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Tick-Bite Injury: Mediation by a Complement-Derived Chemotictic Chemotactic Factor

From the Walter Reed Army Institute of Research, Washington, D. C., The University of Connecticut, Farmington, Connecticut, and Old Dominion University, Norfolk, Virginia

Abstract

The intensely destructive tick-bite injury is dependent on the presence of neutrophils. The present study examines the nature of the tick-host interaction and the attraction of neutrophils to the site of injury. Tick salivary gland extracts have no intrinsic chemotactic activity but can generate this activity from human or dog serum. Activity was also generated from human C5 but not from C3. Antibody to C5 eliminated the chemotactic activity produced in human serum. The chemotactic factor generated in human serum appeared to be a C5 cleavage product of low sedimentation velocity in sucrose gradient ultracentrifugation. Complement depletion of C5 in rats by cobra venom treatment greatly reduced the tissue necrosis and inflammation associated with the tick feeding lesion. These results suggested that this inflammatory lesion was related to the cleavage of host C5 by tick saliva to produce a chemoattractant for neutrophils. This non-immunologic model of tissue injury is analogous to the immunologic models of the Arthus reaction and acute nephrotoxic nephritis. In each case, the complement system provides the chemotactic factors for neutrophils, and the ensuing damage is neutrophil-dependent.