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dc.contributor.authorZhao, Ge
dc.contributor.authorUsui, Marcia L.
dc.contributor.authorUnderwood, Robert A.
dc.contributor.authorSingh, Pradeep K.
dc.contributor.authorJames, Garth A.
dc.contributor.authorStewart, Philip S.
dc.contributor.authorFleckman, Philip
dc.contributor.authorOlerud, John E.
dc.identifier.citationZhao G, Usui ML, Underwood RA, Singh PK, James GA, Stewart PS, Fleckman P, Olerud JE, "Time course study of delayed wound healing in a biofilm-challenged diabetic mouse model," Wound Repair and Regeneration, May 2012 20(3):342–352.en_US
dc.description.abstractBacterial biofilm has been shown to play a role in delaying wound healing of chronic wounds, a major medical problem that results in significant health care burden. A reproducible animal model could be very valuable for studying the mechanism and management of chronic wounds. Our previous work showed that Pseudomonas aeruginosa (PAO1) biofilm challenge 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. Of the biofilm-challenged wounds, 64% healed by 6 weeks, and all of the biofilmchallenged wounds healed by 8 weeks. During the wound-healing process, P. aeruginosa was gradually cleared from the wounds while the presence of Staphylococcus 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 expression increased threefold in 4-week wounds. In summary, our study shows that biofilm-challenged wounds typically heal in approximately 6 weeks, at least 2 weeks longer than nonbiofilm-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 antibiofilm strategies for treating chronic wounds.en_US
dc.titleTime course study of delayed wound healing in a biofilm-challenged diabetic mouse modelen_US
mus.citation.journaltitleWound Repair and Regenerationen_US
mus.identifier.categoryChemical & Material Sciencesen_US
mus.identifier.categoryEngineering & Computer Scienceen_US
mus.identifier.categoryHealth & Medical Sciencesen_US
mus.identifier.categoryLife Sciences & Earth Sciencesen_US
mus.relation.collegeCollege of Agricultureen_US
mus.relation.collegeCollege of Education, Health & Human Developmenten_US
mus.relation.collegeCollege of Engineeringen_US
mus.relation.collegeCollege of Letters & Scienceen_US
mus.relation.departmentCenter for Biofilm Engineering.en_US
mus.relation.departmentChemical & Biological Engineering.en_US
mus.relation.departmentChemistry & Biochemistry.en_US
mus.relation.departmentHealth & Human Development.en_US
mus.relation.departmentMicrobiology & Immunology.en_US
mus.relation.universityMontana State University - Bozemanen_US
mus.relation.researchgroupCenter for Biofilm Engineering.en_US
mus.contributor.orcidStewart, Philip S.|0000-0001-7773-8570en_US

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