Pseudomonas aeruginosa Elastase and Its Role in Pseudomonas Infections

Wretlind, Bengt; Pavlovskis, O R

doi:10.1093/clinids/5.supplement_5.s998

Cited by 176 publications

(130 citation statements)

References 44 publications

Supporting

Mentioning

126

Contrasting

Unclassified

Order By: Relevance

“…A variety of other neutrophil-and bacteria-derived products, particularly proteases, have been suggested to contribute to tissue injury at sites of P. aeruginosa infection (24)(25)(26)(27)(28)(29)(30)(31). A number ofthese proteases have been reported to alter the physicochemical nature of transferrin and lactoferrin.…”

Section: Introductionmentioning

confidence: 99%

Pseudomonas and neutrophil products modify transferrin and lactoferrin to create conditions that favor hydroxyl radical formation.

Britigan

Edeker

1991

J. Clin. Invest.

View full text Add to dashboard Cite

In vivo most extracellular iron is bound to transferrin or lactoferrin in such a way as to be unable to catalyze the formation of hydroxyl radical from superoxide (7O-) and hydrogen peroxide (H202). At sites of Pseudomonas aeruginosa infection bacterial and neutrophil products could possibly modify transferrin and/ or lactoferrin forming catalytic iron complexes. To examine this possibility, diferrictransferrin and diferriclactoferrin which had been incubated with pseudomonas elastase, pseudomonas alkaline protease, human neutrophil elastase, trypsin, or the myeloperoxidase product HOCI were added to a hypoxanthine/xanthine oxidase *02-/H202 generating system. Hydroxyl radical formation was only detected with pseudomonas elastase treated diferrictransferrin and, to a much lesser extent, diferriclactoferrin. This effect was enhanced by the combination of pseudomonas elastase with other proteases, most prominently neutrophil elastase. Addition of pseudomonas elastasetreated diferrictransferrin to stimulated neutrophils also resulted in hydroxyl radical generation. Incubation of pseudomonas elastase with transferrin which had been selectively iron loaded at either the NH2-or COOH-terminal binding site yielded iron chelates with similar efficacy for hydroxyl radical catalysis. Pseudomonas elastase and HOCI treatment also decreased the ability of apotransferrin to inhibit hydroxyl radical formation by a Fe-NTA supplemented hypoxanthine/xanthine oxidase system. However, apotransferrin could be protected from the effects of HOCI if bicarbonate anion was present during the incubation. Apolactoferrin inhibition of hydroxyl radical generation was unaffected by any of the four proteases or HOC. Alteration of transferrin by enzymes and oxidants present at sites of pseudomonas and other bacterial infections may increase the potential for local hydroxyl radical generation thereby contributing to tissue injury. (J. Clin. Invest. 1991.

show abstract

Section: Introductionmentioning

confidence: 99%

Pseudomonas and neutrophil products modify transferrin and lactoferrin to create conditions that favor hydroxyl radical formation.

Britigan

Edeker

1991

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…Many virulence factors of P. aeruginosa are cell surface components, such as lipopolysaccharide (LPS) and alginate, or extracellular products, such as alkaline protease, elastase, exotoxin A, DNase, and phospholipase C (PLC); in concert or acting alone, they contribute to the pathogenesis of infection (1,2,13,14,18,37,48,54). Several studies have demonstrated the secretion of these products to the external environment during the growth of the pathogen (2,3,18,19,21,28,30).…”

mentioning

confidence: 99%

“…aeruginosa secretes several proteases (18,29,30,54). We examined the secretion of elastase and protease in strain ATCC 19660 since the amounts of both enzymes produced by this strain were found to be larger than those for strain H103.…”

mentioning

confidence: 99%

Virulence factors are released from Pseudomonas aeruginosa in association with membrane vesicles during normal growth and exposure to gentamicin: a novel mechanism of enzyme secretion

1995

View full text Add to dashboard Cite

Pseudomonas aeruginosa blebs-off membrane vesicles (MVs) into culture medium during normal growth. Release of these vesicles increased approximately threefold after exposure of the organism to four times the MIC of gentamicin. Natural and gentamicin-induced membrane vesicles (n-MVs and g-MVs, respectively) were isolated by filtration and differential centrifugation, and several of their biological activities were characterized. Electron microscopy of both n-MVs and g-MVs revealed that they were spherical bilayer MVs with a diameter of 50 to 150 nm. Immunoelectron microscopy and Western blot (immunoblot) analysis of the vesicles demonstrated the presence of B-band lipopolysaccharide (LPS), with a slightly higher proportion of B-band LPS in g-MVs than in n-MVs. A-band LPS was occasionally detected in g-MVs but not in n-MVs. In addition to LPS, several enzymes, such as phospholipase C, protease, hemolysin, and alkaline phosphatase, which are known to contribute to the pathogenicity of Pseudomonas infections were found to be present in both vesicle types. Both types of vesicles contained DNA, with a significantly higher content in g-MVs. These vesicles could thus play an important role in genetic transformation and disease by serving as a transport vehicle for DNA and virulence factors and are presumably involved in septic shock.

show abstract

“…14 Therefore, inflammation is likely to have been initiated by enzymatic digestion of substrates in ST including a) b) c) collagen 6 and elastin 15 , and possibly the digestion of fibrinogen; the soluble plasma protein involved in the clotting cascade.…”

Section: Discussionmentioning

confidence: 99%

Effects of Pseudomonas aeruginosa elastase and Exotoxin A on subcutaneous tissue following dermal trauma.

Geerlings

Penhale

Stumbles³

2017

MRAJ

View full text Add to dashboard Cite

Pseudomonas aeruginosa is an opportunistic pathogen of the skin, especially following severe trauma such as burning. It produces a large array of virulence factors, including Exotoxin A and elastase that can kill susceptible cells and digest collagenous tissue. To observe and measure their effects, these purified virulence factors were applied directly to subcutaneous tissue using a transdermal chamber implanted in mice. Elastase disrupted collagen formation in tissue, induced haemorrhage, and increased exudation into the chamber which was quickly resolved by the host. Exotoxin A reduced the number of fibroblasts and leukocytes in tissue, decreased collagen formation, and reduced exudation and the concentration of monocytes in the chamber reservoir; these effects being observed four days post treatment. The ability of these two virulence factors to alter collagen formation and production, and influence local populations of leukocytes, provides further insight into the aetiology of bacteraemia following P.aeruginosa infection of skin.

show abstract

Pseudomonas aeruginosa Elastase and Its Role in Pseudomonas Infections

Cited by 176 publications

References 44 publications

Pseudomonas and neutrophil products modify transferrin and lactoferrin to create conditions that favor hydroxyl radical formation.

Pseudomonas and neutrophil products modify transferrin and lactoferrin to create conditions that favor hydroxyl radical formation.

Virulence factors are released from Pseudomonas aeruginosa in association with membrane vesicles during normal growth and exposure to gentamicin: a novel mechanism of enzyme secretion

Effects of Pseudomonas aeruginosa elastase and Exotoxin A on subcutaneous tissue following dermal trauma.

Contact Info

Product

Resources

About