMed1990

The diagnosis of mild emphysema. Correlation of computed tomography and pathology scores.

Early and accurate diagnosis of emphysema is said to be invaluable for identification of clinically silent and mild emphysema. Recently, computed tomography (CT) has been much advocated for its efficacy in detailed diagnosis of emphysema, and the results have been compared with the pathology grade of emphysema in resected lung specimens. To assess the ability of high resolution CT scan in detecting and grading mild emphysema, we correlated the high resolution CT scan with the pathology grade of emphysema and the destructive index (DI) of lung specimens from 42 patients undergoing thoracotomy for a solitary pulmonary nodule. The high resolution CT scan and the cut surface of the lung, corresponding exactly to the same plane of the CT scan image, were assessed using the picture-grading system of Thurlbeck and coworkers on a scale of zero to 100. The CT scores for all patients ranged from 12 to 57, with a mean +/- SD of 22.1 +/- 9.6 using 1-mm collimation (n = 35), and from 7 to 46 with a mean +/- SD of 16.5 +/- 8.3 using 5-mm collimation (n = 33). The pathology scores ranged from 10 to 57, with a mean +/- SD of 23.2 +/- 9.8 (n = 42). The DI ranged from 15.4 to 67.1, with a mean +/- SD of 31.4 +/- 10.8 (n = 42). The CT scores using 1-mm and 5-mm collimation correlated significantly with the pathology scores (r = 0.68 and 0.76, respectively, p less than 0.001), and with the DI (r = 0.62 and 0.74, respectively, p less than 0.001). The pathology scores correlated significantly with the DI (r = 0.72, p less than 0.001). We therefore concluded that high resolution CT can help to identify the presence and grading of mild emphysema.

Adult↗
PubMed1990

Induction and exacerbation of emphysema in hamsters with human neutrophil elastase inactivated reversibly by a peptide boronic acid.

In solution, MeO-Suc-Ala-Ala-Pro-D,L-boro-Val pinacol ester (Boroval) is a highly effective but reversible inhibitor of both porcine pancreatic elastase and human neutrophil elastase (HNE) (50% inhibition with a 1.5 M ratio of Boroval to elastase). Boroval has been shown to prevent porcine-pancreatic-elastase-induced emphysema in hamsters. But with HNE-induced emphysema in hamsters, pretreatment with as much as a 170-fold M excess of Boroval, given intratracheally 1 h before 0.3 mg HNE, did not prevent emphysema. Indeed, lung volumes were larger after Boroval pretreatment than after HNE alone. Emphysema was also induced by instilling HNE that had been mixed with and inactivated by a 41-fold M excess of Boroval (a molar ratio of 42). When 0.25 or 0.5 mg of HNE were given mixed with a 41-fold M excess of Boroval, the emphysema was much more severe with the 0.5 mg dose. Two hours after instillation of 0.3 mg HNE inactivated with a 34-fold M excess of Boroval, bronchoalveolar lavage contained elastolytic activity but no evidence of hemorrhage. In contrast, hemorrhage was severe in hamsters that had been instilled with 0.3 mg HNE alone. We conclude that Boroval can enhance HNE-induced emphysema. We postulate that Boroval suppresses HNE-induced hemorrhage and the resultant influx of plasma protease inhibitors; the HNE-Boroval complex is transported into the alveolar interstitium, followed by dissociation of the inhibitor from the active site of HNE. Because of its small size, free Boroval is rapidly cleared, and the reactivated HNE attacks elastic fibers, giving rise to emphysema.

Animals↗
PubMed1990

Evaluation of elastase and antielastase balance in patients with chronic bronchitis and pulmonary emphysema.

On the basis of the "protease-antiprotease imbalance" theory for the pathogenesis of pulmonary emphysema, we hypothesized that measurement of elastase burden and antielastase capacity in the alveolar space might correlate with emphysema. To evaluate this, the severity of emphysema, the elastase burden, and the elastase inhibitory capacity were estimated in 28 patients with chronic bronchitis and variable degrees of emphysema, none of whom had congenital deficiency of alpha-1-protease inhibitor, and all of whom underwent bronchoalveolar lavage. Emphysema was assessed by both computed tomography and diffusing capacity. To examine "elastase burden," elastase:alpha-1-protease inhibitor complex and free elastase activity in alveolar lavage fluids were measured. To evaluate "antielastase" capacity, elastase inhibiting capacity in alveolar lavage fluid was measured. Elastase burden correlated directly and antielastase capacity correlated inversely with emphysema. These data provide direct support for the "protease-antiprotease imbalance" theory of emphysema in a group of smokers without congenital deficiency of alpha-1-protease inhibitor.

Adult↗
PubMed1991

Scanning electron microscopic observations of emphysema in humans. A descriptive study.

We have performed dissecting light and scanning electron microscopy (SEM) on 14 lungs with mild centrilobular emphysema, two of which also had mild panacinar emphysema. The lungs were surgically resected, mainly for cancer. The walls of centrilobular emphysema were either thick or thin. The former were less common and represented fibrosis of the walls. The latter were less fibrotic, but some fibrosis was seen. Adjacent alveoli were compressed and distorted, and overlapping walls of air spaces occurred. In panacinar emphysema alveolar ducts were enlarged and flattened with transverse linear bands interpreted as flattened walls of enlarged alveoli. The walls of air spaces were chiefly lined by type I and type II epithelial cells, but occasionally bronchiolar epithelium lined the proximal emphysematous spaces. Supplying bronchioles showed diminished numbers of ciliated cells with cilia of reduced height. SEM was much more sensitive than dissecting microscopy in recognizing emphysema. The apparent fibrosis suggests that the definition of emphysema may have to be reconsidered and that if fibrosis is apparent, the proteolysis-antiproteolysis hypothesis of the pathogenesis of emphysema may have to be modified.

Carcinoid Tumor↗
PubMed1993

Limited contribution of emphysema in advanced chronic obstructive pulmonary disease.

Previous studies on autopsy specimens or surgically resected lobes or lungs have reached varying conclusions regarding the importance of small airways disease and emphysema in causing fixed expiratory airflow limitation in patients with chronic obstructive pulmonary disease (COPD). We obtained high resolution CT scans of the lung and lung function in 56 consecutive patients with fixed expiratory airflow limitation. There was poor correlation between CT emphysema score and either FEV1/FVC% (r = -0.36) or FEV1 % predicted (r = -0.20). In only 10 of the 35 patients with FEV1 < 50% predicted, the CT emphysema score was > 40, indicating significant emphysema. A strong negative correlation between diffusing capacity % predicted and diffusing capacity per alveolar volume and CT emphysema score was found only in patients with FEV1 > or = 1 L (r = -0.75, p < 0.0001). Thus, emphysema does not appear to be primarily responsible for expiratory airflow limitation in COPD. A low diffusing capacity may be spuriously misleading in patients with FEV1 < 1 L and no or trivial emphysema.

Aged↗
PubMed1987

The National Institutes of Health Intermittent Positive Pressure Breathing trial--pathology studies. III. The diagnosis of emphysema.

In an attempt to predict the severity of emphysema in patients with moderately severe and severe chronic air-flow obstruction, antemortem pulmonary function data, including spirometry, subdivisions of lung volumes, diffusing capacity (transfer factor) for carbon monoxide, and elastic recoil were assessed in 46 patients who were autopsied during the National Institutes of Health Intermittent Positive Pressure Breathing Clinical Trial and we compared these to the morphologic severity of emphysema. The severity of emphysema was graded by the panel grading method using whole lung, paper-mounted (Gough-Wentworth) sections and the mean linear intercept (Lm). The FEV1 and FEF25-75 of the FVC, the DLCO, the diffusing capacity for carbon monoxide, and subdivisions of lung volumes showed significant but low order correlations with the emphysema score and Lm. Total lung capacity, determined by plethysmography, was better related to emphysema in this study than in others in which TLC was measured by helium dilution. Volume-pressure data fitted to the exponential equation (V = A - Be-KP) yielded a low order, but a significant relationship between Lm and the exponential constant (K), but not between K and the panel emphysema score. We conclude that the recognition of the presence and severity of emphysema continues to require a multivariate approach including clinical history, assessment of air-flow obstruction via routine spirometry, radiologic assessment of the lung with emphasis on total lung capacity, and evaluation of the diffusing capacity for carbon monoxide.

Biomechanical Phenomena↗
PubMed2006

Predictors of mortality in patients with emphysema and severe airflow obstruction.

PURPOSE: Limited data exist describing risk factors for mortality in patients having predominantly emphysema. SUBJECTS AND METHODS: A total of 609 patients with severe emphysema (ages 40-83 yr; 64.2% male) randomized to the medical therapy arm of the National Emphysema Treatment Trial formed the study group. Cox proportional hazards regression analysis was used to investigate risk factors for all-cause mortality. Risk factors examined included demographics, body mass index, physiologic data, quality of life, dyspnea, oxygen utilization, hemoglobin, smoking history, quantitative emphysema markers on computed tomography, and a modification of a recently described multifunctional index (modified BODE). RESULTS: Overall, high mortality was seen in this cohort (12.7 deaths per 100 person-years; 292 total deaths). In multivariate analyses, increasing age (p=0.001), oxygen utilization (p=0.04), lower total lung capacity % predicted (p=0.05), higher residual volume % predicted (p=0.04), lower maximal cardiopulmonary exercise testing workload (p=0.002), greater proportion of emphysema in the lower lung zone versus the upper lung zone (p=0.005), and lower upper-to-lower-lung perfusion ratio (p=0.007), and modified BODE (p=0.02) were predictive of mortality. FEV1 was a significant predictor of mortality in univariate analysis (p=0.005), but not in multivariate analysis (p=0.21). CONCLUSION: Although patients with advanced emphysema experience significant mortality, subgroups based on age, oxygen utilization, physiologic measures, exercise capacity, and emphysema distribution identify those at increased risk of death.

Adult↗
PubMed2004

Emphysema lung tissue gene expression profiling.

Emphysema occurs in a subgroup of patients with chronic obstructive pulmonary disease and patients with the genetic defect of alpha(1)-antitrypsin deficiency who have a smoking history of many years' duration. Emphysema is generally the result of a chronic and progressive destruction of the alveolar structures, which is believed to be driven by chronic inflammation, infections, oxidative stress, and an imbalance of protease and antiprotease activity. Here, we use microarray technology to characterize the gene expression profile of lung tissue samples obtained from patients with advanced emphysema and that obtained from healthy subjects. We hypothesized that the gene expression profile of emphysema lung tissue is distinct when compared with the expression profile of normal lungs. We report that severely emphysematous tissue is characterized by a global decrease in gene expression and by an increased abundance of transcripts encoding proteins involved in inflammation, immune responses, and proteolysis. Whereas the gene expression profile is to some degree shared between "usual" emphysema and alpha(1)-antitrypsin deficiency-related emphysema, there are statistically significant differences in the modulation of groups of genes associated with protein and energy metabolism, and immune function, which allow distinction between these two emphysema types on the lung tissue level.

Adolescent↗
PubMed1990

Biological effects of inhaled 239PuO2 in rats with pre-existing pulmonary emphysema.

The modifying effects of pre-existing pulmonary emphysema on the deposition, distribution, retention and effects of inhaled 239PuO2 in the rat were investigated. The presence of emphysema in the rats was documented by morphometric and respiratory function measurements. For rats exposed to similar airborne concentrations of 239PuO2, initial lung burdens of 239Pu per kg body mass were lower in rats with emphysema than in those without emphysema; however, the retention of 239Pu over time was similar in both groups. The distribution of 239Pu particles in the lungs of rats with emphysema tended to be more random than in the lungs of control rats. The life span, and incidences of non-neoplastic and neoplastic lesions in the lung, and risk of lung tumours per unit of alpha dose to the lungs in the rats with emphysema were similar to or less than in the control rats, when groups with similar initial lung burdens of 239Pu were compared. The results of this study suggest that humans with uncomplicated pulmonary emphysema are not necessarily more sensitive to the carcinogenic effects of inhaled 239PuO2 than individuals with normal lungs.

Administration, Inhalation↗
PubMedDate not supplied

Orbital emphysema and diplopia following thoracotomy.

PURPOSE: To describe the clinical and radiological findings in a patient with diplopia and orbital emphysema following thoracotomy. METHODS: Reported is a 71-year-old woman who presented with diplopia several days following thoracotomy. RESULTS: Physical examination revealed diffuse subcutaneous emphysema and a right hypertropia. Head computed tomography revealed facial and palpebral subcutaneous emphysema extending into the infratemporal fossa and orbits bilaterally. A chest tube was replaced and her diplopia resolved. CONCLUSIONS: Subcutaneous emphysema can lead to diplopia and orbital emphysema in the absence of orbital trauma. Contrary to previously suggested mechanisms of orbital emphysema associated with subcutaneous emphysema, computed tomography imaging suggested that air entry into the orbit in this case was through the inferior orbital fissure.

Aged↗
PubMed2001

Lymphocyte population and apoptosis in the lungs of smokers and their relation to emphysema.

Previously, it had been shown that T-lymphocytes are the predominant inflammatory cells found in the alveolar wall of smokers and their numbers correlated with the extent of emphysema. However, the phenotype of these cells was not defined. The aim of this study was to describe the different T-cell phenotypes and investigate the possible presence of apoptosis in the lung parenchyma of smokers. Samples from lungs were obtained at surgery from 15 patients who smoked and six who had never smoked. Samples were frozen and prepared for histological and immunocytochemical examination. Slides were stained for CD3+, CD4+, CD8+, gammadelta T-cells, CD56 natural killers ((NK) cells), and elastase (neutrophils). Anti-CD95 monoclonal antibodies and in situ end-labelling techniques were used to detect Fas expression and apoptosis. Positive staining cells were expressed as cells-mm alveolar wall-, percentage of total cells, and Fas/APO and apoptosis index. Emphysema was identified macroscopically, microscopically and reported as present or absent. All subjects had pulmonary function tests before surgery. Neutrophils were the predominant cell in the lung parenchyma of nonsmokers and smokers without emphysema. In smokers with emphysema, the CD3+ and CD8+ were the predominant cells (p<0.05) in the alveolar wall. gammadelta cells were increased in all smokers and no increased numbers of NK cells was found. The T-cell numbers x mm alveolar wall(-1) showed a bilinear relationship with the amount smoked increasing at an inflection point of 30 packs yr(-1) (R2= 0.345; p < 0.01). Apoptosis in smokers showed a bilinear relationship with the amount smoked increasing sharply in smokers with emphysema (R2=0.3613; p < 0.009). It is concluded that the pathogenesis of emphysema might be mediated by T-lymphocytes, mainly CD8+ cytolytic T-cells, and that apoptosis might be one of the mechanisms of lung destruction leading to the development of emphysema. If this is the case, it could be speculated that T-cell inflammation is a response to antigenic stimuli originating in the lung and induced by cigarette smoking.

Aged↗
PubMed2003

Imbalance between vascular endothelial growth factor and endostatin in emphysema.

Vascular endothelial growth factor (VEGF) stimulates endothelial cell proliferation, and endostatin directly antagonises the biological effects of VEGF. The maintenance of pulmonary endothelial cells is also thought to depend upon the local balance of VEGF and endostatin in the lung. Therefore, this study was designed to determine whether there is an imbalance between VEGF and endostatin levels in patients with pulmonary emphysema. VEGF and endostatin levels were simultaneously measured from 25 emphysema patients and 12 normal control subjects, and their correlation and balance in induced sputum was evaluated. VEGF levels in induced sputum were significantly lower in emphysema patients (854 +/- 307 pg x mL(-1)) than in normal controls (1,791 +/- 1,192 pg x mL(-1)). In contrast, there was no significant difference in endostatin levels among the two groups. Therefore, the ratio of VEGF to endostatin levels was markedly lower in emphysema patients (4.5 +/- 1.8) than in normal controls (8.1 +/- 2.6). Moreover, VEGF levels were correlated with endostatin levels in normal controls but not in emphysema patients. In addition, the ratio of VEGF to endostatin levels was correlated with forced expiratory volume in one second (FEV1), FEV1/forced vital capacity and carbon monoxide diffusing capacity of the lung in emphysema patients. The findings in this study suggest that there is an imbalance between vascular endothelial growth factor and endostatin levels in induced sputum from emphysema patients.

Aged↗
PubMed2005

Correlation of lung surface area to apoptosis and proliferation in human emphysema.

Pulmonary emphysema is associated with alterations in matrix proteins and protease activity. These alterations may be linked to programmed cell death by apoptosis, potentially influencing lung architecture and lung function. To evaluate apoptosis in emphysema, lung tissue was analysed from 10 emphysema patients and six individuals without emphysema (normal). Morphological analysis revealed alveolar cells in emphysematous lungs with convoluted nuclei characteristic of apoptosis. DNA fragmentation was detected using terminal deoxynucleotide transferase-mediated dUTP nick-end labelling (TUNEL) and gel electrophoresis. TUNEL revealed higher apoptosis in emphysematous than normal lungs. Markers of apoptosis, including active caspase-3, proteolytic fragment of poly (ADP-ribose) polymerase, Bax and Bad, were detected in emphysematous lungs. Linear regression showed that apoptosis was inversely correlated with surface area. Emphysematous lungs demonstrated lower surface areas and increased cell proliferation. There was no correlation between apoptosis and proliferation, suggesting that, although both events increase during emphysema, they are not in equilibrium, potentially contributing to reduced lung surface area. In summary, cell-based mechanisms associated with emphysematous parenchymal damage include increased apoptosis and cell proliferation. Apoptosis correlated with airspace enlargement, supporting epidemiological evidence of the progressive nature of emphysema. These data extend the understanding of cell dynamics and structural changes within the lung during emphysema pathogenesis.

Adult↗
PubMed1997

Arterial endothelin-1 level in pulmonary emphysema and interstitial lung disease. Relation with pulmonary hypertension during exercise.

This study was undertaken to assess the arterial plasma levels of endothelin-1 (ET-1) and their relationship with pulmonary haemodynamic and gas exchange variables during exercise in patients with emphysema and interstitial lung disease (ILD). Incremental cycle ergometry was performed in all patients up to maximal capacity. At rest, arterial ET-1 levels were higher in emphysema (1.86 +/- 0.35 pg.mL-1; p < 0.02) and ILD (1.75 +/- 0.25 pg.mL-1; p < 0.03) patients than in controls (1.35 +/- 0.18 pg.mL-1). Emphysema (2.08 +/- 0.26 versus 1.70 +/- 0.40 pg.mL-1) and ILD (1.98 +/- 0.21 versus 1.67 +/- 0.02 pg.mL-1) patients with pulmonary hypertension (PH) presented significantly (p < 0.05) higher arterial ET-1 levels than those without. At rest, arterial ET-1 levels were significantly correlated with mean pulmonary arterial pressure (Ppa) in both ILD (r = 0.8, p = 0.01) and emphysema (r = 0.5, p = 0.03) patients. During exercise, the arterial ET-1 levels were significantly correlated with arterial oxygen (Pa,O2) (r = -0.6, p = 0.04), alveolar-arterial oxygen difference (r = 0.8, p = 0.01), and Ppa (r = 0.6, p = 0.04) in ILD patients, but not in those with emphysema. In brief, the results of this study suggest that arterial endothelin-1 is markedly increased in interstitial lung disease and emphysema patients, and that, it is related to the exercise-induced exacerbation of pulmonary hypertension in patients with interstitial lung disease, but not in those with emphysema.

Aged↗
PubMed2005

Marked alveolar apoptosis/proliferation imbalance in end-stage emphysema.

BACKGROUND: Apoptosis has recently been proposed to contribute to the pathogenesis of emphysema. METHODS: In order to establish if cell fate plays a role even in end-stage disease we studied 16 lungs (9 smoking-associated and 7 alpha1antitrypsin (AAT)-deficiency emphysema) from patients who had undergone lung transplantations. Six unused donor lungs served as controls. Apoptosis was evaluated by TUNEL analysis, single-stranded DNA laddering, electron microscopy and cell proliferation by an immunohistochemical method (MIB1). The role of the transforming growth factor (TGF)-beta1 pathway was also investigated and correlated with epithelial cell turnover and with the severity of inflammatory cell infiltrate. RESULTS: The apoptotic index (AI) was significantly higher in emphysematous lungs compared to the control group (p < or = 0.01), particularly if only lungs with AAT-deficiency emphysema were considered (p < or = 0.01 vs p = 0.09). The proliferation index was similar in patients and controls (1.9 +/- 2.2 vs 1.7 +/- 1.1). An increased number of T lymphocytes was observed in AAT-deficiency lungs than smoking-related cases (p < or = 0.05). TGF-beta1 expression in the alveolar wall was higher in patients with smoking-associated emphysema than in cases with AAT-deficiency emphysema (p < or = 0.05). A positive correlation between TGF-betaRII and AI was observed only in the control group (p < or = 0.005, r2 = 0.8). A negative correlation was found between the TGF-beta pathway (particularly TGF-betaRII) and T lymphocytes infiltrate in smoking-related cases (p < or = 0.05, r2 = 0.99) CONCLUSION: Our findings suggest that apoptosis of alveolar epithelial cells plays an important role even in end-stage emphysema particularly in AAT-deficiency disease. The TGFbeta-1 pathway does not seem to directly influence epithelial turnover in end-stage disease. Inflammatory cytokine different from TGF-beta1 may differently orchestrate cell fate in AAT and smoking-related emphysema types.

Apoptosis↗