We investigated the bacteriolytic activity of gingival crevicular fluid (CF) on 14C-labeled Streptococcus faecalis, Streptococcus mutans, Staphylococcus aureus, and on whole dental plaque. CF was collected from 100 healthy donors pooled and centrifuged at 200 g. CF supernate and a frozen and thawed extract of the pellet were interacted with the different bacterial strains, while Streptococcus faecalis and Staphylococcus aureus released 60% and 75% of the radioactive label, only 38% of it was solubilized from Streptococcus mutans, following their incubation with the CF supernate. The findings agreed with results obtained by interacting bacteria with a frozen and thawed lysate of human peripheral blood leukocytes. On the other hand, extracts from frozen and thawed CF pellet were inactive. Further, lipoteichoic acid and lipopolysaccharide were released by CF from Gram-positive and Gram-negative bacteria, respectively. The role of bacteriolytic factors, present in CF, as a result of the interaction between microorganisms and leukocytes at inflammatory sites is discussed.

Streptococcal and staphylococcal arthritis: can chronic arthritis in the human be caused by highly chemotactic degradation products generated from bacteria by leukocyte enzymes and by the deactivation of leukocytes by inflammatory exudates, polyelectrolytes, leukocyte hydrolases and by cell sensitizing agents derived from bacteria?

Human polymorphonuclear leukocytes (PMN) chemotaxis was tested during exposure to leukocyte and platelet extracts, a variety of polyelectrolytes, inflammatory exudates, and bacterial products. The chemoattractants employed were either zymosan-activated serum or supernatant from autolyzed Staphylococcus aureus. Chemotaxis to both chemoattractants was markedly inhibited by leukocyte and platelet extracts; inflammatory exudates; anionic polyelectrolytes, DNA, hyaluronic acid, liquoid; and by cationic polyelectrolytes, histone, protamine base, protamine sulfate, and myeloperoxidase. Inhibition was also found with elastase, collagenase, pepstatin, and epsilon-amino-caproic acid. Bacterial products, such as lipoteichoic acid and lipopolysaccharides, and extracts of human dental plaque inhibited chemotaxis. No inhibition of chemotaxis was observed with heparin (< 10 micrograms/ml), chondroitin sulfate, phosphatidylethanolamine and phospatidylserine. Indeed, chondroitin sulfate markedly enhanced chemotaxis and antagonized the inhibitory effect of leukocyte or platelet extract. None of the agents employed was toxic to PMN as judged by trypan blue exclusion. These observations suggest that cationic polyelectrolytes and inflammatory exudates influence PMN surfaces, modifying interaction with chemoattractants. Assessment of the role of PMN chemotaxis in host defense against microbial invaders requires evaluation of the response in the presence of agents likely to be present in inflamed tissues.