Experimental Models of Streptococcal Arthritis: Pathogenetic Role of Streptococcal Products and Prostaglandins and Their Modification by Anti-Inflammatory Agents

Is Bacteriolysis In vivo a Friend or a Foe? Relation to Sepsis, Chronic Granulomatous Inflammation and to Oral Disorders: an Overview Hypothesis

“…The use of experimental models, mostly in rats, showed a long persistence of microbial cell-walls residing within large macrophages due probably to their inability to degrade the PPG [43][44][45][46][47][48].Such stimulated macrophages probably release into the surrounding media chemotactic agents, enzymes and cytokines, which can amplify and also further perpetuate the inflammatory responses (Figures 1 and figure 2) Are Microbial Cell-Walls also involved in the Pathophysiology of Periodontal Disease and in Pulpitis?…”

“…Extensive studies have been performed to explain the possible mechanisms involved in the pathogenesis of septic shock [1,2,5], chronic inflammatory processes such as seen in tuberculosis, arthritis, microbial-and fungal infections, periodontal disease and pulpitis, which many of them are also characterized by longlasting granuloma formation [15,38,[43][44][45][46][47][48][49]. Since cell and tissue damage in post-infectious sequelae is probably an end-result of "cross-talks" among a multiplicity of pro inflammatory agents and the immune responses of the host [7][8][9][10]12], it may suggest that multi-drug strategies, but not single antagonists, could prove more effective protectors against the aftermath of chronic inflammatory episodes [16].…”

Cationic polyelectrolytes: A new look at their possible roles as opsonins, as stimulators of respiratory burst in leukocytes, in bacteriolysis, and as modulators of immune-complex diseases (A review hypothesis)

“…The persistence of nonbiodegradable microbial cell walls in vivo is probably central in the initiation of chronic inflammatory sequellae. The activation of macrophages by bacterial PPG-PS complexes (149) has been suggested to be the major cause of tissue damage seen in infectious granulomas (142)(143)(144)(145)(146)(147)(148)(149). Even penicillin-grown bacteria (121,147) persisted with apparently intact cell walls within macrophages in joint (t21) and liver (147) lesions for long periods.…”

“…Even penicillin-grown bacteria (121,147) persisted with apparently intact cell walls within macrophages in joint (t21) and liver (147) lesions for long periods. Resistance of the PPG-PS complexes to degradation in vivo could therefore also be a result of the selective inactivation either of leukocyte hydrolases and CPs or of the bacterial autolysins by proteinase, glycosaminoglycans, and oxygen radicals, known to accumulate in large amounts in inflammatory and infectious foci (46)(47)(48)(143)(144)(145)(146)(147)(148)(149).…”