Abstract:

Mechanisms of biodegradation of staphylococci by leukocyte factors and its modulation by serum proteins, inflammatory exudates, polyelectrolytes, antibiotics and by lipoteichoic acid: Relation to chemotaxis and to the survival of bacteria in inflammatory sites After phagocytosis of opsonized and non-opsonized bacteria by phagocytes, there is fusion of lysosomes discharge of lysosomal factors into phagosomes and activation of metabolic pathways leading to the generation of hydrogen peroxide, singlet oxygen, and other oxygen radicals, and death of the engulfed bacteria. Although much is known today about the mechanism by which phagocytes kill bacteria following phagocytosis, very little is known about the mechanisms of biodegradation of the engulfed bacteria. Biodegradation of bacteria within PMN involves action of lysosomal enzymes, neutral protease collagenases and proteases as well as reactive oxygen radical and release of these products from phagocytes may lead to destruction of host tissue. The propagation of chronic inflammatory sequellae following infections with staphylococci may also be mediated by delayed and immediate hypersensitivity reactions. Degradation of products of microbes also may diffuse into tissue and the chemotactic properties of these exudates attracts more phagocytic cells. Inflammatory exudates induced by bacterial infections are rich in acid and neutral hydrolases of leukocyte origin as well as bacterial products. The purpose of the present communication is to summarize several years of investigation of the pathogenesis of staphylococcal lesions with emphasis on the role played by anionic and cationic polyelectrolytes and degradation products of bacteria in the modulation of leukocyte-bacteria interactions (10, 14).