Pseudomonas aeruginosa pili as ligands for nonopsonic phagocytosis by fibronectin-stimulated macrophages

Kelly, N. M.; Kluftinger, J. L.; Pasloske, Brittan L.; Paranchych, W.; Hancock, Robert E. W.

doi:10.1128/iai.57.12.3841-3845.1989

Cited by 33 publications

(30 citation statements)

References 30 publications

(25 reference statements)

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“…The phagocytosis resistance of nonmotile bacteria could not be attributed solely to lack of contact between bacteria and macrophages; performing the phagocytic assays on a rocking platform or forcing the bacteria down onto the monolayer by centrifugation both failed to enhance the nonopsonic ingestion of the nonmotile CF isolates examined (data not shown). The ability of the nonflagellated and RpoN -CF isolates examined in this study to resist nonopsonic uptake by macrophages is consistent with studies indicating that RpoNdependent ligands play a major role in the recognition of P. aeruginosa by macrophages in the absence of serum opsonins (13,21). The phagocytosis resistance of nonmotile bacteria together with the finding that macrophage phagocytosis of P. aeruginosa is critically dependent on the presence of glucose (32) may also help to explain why P. aeruginosa is such an efficient respiratory pathogen in CF.…”

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confidence: 89%

Nonmotility and phagocytic resistance of Pseudomonas aeruginosa isolates from chronically colonized patients with cystic fibrosis

1994

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Although Pseudomonas aeruginosa chronically colonizes most older patients with cystic fibrosis (CF), bacterial features responsible for its persistence are understood poorly. We observed that many P. aeruginosa isolates from chronically colonized patients were nonmotile and resistant to phagocytosis by macrophages. P. aeruginosa isolates were collected from 20 CF patients for up to 10 years. Isolates from early colonization were highly motile and expressed both flagellin and pilin. However, many isolates from chronically colonized patients lacked flagellin expression and were nonmotile; a total of 1,030 P. aeruginosa CF isolates were examined, of which 39%O were nonmotile. Moreover, sequential isolates recovered from several of the CF patients were consistently nonmotile for up to 10 years. Lack of motility was rare among environmental isolates (1.4%) and other clinical isolates (3.7%) of P. aeruginosa examined. Partial complementation of motility in nonmotile P. aeruginosa isolates was achieved by introduction of extra copies of the rpoN locus carried on plasmid pPT212, indicating that the alternate sigma factor, RpoN, may be involved in the coordinate regulation of virulence factors during CF infection. We hypothesize that the nonmotile phenotype may provide P. aeruginosa a survival advantage in chronic CF infection by enabling it to resist phagocytosis and conserve energy.

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confidence: 89%

Nonmotility and phagocytic resistance of Pseudomonas aeruginosa isolates from chronically colonized patients with cystic fibrosis

1994

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“…Certainly, microcolonies of P. aeruginosa in the lung sputum of chronically infected patients with CF have been observed and resemble mucoid colonies grown in the laboratory (Bjarnsholt et al, 2009). Conversely, pili are the major adhesin involved in nonopsonic phagocytosis of Pseudomonas (Kelly et al, 1989). Pilin-deficient mutants or those impaired in twitching motility demonstrate reduced virulence in various models.…”

Section: Flagella and Type 4 Pilimentioning

confidence: 99%

Pseudomonas aeruginosa: new insights into pathogenesis and host defenses

2013

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This review about Pseudomonas aeruginosa acute and chronic virulence is timely and extremely well presented. It presents both the response of the host and the virulence factors produced by the bacterium. AbstractPseudomonas aeruginosa is a metabolically versatile bacterium that can cause a wide range of severe opportunistic infections in patients with serious underlying medical conditions. These infections are characterized by an intense neutrophilic response resulting in significant damage to host tissues and often exhibit resistance to antibiotics leading to mortality. Treatment of persistent infections is additionally hampered by adaptive resistance, due to the growth state of the bacterium in the patient including the microorganism's ability to grow as a biofilm. An array of P. aeruginosa virulence factors counteract host defences and can cause direct damage to host tissues or increase the bacterium's competitiveness. New prevention and treatment methods are urgently required to improve the outcome of patients with P. aeruginosa infections. This review describes the two main types of P. aeruginosa lung infections and provides an overview of the host response and how the genomic capacity of P. aeruginosa contributes to the pathogenesis and persistence of these infections.

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“…In addition, the host's inflammatory response is ineffective in combating biofilms. 15 In order to systematically study pathologenic mechanisms and test new therapies for chronic wounds, a reliable animal model would be a valuable tool. Researchers have tried several methods to delay wound healing, such as the ischemic rabbit ear model, 16,17 radiation-impaired rats, 18 and diabetic mice.…”

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confidence: 99%

Time course study of delayed wound healing in a biofilm‐challenged diabetic mouse model

Zhao

Usui

Underwood

et al. 2012

Wound Repair Regeneration

104

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Bacterial biofilm has been shown to play a role in delaying wound healing of chronic wounds, a major medical problem that results in significant healthcare burden. A reproducible animal model could be very valuable for studying the mechanism and management of chronic wounds. Our previous work demonstrated that Pseudomonas aeruginosa (PAO1) biofilmchallenge on wounds in diabetic (db/db) mice significantly delayed wound healing. In this wound time course study, we further characterize the bacterial burden, delayed wound healing and certain aspects of the host inflammatory response in the PAO1 biofilm-challenged db/db mouse model. PAO1 biofilms were transferred onto 2 day old wounds created on the dorsal surface of db/db mice. Control wounds without biofilm-challenge healed by 4 weeks, consistent with previous studies; none of the biofilm-challenged wounds healed by 4 weeks; 64% of the biofilm-challenged wounds healed by 6 weeks; and all of the biofilm-challenged wounds healed by 8 weeks. During the wound healing process, P. aeruginosa were gradually cleared from the wounds while the presence of S. aureus (part of the normal mouse skin flora) increased. Scabs from all unhealed wounds contained 107 P. aeruginosa, which was 100 fold higher than the counts isolated from wound beds (i.e. 99% of the P. aeruginosa was in the scab). Histology and genetic analysis showed proliferative epidermis, deficient vascularization and increased inflammatory cytokines. Hypoxia inducible factor (HIF) expression increased 3 fold in 4 week wounds. In summary, our study demonstrates that biofilm-challenged wounds typically heal in approximately 6 weeks, at least 2 weeks longer than non biofilm-challenged normal wounds. These data suggest that this delayed wound healing model enables the in vivo study of bacterial biofilm responses to host defenses and the effects of biofilms on host wound healing pathways. It may also be used to test anti-biofilm strategies the treatment of chronic wounds.

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Pseudomonas aeruginosa pili as ligands for nonopsonic phagocytosis by fibronectin-stimulated macrophages

Cited by 33 publications

References 30 publications

Nonmotility and phagocytic resistance of Pseudomonas aeruginosa isolates from chronically colonized patients with cystic fibrosis

Nonmotility and phagocytic resistance of Pseudomonas aeruginosa isolates from chronically colonized patients with cystic fibrosis

Pseudomonas aeruginosa: new insights into pathogenesis and host defenses

Time course study of delayed wound healing in a biofilm‐challenged diabetic mouse model

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