Electromorphic Association of Alpha-1-antitrypsin with Arthritides and Alteration of Immunomodulatory Response

Alpha-1-antitrypsin (AAT) plays a central role as a protease inhibitor of matrix metalloproteinase, collagenase, elastase in controlling synovium and cartilage degradation and appears to be involved in regulation of the immune system, perhaps through the production of proteases by ‘T’ cells. Deficiency of AAT may contribute to diseases with the involvement of an immune component of the synovium/synovial fluid. The present study aims at evaluating the role of AAT and its specific polymorphic variation with arthritides, which is an inflammatory bone disorder. AAT serum samples were carried out on PAGE in 150 Rheumatoid arthritis, 100 osteoarthritis and 125 adult control subjects. AAT phenotype distribution revealed an association of PiS, PiF and PiZ alleles with inflammatory condition. An increased frequency of Pi FM phenotype in the disease condition could lead to an increased sensitivity of the ‘F’ variant to oxidation. Further, the S & Z alleles when present may contribute to the decreased enzyme activity of AAT, which in turn may influence the molar complex formation with proteolytic enzymes in cartilage degradation process.