Pseudomonas aeruginosa uses T3SS to inhibit diabetic wound healing. Issue 4 (27th July 2015)

• Record Type: Journal Article
• Authors: Goldufsky, Josef; Wood, Stephen J.; Jayaraman, Vijayakumar; Majdobeh, Omar; Chen, Lin; Qin, Shanshan; Zhang, Chunxiang; DiPietro, Luisa A.; Shafikhani, Sasha H.
• Is Part Of: Wound repair and regeneration. Volume 23:Issue 4(2015)
• Page Start: 557
• Page End: 564
• Publication Date: 2015-07-27
• Subjects: Wound healing -- Periodicals; Regeneration (Biology) -- Periodicals; 617.14
• DOI: 10.1111/wrr.12310
• Languages: English
• ISSNs: 1067-1927

Abstract

<abstract abstract-type="main"> <title>ABSTRACT</title> <p>Diabetic foot ulcers are responsible for more hospitalizations than any other complication of diabetes. Bacterial infection is recognized as an important factor associated with impaired healing in diabetic ulcers. <italic>Pseudomonas aeruginosa</italic> is the most frequently detected Gram‐negative pathogen in diabetic ulcers. <italic>P. aeruginosa</italic> infection has been shown to impair healing in diabetic wounds in a manner that correlates with its ability to form biofilm. While the majority of infections in diabetic ulcers are biofilm associated, 33% of infections are nonbiofilm in nature. <italic>P. aeruginosa</italic> is the most prevalent Gram‐negative pathogen in all diabetic wound types, which suggests that the deleterious impact of <italic>P. aeruginosa</italic> on healing in diabetic wounds goes beyond its ability to form biofilm and likely involves other factors. The Type III Secretion System (T3SS) virulence structure is required for the pathogenesis of all <italic>P. aeruginosa</italic> clinical isolates, suggesting that it may also play a role in the inhibition of wound repair in diabetic skin ulcers. We evaluated the role of T3SS in mediating <italic>P. aeruginosa</italic>–induced tissue damage in the wounds of diabetic mice. Our data demonstrate that <italic>P. aeruginosa</italic> establishes a robust and persistent infection in diabetic wounds independent of its ability to form biofilm and causes severe wound damage in a manner that primarily depends on its T3SS.</p> </abstract>