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Fig. 1 | BMC Pulmonary Medicine

Fig. 1

From: Alpha-1 antitrypsin (AAT) augmentation therapy in individuals with the PI*MZ genotype: a pro/con debate on a working hypothesis

Fig. 1

Potential mechanism for increased disease risk in individuals with the PI*MZ genotype. Left panel: In MM non-smokers, a normal protease/antiprotease balance exists with normal alveoli. Central panel: MZ non-smokers have a slight imbalance of AAT and neutrophil elastase, IL-8 levels may increase in the lungs causing neutrophil activation and inflammation and progressive damage in the lungs in some patients. Right panel: MZ smokers have a greater imbalance between AAT and neutrophil elastase as a result of reactive oxygen species in cigarette smoke inactivating AAT. Additional factors such as Z polymers and IL-8 inflammatory markers cause greater production of neutrophil elastase in the lung, causing irreversible damage. Figure adapted from Carroll et al. 2014; https://doi.org/10.5772/58602 [23] under the Creative Commons Attribution 3.0 License. AAT alpha-1 antitrypsin, IL interleukin

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