However, in the current study, neither bacterial nor viral infections were associated with significant changes in the levels of MMPs and TIMPs in BAL, indicating that the observed increase of MMP-9, TIMP-1 and TIMP-2 in BAL during AE-COPD resulted from increased secretion by lung resident cell types or by inflammatory cells such as macrophages and neutrophils invading the lung during AE-COPD. This evidence concerns the gene TIMP1 and viral infectious disease.