Inhibition of neutrophil superoxide production by human plasma alpha 1-antitrypsin.
We report here that human plasma alpha 1-antitrypsin (alpha 1-AT) inhibited human neutrophil O2.- release elicited by a variety of stimulants. In comparison, the inhibitory capacities of two serine protease inhibitors, L-1-tosylamide 2-phenylethyl chloromethyl ketone (TPCK) and soybean trypsin inhibitor (SBTI), and the human recombinant alpha 1-AT mutant, alpha 1-AT-Arg358 were in the order: alpha 1-AT = TPCK much greater than alpha 1-AT-Arg358 greater than SBTI when cells were stimulated with concanavalin A plus cytochalasin E. These data suggest that, in human inflammatory fluids containing relatively high concentrations of alpha 1-AT (such as rheumatoid arthritis synovial fluid), (i) alpha 1-AT may down-regulate the inflammatory process by inhibiting the neutrophil respiratory burst and (ii) serpin oxidation by neutrophil-released reactive oxygen species is unlikely to occur.
Bucurenci
N
N
Inflammation Research Group, London Hospital Medical College, England.
Blake
D R
DR
Chidwick
K
K
Winyard
P G
PG
D000328:Adult; D006801:Humans; D007700:Kinetics; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism*; D015842:Serine Proteinase Inhibitors / Q000494:pharmacology; D013481:Superoxides / Q000378:metabolism*; D000515:alpha 1-Antitrypsin / Q000378:metabolism*
D015842:Serine Proteinase Inhibitors; D000515:alpha 1-Antitrypsin; D013481:Superoxides