Abstract Background: Pulmonary fibrosis, the final result of a large variety of interstitial lung diseases,
is characterized by an aberrant remodeling of extracellular matrix (ECM) with a profound
disturbance of the normal lung architecture. This remodeling includes the exaggerated accumulation
of ECM components in the interstitial and alveolar spaces and the disruption of the basement
membranes. It has long been accepted that MMPs play an important role in the pathogenesis of
pulmonary fibrosis, but the exact mechanisms are not well characterized. There are several interrelated
processes—such as ECM remodeling, basement-membrane disruption, epithelial-cell apoptosis,
cell migration, and angiogenesis—in which MMPs may play a central role, either by ECM direct
cleavage or by generating bioactive mediators. TIMPs can modulate cellular processes such as cell
growth, apoptosis and migration, and can be both anti- and pro-tumorigenic. This study aimed to
examine the changes in induced sputum as regards MMP-9, TIMP-1 and levels of inflammatory
cells in ILD patients compared with sputum of healthy non smokers.
Subjects and methods: Thirty subjects were included in this study and were classified into the following
two groups: Group I included twenty patients diagnosed clinically, radiologically and physiologically
as interstitial lung diseases. Group II included ten healthy non smoker subjects. Sputum
induction was done and processed to assess matrix metalloproteinase-9 (MMP-9), tissue inhibitor of
metalloproteinase-1(TIMP-1) and cytological examination with cellular count.
Results: In this study, we have demonstrated that levels of sputum MMP-9 and TIMP-1 were
significantly increased in patients with interstitial lung diseases than normal persons with highly
significant statistical differences (p=0.001). MMP-9 was positively correlated with number of
neutrophils in the airway with highly significant statistical difference (p= 0.001). |