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Subsequent research on murine model revealed that A1AT can inhibit both macrophages metalloproteinase (MMP-12) production and the release of TNF-alpha from alveolar macrophages, thereby reducing smoke-induced inflammation and the influx of inflammatory cells ( One proposed mechanism for the increased production of MMP-12 is the activation of proteinase-activated receptor-1 (PAR-1) by serum constituents, such as plasmin/plasminogen and thrombin, which leak into the lung after smoke exposure

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10.1093/jxb/erh138 J

Results from stage 1 (prior to interim) and stage 2 (post-interim) were combined using the inverse normal method and the median unbiased estimate calculated