In a smoking patient, is the lung over digested because of a combination of smoking and a defect in the antitrypsin gene (prevents digestion from protease)? Or does smoking act the same as a patient with a defect in the gene?

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    $\begingroup$ Do you have any proof for this claim? Usually proteases are not active in lung tissues. $\endgroup$ – Chris Nov 7 '17 at 15:07

Wikipedia has a fine article on the disease.


from that article

Alpha-1 antitrypsin (A1AT) is produced in the liver, and one of its functions is to protect the lungs from neutrophil elastase, an enzyme that can disrupt connective tissue.

Neutrophil proteases are active anywhere neutrophils are. People who don't smoke can get COPD just from having the double recessive form of this disease (no active alpha-1 antitrypsin). But if that is the case with you and you also smoke you get accelerated COPD. COPD is already an inflammatory disease associated with mucus and neutrophil action and the damage this causes is no doubt augmented with the lack of protective alpha-1 antitrypsin.

If you suffer this condition you can get infusions of alpha-1 antitrypsin - sort of like type 1 diabetics get insulin.


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