Animal Models of Emphysema^1–3

Smoke Extract Stimulates Lung Epithelial Cells to Release Neutrophil and Monocyte Chemotactic Activity

“…29 -31 Anti-LTB 4 serum, [5,6,8,9,11,12,14,15,3 H(N)]-LTB 4 , and synthetic LTB 4 were purchased from Amersham Co. (Arlington Heights, IL). Briefly, ethanol and supernatant mixtures were centrifuged at 5500 ϫ g at 0°C.…”

“…4 Studies in animal models have demonstrated that cigarette smoking is associated with the chronic accumulation of inflammatory cells in the lung. 5 Increased numbers of neutrophils and monocytes, activated by cigarette smoke, produce large amounts of proteases and oxidants. 6,7 The cigarette smoke can inactivate antiprotease protection.…”

Neutrophil elastase-initiated EGFR/MEK/ERK signaling counteracts stabilizing effect of autocrine TGF-β on tropoelastin mRNA in lung fibroblasts

“…Smoking-induced chronic pulmonary inflammation and inherited deficiency of ␣1-protease inhibitor are some of the known risk factors associated with the excessive activity of elastases, primarily of neutrophil and macrophage origin, which predispose the lung to the degradation of interstitial elastin. Persistent elastolysis and accompanying elastin repair insufficiency in the chronically elastase/anti-elastase-imbalanced lung are thought to result in irreversible loss of alveoli and lead to emphysema in humans and experimental animals (9,28,35,38). The molecularcellular mechanisms underlying the insufficiency of elastin repair in the elastase/anti-elastase-imbalanced lung are still under investigation.…”

N-acetylcysteine prevents cigarette smoke induced small airways alterations in rats

“…A later SBW study by VAN MUYLEM et al [4], which included helium and sulphur hexafluoride tracer concentrations, also revealed distinct correlations between indices derived from He and SF 6 slopes and airway pathology scores. Due to the fact that the diffusion front is located more peripherally for SF 6 than for He, the respective phase III slopes are indicative of the site where ventilation inhomogeneities occur.Although animal studies are well-suited for the study of lung function in the diseased lung, the difficulty often resides in reproducing a lesion which is comparable to that encountered in the human lung [5]. Previous studies in rats have led to conflicting results as to whether the cigarette smoke induces emphysematous lesions [6,7] or not [8,9] and not all studies provide any information about the extent to which the nonalveolated airways are affected [10].…”

“…Although animal studies are well-suited for the study of lung function in the diseased lung, the difficulty often resides in reproducing a lesion which is comparable to that encountered in the human lung [5]. Previous studies in rats have led to conflicting results as to whether the cigarette smoke induces emphysematous lesions [6,7] or not [8,9] and not all studies provide any information about the extent to which the nonalveolated airways are affected [10].…”