Chemotaxis of polymorphonuclear leukocytes in corneal inflammation: tissue injury in herpes simplex virus infection.

The generation of complement-dependent chemotactic activity was demonstrated by herpes simplex virus (HSV) antigen, HSV antigen-antiviral antibody complexes, and HVS-infected cell lysates using the Boyden in vitro assay. In the presence of normal serum, chemotactic activity was generated by lysates of uninfected cells when nonspecific cell damage released chemotactic intracellular proteolytic enzymes. In order to determine the role that chemotaxis might play in the pathogenesis of stromal herpes keratitis which is accompanied by an infiltrate of polymorphonuclear leukocytes (PMN), lysates of corneal tissue obtained from rabbits with herpes virus epithelial and stromal keratitis were assayed in vitro for chemotactic activity. In the presence of serum both the lysates of HSV-infected corneal tissue as well as lysates of uninfected control tissue produced chemotaxis. This chemotactic activity could be explained by the release of normally intracellular enzymes from the damaged cells. Corneal stroma from animals with disciform keratitis showed significantly more chemotactic activity than similar tissue from the opposite uninfected control eye. This difference could be explained by the presence of HSVantigen-antiviral antibody complexes which activate the complement system resulting in leukotactic factors. However, it is more likely that the chemotactic factors liberated by the PMN cells found in the stroma in disciform keratitis are responsible for the major portion of this difference. Corneal tissue lysates from rabbits with an immune corneal ring of HSV antigenantiviral antibody demonstrated serum-dependent chemotactic activity in vitro. The experimental design of this study did not permit differentiation of the relative roles played by the antigenantibody complexes or by the PMN in activating complement-dependent chemotaxis.