Key result
Ovalbumin challenge in a guinea pig asthma model resulted in significantly higher levels of MMP-9 compared to saline controls, with no significant difference in TIMP-1 levels.
In a guinea pig asthma model, MMP-9 is significantly elevated following ovalbumin challenge, suggesting a role in tissue remodeling and early bronchial injury.
No immediate clinical implications; leaves open MMP-9 role in human asthma remodeling.
Our objective was to investigate the role of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) and their cellular sources in guinea pig asthma model following ovalbumin (OA) challenge. Twenty guinea pigs were divided into 2 groups: OA-challenged group were sensitized by intraperitoneal injection with OA and exposed to OA while the control group used saline in a similar manner. The positive level index (PLI), defined as the percentage of positive-stained cells x average optical density, was used to assess the expressing levels of MMP-9 and TIMP-1. The levels of MMP-9 from OA-challenged group were significantly higher than those of controls. However, no significant difference of the TIMP-1 levels between the OA-challenged group and controls were found. MMP-9 was expressed strongly in both inflammatory and structural cells while TIMP-1 was expressed weakly in inflammatory cells and structural cells. Our results implied that MMP-9 may contribute to tissue remodeling in asthma and both structural and inflammatory cells within lung tissue are the main cellular sources of MMP-9. Excessive expression of MMP-9 in the early or acute stage of asthma may be associated with the initiation of bronchial injury and inflammatory cells accumulation.
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Tang et al. (2005) studied Asthma (n=20). Ovalbumin (OA) challenge vs. Saline was evaluated on Levels of MMP-9 and TIMP-1 (positive level index). Ovalbumin challenge in a guinea pig asthma model resulted in significantly higher levels of MMP-9 compared to saline controls, with no significant difference in TIMP-1 levels.
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