Overexpression of CD163, CD204 and CD206 on alveolar macrophages in the lungs of patients with severe chronic obstructive pulmonary disease.
PLoS One
; 9(1): e87400, 2014.
Article
em En
| MEDLINE
| ID: mdl-24498098
ABSTRACT
We have previously reported that the lungs of patients with very severe chronic obstructive pulmonary disease (COPD) contain significantly higher numbers of alveolar macrophages than those of non-smokers or smokers. M1 and M2 macrophages represent pro- and anti-inflammatory populations, respectively. However, the roles of M1 and M2 alveolar macrophages in COPD remain unclear. Immunohistochemical techniques were used to examine CD163, CD204 and CD206, as M2 markers, expressed on alveolar macrophages in the lungs of patients with mild to very severe COPD (Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage I (mild) nâ=â11, II (moderate) nâ=â9, III (severe) nâ=â2, and IV (very severe) nâ=â16). Fifteen smokers and 10 non-smokers were also examined for comparison. There were significantly higher numbers of alveolar macrophages in COPD patients than in smokers and non-smokers. The numbers and percentages of CD163(+), CD204(+) or CD206(+) alveolar macrophages in patients with COPD at GOLD stages III and IV were significantly higher than in those at GOLD stages I and II, and those in smokers and non-smokers. In patients with COPD, there was a significant negative correlation between the number of CD163(+), CD204(+) or CD206(+) alveolar macrophages and the predicted forced expiratory volume in one second. Overexpression of CD163, CD204 and CD206 on lung alveolar macrophages may be involved in the pathogenesis of COPD.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Alvéolos Pulmonares
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Antígenos de Diferenciação Mielomonocítica
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Antígenos CD
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Macrófagos Alveolares
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Receptores de Superfície Celular
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Doença Pulmonar Obstrutiva Crônica
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Lectinas Tipo C
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Lectinas de Ligação a Manose
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Receptores Depuradores Classe A
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Pulmão
Limite:
Aged
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Ano de publicação:
2014
Tipo de documento:
Article