RESUMO

Cigarette smoking produces peripheral airway inflammation in all smokers, and chronic airways obstruction in approximately 20% of heavy smokers. The present study was designed to test the hypothesis that airways obstruction is related to changes in the expression of adhesion molecules involved in the recruitment of cells to sites of inflammation in the lung. Freshly resected lungs from heavy smokers with airways obstruction (n = 10) and from heavy smokers with normal lung function (n = 10) were collected in the operating room, inflated with optimal cutting temperature (OCT) medium and frozen over liquid nitrogen. Six micrometres thick cryostat sections cut from random samples of this tissue were stained, using immunohistochemistry, with monoclonal antibodies to the adhesion molecules on leucocytes: L-selectin, very late activation antigen-4 (VLA-4), CD11a/CD18, CD11b/CD18, CD11c/CD18; and on endothelial and epithelial surfaces: E-selectin, P-selectin, vascular cell adhesion molecule (VCAM-1), intercellular adhesion molecule (ICAM)-1 and ICAM-2 using the alkaline phosphatase anti-alkaline phosphatase (APAAP) technique. The slides were coded and the expression of each molecule scored by three observers using a semiquantitative grading system. Two inducible adhesion molecules, E-selectin on endothelium and CD11b on leucocytes, were also evaluated using quantitative morphometric analysis. The results showed a distribution of adhesion molecules that was consistent with the inflammatory response in the airways and parenchyma of all subjects but failed to show any differences between those with or without airways obstruction. We conclude that development of airways obstruction in heavy smokers cannot be explained by differences in the expression of adhesion molecules known to be involved in the control of cell traffic in the lung.

Assuntos

Moléculas de Adesão Celular/genética , Regulação da Expressão Gênica , Pneumopatias Obstrutivas/metabolismo , Fumar/metabolismo , Idoso , Anticorpos Monoclonais , Antígenos CD/análise , Antígenos CD/genética , Antígenos CD11/análise , Antígenos CD11/genética , Antígenos CD18/análise , Antígenos CD18/genética , Moléculas de Adesão Celular/análise , Selectina E/análise , Selectina E/genética , Endotélio/metabolismo , Endotélio/patologia , Epitélio/metabolismo , Epitélio/patologia , Feminino , Humanos , Imuno-Histoquímica , Integrina alfa4beta1 , Integrina beta1/análise , Integrina beta1/genética , Integrinas/análise , Integrinas/genética , Molécula 1 de Adesão Intercelular/análise , Molécula 1 de Adesão Intercelular/genética , Selectina L/análise , Selectina L/genética , Leucócitos/metabolismo , Leucócitos/patologia , Pulmão/metabolismo , Pulmão/patologia , Pneumopatias Obstrutivas/genética , Pneumopatias Obstrutivas/patologia , Masculino , Pessoa de Meia-Idade , Selectina-P/análise , Selectina-P/genética , Pneumonia/genética , Pneumonia/metabolismo , Pneumonia/patologia , Receptores de Retorno de Linfócitos/análise , Receptores de Retorno de Linfócitos/genética , Receptores de Antígeno muito Tardio/análise , Receptores de Antígeno muito Tardio/genética , Fumaça , Fumar/genética , Fumar/patologia , Molécula 1 de Adesão de Célula Vascular/análise , Molécula 1 de Adesão de Célula Vascular/genética