Deficient phagocytosis secondary to breakdown of opsonic factors in infected exudates.
Pleural empyema, a clinical entity characterized by the simultaneous presence of large number of PMNLs and viable bacteria, is a biological paradox which has not been fully explained yet. Our preliminary studies suggest that receptor and bactericidal functions of PMNL isolated from purulent exudates, can be close to normal in this condition. Supernatants of these empyemas however have been shown to be low in heat labile opsonic activity and complement hemolytic activity. These observations have been extended by the demonstration of breakdown of IgG, C3 and factor B in infected pleural effusions as opposed to pleural fluids obtained under other conditions. The breakdown of Ig and C3 seems to be enzymatic and to occur, at least for C3, even in the absence of Ca and Mg ions: thus, direct cleavage of C3, possibly by PMNL enzymes, has to be postulated to explain these results. Present work in our laboratory is trying to explore this possibility.
D000038:Abscess / Q000503:physiopathology; D001770:Blood Bactericidal Activity; D003167:Complement Activation; D004653:Empyema / Q000503:physiopathology*; D005122:Exudates and Transudates / Q000502:physiology; D006801:Humans; D009504:Neutrophils / Q000502:physiology; D009895:Opsonin Proteins / Q000502:physiology*; D010587:Phagocytosis
D009895:Opsonin Proteins