Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine which proteinases are responsible for the lung destruction characteristic of pulmonary emphysema, macrophage elastase-deficient (MME-/-) mice were subjected to cigarette smoke. In contrast to wild-type mice, MME-/- mice did not have increased numbers of macrophages in their lungs and did not develop emphysema in response to long-term exposure to cigarette smoke. Smoke-exposed MME-/- mice that received monthly intratracheal instillations of monocyte chemoattractant protein-1 showed accumulation of alveolar macrophages but did not develop air space enlargement. Thus, macrophage elastase is probably sufficient for the development of emphysema that results from chronic inhalation of cigarette smoke.
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PMID:Requirement for macrophage elastase for cigarette smoke-induced emphysema in mice. 930 97

Methyl methacrylate (MMA) is a monomer, commonly used in neurosurgery, orthopedic surgery, and in dental clinics. The adverse effects of this monomer are well described in the literature. This study was designed to evaluate the effects of MMA on nasal cavity, lung, and antioxidant status. For this purpose, two experimental groups of rats were exposed to MMA (at 1,000 ppm, 6 h/day, 5 days/week for 4 weeks) by inhalation under poor (group A, n = 12) and normal ventilation (group B, n = 11) conditions. A control group (group C, n = 10) received normal air. Degeneration of olfactory epithelium, bronchopneumonia, interstitial pneumonia, hemorrhage, atelectasis, edema, emphysema, and bronchial epithelial hyperplasia were observed in groups A and B. Emphysema was the most common lesion. Bronchopneumonia with abscesses was only observed in group A. Glutathione levels were significantly decreased and malondialdehyde levels were significantly increased in group A. No significant difference was observed in superoxide dismutase levels between the groups. The data presented indicate that before using MMA, adequate protection systems should be in place to prevent occupationally related MMA respiratory-tract injuries.
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PMID:The effects of methyl methacrylate on nasal cavity, lung, and antioxidant system (an experimental inhalation study). 1205 52

The cells/proteases responsible for the development of smoke-induced emphysema is an area of intense investigation. Mice with knockout of macrophage metalloelastase genes (MME(-/-)) do not develop emphysema after smoke exposure, but we also observed that neutrophils (PMN) in lavage appeared to be a requirement for acute connective tissue breakdown. In this study we exposed mice to cigarette smoke and examined lavage PMN, macrophages (MAC), desmosine (DES, a measure of elastin breakdown) and hydroxyproline (HP, a measure of collagen breakdown) 24 h afterwards. MME(+/+) mice exposed to smoke showed elevations in PMN, DES, and HP, but no elevations were seen in MME-deficient mice. Both PMN influx and increased levels of DES/HP could be restored by administering MAC from MME(+/+) mice to MME-deficient mice and then exposing them to smoke. RS113456, a metalloprotease inhibitor, also prevented PMN influx and connective tissue breakdown. Western blots against mouse alpha(1)-antitrypsin (alpha(1)AT) showed that alpha(1)AT was not protected in MME-deficient mice, nor by administration of RS113456. We conclude that, in mice, acute smoke-induced connective tissue breakdown, the precursor to emphysema, requires both PMN and MME, that PMN influx appears to be secondary to MAC activation, and that this process initially does not involve protection of alpha(1)AT from metalloprotease attack.
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PMID:Acute cigarette smoke-induced connective tissue breakdown requires both neutrophils and macrophage metalloelastase in mice. 1220