Normal sera and plasma, derived from humans, calves, rats, rabbits, horses, human synovial fluids, inflammatory exudates, and leukocyte extracts, when sufficiently diluted are highly bacteriolytic for Staph, aureus, Strep. faecalis, B. sutilis and to a variety of gram-negative rods. On the other hand, concentrated serum or the other body fluids are usually not bacteriolytic for these bacterial species. While the lysis of Staph, aureus and B. subtilis by diluted serum is not lysozyme dependent, lysis of Strep. faecalis is absolutely dependent on the concentration of lysozyme. The lytic factor in human serum is present in Cohn's fractions III, IV, and V. It is nondialyzable, resistant to heating for 75 degrees C and 20 min, and acts optimally at pH 5.0. Like leukocyte extracts, synovial fluids, and inflammatory exudates, it lyses only young staphylococci. The inability of concentrated serum to lyse Staph. aureus and Strep. faecalis is due to the presence in the gamma globulin fraction of a potent inhibitor, which can be partly removed by dilution of by adsorption upon the homologous bacteria. Lysis of the bacteria is also strongly inhibited by Cohn's fraction II (gamma globulin) by high-molecular-weight DNA, heparin, liquoid, and histone. The possible role played by serum globulin in the protection of bacteria against degradation by leukocyte is discussed.
Leukocyte extracts, trypsin, and lysozyme are all capable of releasing the bulk of the LPS from S. typhi, S. typhimurium, and E. coli. Bacteria which have been killed by heat, ultraviolet irradiation, or by a variety of metabolic inhibitors and antibiotics which affect protein, DNA, RNA, and cell wall synthesis no longer yield soluble LPS following treatment with the releasing agents. On the other hand, bacteria which are resistant to certain of the antibiotics yield nearly the full amount of soluble LPS following treatment, suggesting that certain heatlabile endogenous metabolic pathways collaborate with the releasing agents in the release of LPS from the bacteria. It is suggested that some of the beneficial effects of antibiotics on infections with gram-negative bacteria may be the prevention of massive release of endotoxin by leukocyte enzymes in inflammatory sites.
Severe inflammatory lesions were induced in the periodontal tissues of the rat following the intragingival injection of lipoteichoic acid (LTA) from Streptococcus mutans. There was no difference in the severity and distribution of the lesions between nonimmunized rats and animals immunized against LTA after antigenic challenge. The lesions are characterized by the occurrence of granulation tissue, massive infiltration of PMNs, abscess formation, bone resorption, and new bone formation. Deacylated LTA and saline caused relatively mild inflammation, and no significant bone resorption or new bone formation was evident. The peak response was reached after 3 intragingival infections. The mechanisms by which LTA caused the pathological alterations in the rat periodontium and the possible relations of this experimental model to periodontal disease in the human are discussed.