Pulmonary opsonins in Klebsiella pneumoniae pneumonia in rats

Abstract

Klebsiella pneumoniae was inoculated intrabronchially into rats, and bronchoalveolar lavage fluid and sera were obtained during the ensuing pneumonia. Klebsiellae recovered by lavage were not maximally coated with C3, as judged by studies with fluorescent antibody, whereas the organisms could be coated fully with C3 by a brief incubation in rat serum. The levels of Cl and C3 in lavage fluid obtained during infection were only a small fraction of the levels in the serum, and klebsiellae were not opsonized during incubation with concentrated lavage fluid. Systemic decomplementation did not affect the severity of K. pneumoniae pneumonia, as judged by the measurement of lung weight or by the numbers of klebsiellae in the lungs, but decomplemented rats had a larger number of klebsiellae in the blood at 24 h of infection than did controls. There were fewer klebsiellae in the lungs 4 h after inoculation of preopsonized organisms than after inoculation of organisms which were incubated in control (heat-inactivated) sera. These studies indicate that the concentration of complement and heat-labile opsonins within the alveoli is lower than that in the systemic circulation and is not adequate for effective opsonization of klebsiellae. Complement has been shown to exert a protective effect in a variety of bacterial infections. The precise role of complement in pulmonary defenses, however, has not been well defined. Normal bronchoalveolar lavage fluid contains functional components of both the classical and the alternative complement pathways (10, 12-14), but there is little information about the levels of these components in the lungs during bacterial infection. To assess the role of complement within the pulmonary alveoli during infection, bronchoalveolar lavage fluids of rats with Klebsiella pneumoniae pneumonia were studied. The course of pneumonia in decomplemented rats and in rats injected with preopsonized klebsiellae was also studied. The results of the studies suggest that complement levels within the alveoli are much lower than the levels in the circulation and are not optimal for opsonization of klebsiellae. MATERIALS AND METHODS Animals. Adult (200to 300-g) male Sprague-Dawley rats (Charles River Breeding Laboratories, Wilmington, Mass.) were used throughout. Experimental pneumonia. K. pneumoniae type

Bacterial isolation from internal organs of rats (Rattus rattus) captured in Baghdad city of Iraq

“…Many opportunistic pathogens, for example, Klebsiella , Enterobacter , and Pseudomonas have become increasingly relevant as the causative agents of clinical diseases and pathological lesions in laboratory animals [72,75]. As K. pneumoniae can cause severe fatal pyogenic pneumonia in humans, with a lesser extent in K. oxytoca , it serves experimentally as a model for many diseases, while K. oxytoca is infrequent naturally occur [75-77]. Our finding regarding Klebsiella , despite its species, reported six cases from intestinal content, putting the risk of contaminating the surroundings by rat droppings is highly predicted.…”

Lung Antimicrobial Defenses in the Newborn

“…These studies suggest that complement plays a role in lung clearance of pneumococci and Pseudomonas, but not in lung clearance of staphylococci and Klebsiella. 6,[21][22][23] Complement appears to function in the lung primarily as a chemoattractant and less as an opsonin. 6,21,22 Neonatal serum has deficient alternative and classic complement activity, [24][25][26][27] which may predispose to bacterial infection in the lung.…”

Nonphagocytic clearance of Staphylococcus aureus from murine lungs

“…Furthermore, there is no experimental basis for any assumption that inhaled staphylococci are chemotactic for alveolar macrophages. In fact, S. aureus does not appear to be inherently chemotactic and attracts phagocytes only through its capacity to activate the complement cascade (24), a chemotactic system which attracts alveolar macrophages weakly (6,27) and which is in low concentration in alveolar spaces even during inflammation (5).…”