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Clinical Investigations: COPD |

Matrix Metalloproteinases Activity in COPD Associated With Wood Smoke*

Martha Montaño; Carina Beccerril; Victor Ruiz; Carlos Ramos; Raul H. Sansores; Georgina González-Avila
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*From the Department of Molecular Biology (Drs. Montaño, Beccerril, Ruiz, and Ramos) and the Extracellular Matrix Laboratory (Drs. Sansores and González-Avila), Department of Immunology, Instituto Nacional de Enfermedades Respiratorias, Calzada de Tlalpan, México.

Correspondence to: Georgina González-Avila MD, PhD, Laboratorio de Matriz Extracelular, Departamento de Inmunología, Instituto Nacional de Enfermedades Respiratorias, Calzada de Tlalpan 4502, CP 14080, México, D.F., México; e-mail: ggonzalezavila@yahoo.com



Chest. 2004;125(2):466-472. doi:10.1378/chest.125.2.466
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Background: Wood smoke (WS) exposure causes COPD with respiratory alterations that are similar to those described for COPD associated with tobacco smoke (TS). The aim of the present study was to analyze the effects of WS on matrix metalloproteinase (MMP) activity and expression.

Design: BAL fluid and macrophages were obtained from patients exposed to WS and TS, and from control subjects. Macrophage elastolytic activity was assayed by radiolabeled elastin degradation. Gelatinolytic activity was measured by zymography in BAL fluid samples. MMP-2, MMP-9, and MMP-12 expression were analyzed by reverse transcription polymerase chain reaction in macrophages from each group.

Results: Macrophage elastolytic activity was increased significantly in WS and TS cells in comparison to control subjects with no differences between WS and TS samples. MMP-2 was identified in all groups as a 72-Kd band (proMMP-2), with the highest activity in the WS samples. MMP-9 was present in its latent and active forms with the highest gelatinolytic activity in the WS group. MMP-2 expression was increased in both groups as well as MMP-12 compared with the control. Two of three subjects studied in each COPD group had a significant increase in MMP-9 expression.

Conclusion: These findings demonstrate that WS increases MMP activity and expression that might produce lung damage similar to that observed in COPD associated with TS.

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