Is Bacteriolysis In vivo a Friend or a Foe? Relation to Sepsis, Chronic Granulomatous Inflammation and to Oral Disorders: an Overview Hypothesis (original) (raw)
2015, SOJ Microbiology & Infectious Diseases
vascular endothelial cells via pathogen recognition receptors. This may lead to host responses and to the mobilization of the complement system, resulting in endothelial cells disruption. It was recently suggested that histones, released from leukocyte nuclei, may be major mediators of death in sepsis [3,4]. Since sepsis may be caused mainly by Gram positives and by Gram negatives, the question was addressed whether we deal with two different clinical manifestations [5]. The authors stated that: "It has been assumed that the initiation of the systemic inflammatory response with activation of the pro inflammatory cytokine networks and other mediators results in a similar organisms. Systemic immune activation during sepsis may promote the clearance of the microbial pathogen; however, generalized inflammation also contributes to the pathogenesis of septic shock. The balance between these beneficial and deleterious effects may differ between Gram-positive and Gram-negative pathogens pathophysiologic process, regardless of the causative microbic pathogen. Yet, there is increasing experimental evidence that fundamental differences exist in the host response to Gram-positive bacterial pathogens, compared with the host response to Gramnegative." The main pro inflammatory agonists that may be released into the blood stream following lysis of microorganisms include: • Cell surface Lipopolysaccharides (LPS) from Gram negatives • Membrane-associated Lipoteichoic Acid (LTA) from Gram-positives • Capsular polysaccharides from pneumococci • Microbial hemolysins and additional membranedamaging agents • The host may supply : toxic amounts H 2 O 2 , hydroxyl radical, HOCl, Nitric Oxide (NO) and peroxynitrite, Lysosomal acid hydrolases, bactericidal cationic peptides
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