Deficiency of the chemotactic factor inactivator in human sera with   1 -antitrypsin deficiency.
As revealed by appropriate fractionation procedures, human serum deficient in alpha(1)-antitrypsin (alpha(1)-AT) is also deficient in the naturally occurring chemotactic factor inactivator. These serum donors had severe pulmonary emphysema. Serum from patients with clinically similar pulmonary disease, but with presence of alpha(1)-AT in the serum, showed no such deficiency of the chemotactic factor inactivator. When normal human serum and alpha(1)-AT-deficient human sera are chemotactically activated by incubation with immune precipitates, substantially more chemotactic activity is generated in alpha(1)-AT-deficient serum. These data indicate that in alpha(1)-AT-deficient serum there is an imbalance in the generation and control of chemotactic factors. It is suggested that the theory regarding development of pulmonary emphysema in patients lacking the alpha(1)-antitrypsin in their serum should be modified to take into account a deficiency of the chemotactic factor inactivator.
D002633:Chemotaxis; D006801:Humans; D009504:Neutrophils; D011656:Pulmonary Emphysema / Q000209:etiology*; D014361:Trypsin Inhibitors / Q000097:blood*
D014361:Trypsin Inhibitors