A Wound-Isolated Pseudomonas aeruginosa Grows a Biofilm In Vitro Within 10 Hours and Is Visualized by Light Microscopy

Harrison-Balestra, Catherine; Cazzaniga, Alejandro L.; Davis, Stephen C.; Mertz, Patricia M.

doi:10.1097/00042728-200306000-00016

Cited by 23 publications

(27 citation statements)

References 34 publications

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“…Furthermore, there is evidence that neutrophil-and antibiotic-resistant biofilms may develop in ulcers. 37,45 The observations on the inhibition of keratinocyte migration in vitro, caused by LPS, provide one explanation for the lack of reepithelialization seen in chronic wounds and the beneficial effect of sharp debridement, 46 which can remove biofilm. Sharp debridement also causes bolus release of platelet-derived antibacterial products such as NAP-2 and other antibacterial agents, 47 which act to discourage recolonization and promote healing in a manner similar to acute wounds.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of keratinocyte migration by lipopolysaccharide

Loryman

Mansbridge

2007

Wound Repair Regeneration

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A critical process in cutaneous wound healing is reepithelialization by keratinocytes that closes the breach in the epidermis. Chronic wounds fail to reepithelialize despite the presence of activated and proliferative keratinocytes around the wound perimeter. This type of wound is generally colonized to a greater or lesser extent by bacteria. This study examines the possibility that bacterial products might directly inhibit keratinocyte migration. Using conventional scratch assays, we observed a dose-dependent inhibition of keratinocyte migration by lipopolysaccharide (LPS) derived from either Pseudomonas aeruginosa or Escherichia coli. Although the P. aeruginosa preparation appeared to be slightly more inhibitory, both gave half-maximal inhibition at 0.5-0.6 ng/mL. Migration of fibroblasts was not inhibited. The result could not be attributed to a cytotoxic effect of the LPS. LPS inhibition of migration was relieved by neutralizing antibodies to toll-like receptors (TLR), 40% by anti-TLR2 and 75% by anti-TLR4. We conclude that keratinocyte migration is inhibited by bacterial products, detected through TLR4 and also through TLR2. Because chronic wounds always show some presence of bacteria, these findings provide a possible explanation for the lack of healing found in ulcers.

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Section: Discussionmentioning

confidence: 99%

Inhibition of keratinocyte migration by lipopolysaccharide

Loryman

Mansbridge

2007

Wound Repair Regeneration

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“…[1][2][3][4][5][6][7][8][9][10] Defined as a surfaceadhered, complex community of aggregated bacteria encased within a self-secreted matrix of extracellular polymeric substance, biofilm bacteria possess a diverse set of virulence, defense, and survival mechanisms that distinguish them from traditionally studied, free-floating, "planktonic" bacteria. These include an inherent, physical protection against host inflammatory cells and antibiotic penetration by its self-secreted extracellular polymeric substance, 11,12 and intricate cell-to-cell signaling pathways that are specific to different bacterial species.…”

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confidence: 99%

Bacteriophage Therapy for Staphylococcus aureus Biofilm–Infected Wounds

Seth

Geringer

Nguyen³

et al. 2013

Plastic and Reconstructive Surgery

107

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Bacteriophages can be an effective topical therapy against S. aureus biofilm-infected wounds in the setting of a deficient (mutant) or disrupted (débridement) biofilm structure. Combination treatment aimed at disturbing the extracellular biofilm matrix, allowing for increased penetration of species-specific bacteriophages, represents a new and potentially effective approach to chronic wound care. These results establish principles for biofilm therapy that may be applied to several different clinical and surgical problems.

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“…11,12 He, with others, developed the growth factor trap hypothesis to explain venous ulcer pathophysiologic characteristics, 13 put forth the idea that skin grafts do not act solely as a tissue replacement but as pharmacologic agents in healing, 14 and influenced his department's faculty to develop the concept that biofilms play a role in chronic wound healing. 15 This and other work has led to or popularized the use of occlusive dressings, [16][17][18] tissue-engineered skin, [19][20][21][22][23] and cyanoacrylate dressings. 24,25 Equally important to his scientific contributions has been Dr Eaglstein's mentorship of members of his departments and of the field.…”

Section: T Is a Pleasure To Serve As The Guest Editormentioning

confidence: 99%

Wound Healing

Kirsner¹

2007

Arch Dermatol

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A Wound-Isolated Pseudomonas aeruginosa Grows a Biofilm In Vitro Within 10 Hours and Is Visualized by Light Microscopy

Cited by 23 publications

References 34 publications

Inhibition of keratinocyte migration by lipopolysaccharide

Inhibition of keratinocyte migration by lipopolysaccharide

Bacteriophage Therapy for Staphylococcus aureus Biofilm–Infected Wounds

Wound Healing

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