Inhibition of C3a and C5a-Mediated Human Leukocyte Chemotaxis by Human C1 Inhibitor (C1 INH)

It has recently been reported (Smith et al., J. Immunol. 114:216, 1975) that C1 INH can influence complement-mediated chemotactic responsiveness of human blood leukocytes. Depending on the generating source of cytotaxin, the total number of cells responding may be either increased (enhancement) or decreased (inhibition) in the presence of C1 INH. A marked enhancement of chemotaxis was observed when chemotaxin(s) was generated from plasma with lipopolysaccharide (LPS), zymosan, or immune complexes. Results of experiments using anti-C3 and/or anti-C5 suggested that C5a was involved in enhancement whereas C3a-mediated chemotaxis was inhibited with C1 INH. The action of C1 INH appeared to be reversible since washing the cells free of C1 INH led to an unaltered chemotactic response.

These experiments have been extended to include trypsin generated cytotaxin from human C3 and C5.

Modified Boyden chambers are routinely charged with 2 × 10⁶ neutrophils/ml and supported in Hanks' balanced salt solution or medium 199 containing either 10% plasma or 1% BSA.