Interaction of complement with serum-sensitive and serum-resistant strains of Pseudomonas aeruginosa

Schiller, Neal L.; Joiner, K A

doi:10.1128/iai.54.3.689-694.1986

Cited by 51 publications

(24 citation statements)

References 28 publications

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“…Sputum sol phase samples from CF patients infected with P. aeruginosa have been shown to contain split products of complement component C3, which was seen as evidence of complement activation occurring in vivo in the lungs (37). It has also been found that mucoid P. aeruginosa can activate complement (34), but, according to our results, this is not likely to be caused by the alginate extracellular matrix. We suggest that alginate, by its inability to active complement, protects the alginate-producing bacteria from lysis and complement opsonization which may contribute to the persistence of mucoid strains.…”

Section: Discussionsupporting

confidence: 78%

Pseudomonas aeruginosa alginate in cystic fibrosis sputum and the inflammatory response

et al. 1990

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Alginate, a viscous polysaccharide from mucoid Pseudomonas aeruginosa, may interfere with the host defenses in patients with cystic fibrosis and chronic P. aeruginosa lung infection. The alginate concentration in the sol phase of expectorated sputum was quantitated by a biochemical method and a newly developed enzyme-linked immunosorbent assay. There was a high degree of correlation between the methods, and the concentration of alginate ranged from 4 to 101 Fig/ml with a median of 35.5 ,ug/ml when measured by enzyme-linked immunosorbent assay. Alginate could not be detected in the bronchial secretions from patients without P. aeruginosa infection. In vitro investigation of alginate did not show any activation of the alternative pathway of complement, as determined by a hemolytic kinetic assay and by testing for neutrophil chemotaxis. At a high concentration, P. aeruginosa alginate caused a slight activation of the classical pathway of complement. Alginate did not cause neutrophil chemotaxis by itself but was able to reduce the neutrophil chemotactic response to N-formylmethionylieucylphenylalanine and for zymosan-activated serum. P. aeruginosa and seaweed alginates were able to prime neutrophils for increased N-formylmethionylieucylphenylalanine-induced neutrophil oxidative burst, as determined by chemiluminescence. Because of its ability to prevent attraction of neutrophils to the site of infection, lack of complement activation, and ability to enhance neutrophil oxidative burst, alginate from P. aeruginosa may contribute to the persistence and pathogenesis of chronic P. aeruginosa infection in cystic fibrosis.on August 5, 2020 by guest http://iai.asm.org/ Downloaded from

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Section: Discussionsupporting

confidence: 78%

Pseudomonas aeruginosa alginate in cystic fibrosis sputum and the inflammatory response

et al. 1990

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“…The surface assembly of terminal complement components was next examined. It has been postulated that for some gramnegative organisms, mechanisms contributing to serum resistance include inhibition of C5b-9 formation (25,30,31) and surface deposition of normal but nonlytic MAC (18)(19)(20)35) or of altered, nonproductive complexes (14). C5b-9 was rapidly deposited on the surface of B. pseudomallei, with kinetics of deposition similar to that of C3.…”

Section: Discussionmentioning

confidence: 99%

Burkholderia pseudomallei activates complement and is ingested but not killed by polymorphonuclear leukocytes

Egan

Gordon

1996

Infect Immun

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The mechanism by which Burkholderia pseudomallei is resistant to lysis by human serum is unknown but may include interference with complement activation, effective opsonization, or complement-mediated lysis. We investigated the interaction of B. pseudomallei with complement in the presence and absence of specific antibody to determine potential mechanisms of serum resistance. We demonstrated rapid activation and consumption of complement by B. pseudomallei which, in the absence of specific antibody, occurred predominantly via the alternative pathway. Complement activation was associated with deposition of the opsonically active C3b and iC3b fragments on the bacterial surface. C5b-9, detected on the bacterial surface after opsonic periods of 1 to 60 min, was susceptible to elution by 1 M NaCl, indicating that resistance to complement-mediated lysis may result from deposition of the membrane attack complex in a nonmicrobicidal location. To define the role of opsonins, we investigated the ability of polymorphonuclear leukocytes (PMNL) to phagocytose B. pseudomallei. Phagocytosis of bacteria by PMNL, and the observed oxidative response, was significantly increased by opsonization of organisms with complement and/or specific antibody. Despite opsonophagocytosis by PMNL and the production of an oxidative response, no significant bacterial killing was observed.

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“…significantly less C9 was deposited on serum resistant strains as compared with serum sensitive strains. Both types of strains activate complement cascades equally; the remarkable property of resistant strains is the reduced insertion of C5b-9 in the membrane and hence results in increased survival (Schiller and Joiner, 1986). In a more recent report, P. aeruginosa complement regulator-acquiring surface proteins (CRASP-2) showed direct binding to Vn heparin-binding domains and inhibited the complement mediated lysis (Hallström et al, 2010).…”

Section: Figmentioning

confidence: 99%

Vitronectin in bacterial pathogenesis: a host protein used in complement escape and cellular invasion

Singh

Riesbeck³

2010

Molecular Microbiology

177

238

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SummaryThe multifunctional human glycoprotein vitronectin (Vn) plays a significant role in cell migration, tissue repair and regulation of membrane attack complex (MAC) formation. It also promotes neutrophil infiltration and, thus, enhances the inflammatory process during infection. In the host, a balanced homeostasis is maintained by Vn due to neutralization of the selfreactivity of the MAC. On the other hand, Vn bound to the bacterial surface protects from MAC-mediated lysis and enhances adhesion. Gram-negative bacterial pathogens including Moraxella catarrhalis, Haemophilus influenzae and Neisseria gonorrhoeae use Vn recruitment to prevent MAC deposition at their surface. Moreover, Gram-positive bacterial pathogens such as Streptococcus pneumoniae and S. pyogenes utilize Vn for effective adhesion to host cells and subsequent internalization. Vitronectin has an ArgGly-Asp (RGD) sequence for binding the host cell integrin receptors and a separate bacterial-binding domain for pathogens, and thus more likely functions to cross-link bacteria and epithelial cells. Once bacteria are attached to the vitronectin-integrin complex, various host cell-signalling events are activated and promote internalization. In this review, we focus on the important roles of vitronectin in bacterial pathogenesis and describe different strategies used by pathogens to evade the host response by the help of this intriguing molecule.

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Interaction of complement with serum-sensitive and serum-resistant strains of Pseudomonas aeruginosa

Cited by 51 publications

References 28 publications

Pseudomonas aeruginosa alginate in cystic fibrosis sputum and the inflammatory response

Pseudomonas aeruginosa alginate in cystic fibrosis sputum and the inflammatory response

Burkholderia pseudomallei activates complement and is ingested but not killed by polymorphonuclear leukocytes

Vitronectin in bacterial pathogenesis: a host protein used in complement escape and cellular invasion

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