Pseudomonas aeruginosa uses T3SS to inhibit diabetic wound healing.
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. Pseudomonas aeruginosa is the most frequently detected Gram-negative pathogen in diabetic ulcers. P. aeruginosa 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. P. aeruginosa is the most prevalent Gram-negative pathogen in all diabetic wound types, which suggests that the deleterious impact of P. aeruginosa 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 P. aeruginosa 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 P. aeruginosa-induced tissue damage in the wounds of diabetic mice. Our data demonstrate that P. aeruginosa 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.
Department of Immunology/Microbiology, Rush University Medical Center, Chicago, Illinois.
Josef
J
Goldufsky
Department of Immunology/Microbiology, Rush University Medical Center, Chicago, Illinois.
Stephen J
SJ
Wood
Department of Immunology/Microbiology, Rush University Medical Center, Chicago, Illinois.
Vijayakumar
V
Jayaraman
Department of Immunology/Microbiology, Rush University Medical Center, Chicago, Illinois.
Omar
O
Majdobeh
Center for Wound Healing and Tissue Regeneration, College of Dentistry, University of Illinois at Chicago, Chicago, Illinois.
Lin
L
Chen
Department of Pharmacology, Rush University Medical Center, Chicago, Illinois.
Shanshan
S
Qin
Department of Pharmacology, Rush University Medical Center, Chicago, Illinois.
Chunxiang
C
Zhang
Center for Wound Healing and Tissue Regeneration, College of Dentistry, University of Illinois at Chicago, Chicago, Illinois.
Luisa A
LA
DiPietro
Department of Immunology/Microbiology, Rush University Medical Center, Chicago, Illinois.|Department of Internal Medicine, Rush University Medical Center, Chicago, Illinois.|Cancer Center, Rush University Medical Center Chicago, Illinois.
Sasha H
SH
Shafikhani
D000818:Animals; D018441:Biofilms; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000378:metabolism / Q000382:microbiology; D017719:Diabetic Foot / Q000209:etiology / Q000378:metabolism / Q000382:microbiology*; D004195:Disease Models, Animal; D051379:Mice; D008810:Mice, Inbred C57BL; D011552:Pseudomonas Infections / Q000150:complications / Q000382:microbiology*; D011550:Pseudomonas aeruginosa / Q000378:metabolism / Q000472:pathogenicity*; D000069296:Type III Secretion Systems / Q000378:metabolism*; D014774:Virulence; D014945:Wound Healing / Q000502:physiology*; D014946:Wound Infection / Q000150:complications / Q000378:metabolism / Q000382:microbiology*
D000069296:Type III Secretion Systems