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Inflammatory mediators such as the vasoactive and chemotactic factors derived from the activation of the complement system are extremely potent biological peptides that are under rigid control of specific serum-derived regulators, e.g., the anaphylatoxin inactivator (AI) and the chemotactic factor inactivator (CFI). We have previously demonstrated that serum chemotactic factor inactivator concentrations are altered during chronic inflammatory states; here we demonstrate that a rapid elevation of serum CFI activity occurs during acute inflammatory reactions in patients suffering from hypersensitivity pneumonitis. Specifically, serum CFI concentrations were evaluated in patients with hypersensitivity pneumonitis (pigeon breeder's disease) and control subjects (asymptomatic) after aerosol challenge with 2 ml of sterile pigeon serum. At 4 h postchallenge, serum CFI concentrations in the patients with hypersensitivity pneumonitis increased rapidly to 3 times the prechallenge serum concentrations. Asymptomatic (control) subjects showed no increase in serum CFI concentrations after exposure to pigeon serum. In independent studies, we have also demonstrated that serum CFI concentrations are elevated in (1) rabbits with glycogen-induced peritonitis, (2) rabbits after intravenous infusion of C5-derived chemotactic factors, and (3) patients undergoing hemodialysis. These combined data clearly demonstrate that serum CFI activity is rapidly elevated during acute inflammatory reactions within both patient and animal populations, and suggest that serum CFI may represent a "hyperacute" phase reactant that is elevated during inflammation. Possibly, this elevation of CFI may be induced in response to inflammatory mediators produced during inflammation. Thus, the acute elevation of serum CFI concentrations that occurs during acute inflammation may represent the control system that would be responsive to the regulatory needs of the body during inflammatory reactions.