Cyclic AMP placed in the bottom of the modified Boyden chemotaxis chamber is weakly chemotactic for rabbit peritoneal neutrophils. Dibutyryl-cyclic AMP under similar conditions gives a biphasic response, being weakly chemotactic at low concentrations and inhibiting cell movement at higher concentrations. When mixed with the cells in the upper compartment of the chemotaxis chamber, cyclic AMP and dibutyryl-cyclic AMP enhance neutrophil spontaneous motility; on the other hand, dibutyryl-cyclic AMP mixed with the cells in the upper compartment consistently inhibits neutrophil chemotactic responsiveness, while cyclic AMP has a variable effect on chemotaxis. The only effect of ADP and ATP was to inhibit chemotaxis and spontaneous motility. AMP is totally without effect.
The anti-inflammatory agents, phenylbutazone, naproxen and niflumic acid inhibited in vitro rabbit peritoneal neutrophil chemotactic responsiveness to Escherichia coli derived chemotactic factor/s when added to cells suspended in 0.1% bovine serum albumin (BSA). Inhibition of chemotaxis by these drugs was markedly diminished as the BSA concentration was increased to 2%. Experiments with phenylbutazone demonstrated that inhibition of chemotaxis could be observed using neutrophils suspended in 2% BSA by either increasing the drug concentration or by preincubating the cells suspended in 0.1% with the drug prior to the addition of the additional BSA. These data suggest that protein binding can prevent in vitro inhibition of neutrophil chemotaxis by anti-inflammatory agents.
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