{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T07:25:18Z","timestamp":1789629918084,"version":"build-2803163510"},"reference-count":42,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2013,10,9]],"date-time":"2013-10-09T00:00:00Z","timestamp":1381276800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Wound Repair Regeneration"],"published-print":{"date-parts":[[2013,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Diabetic patients exhibit dysregulated inflammatory and immune responses that predispose them to chronic wound infections and the threat of limb loss. The molecular underpinnings responsible for this have not been well elucidated, particularly in the setting of wound biofilms. This study evaluates host responses in biofilm\u2010impaired wounds using the\n                    <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                    ally\n                    <jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>\n                    o mouse, a clinically relevant polygenic model of type 2 diabetes. No differences in cytokine or Toll\u2010like receptor (\n                    <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>\n                    ) expression were noted in unwounded skin or noninoculated wounds of diabetic and wild\u2010type mice. However, diabetic biofilm\u2010containing wounds had significantly less\n                    <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>\n                    2,\n                    <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>\n                    4, interleukin\u20101\u03b2, and tumor necrosis factor\u2010\u03b1 expression than wild\u2010type wounds with biofilm (all\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.001). Both groups had similar bacterial burden and neutrophil infiltration after development of biofilms at 3 days postwounding, but diabetic wounds had significantly less neutrophil oxidative burst activity. This translated into a log\u2010fold greater bacterial burden and significant delay of wound epithelization for biofilm\u2010impaired diabetic wounds at 10 days postwounding. These results suggest that impaired recognition of bacterial infection via the\n                    <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>\n                    pathway leading to inadequate cytokine stimulation of antimicrobial host responses may represent a potential mechanism underlying diabetic susceptibility to wound infection and ulceration.\n                  <\/jats:p>","DOI":"10.1111\/wrr.12109","type":"journal-article","created":{"date-parts":[[2013,10,11]],"date-time":"2013-10-11T22:24:59Z","timestamp":1381530299000},"page":"833-841","source":"Crossref","is-referenced-by-count":80,"title":["Deficient cytokine expression and neutrophil oxidative burst contribute to impaired cutaneous wound healing in diabetic, biofilm\u2010containing chronic wounds"],"prefix":"10.1111","volume":"21","author":[{"given":"Khang T.","family":"Nguyen","sequence":"first","affiliation":[{"name":"Division of Plastic Surgery Feinberg School of Medicine Northwestern University  Chicago Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akhil K.","family":"Seth","sequence":"additional","affiliation":[{"name":"Division of Plastic Surgery Feinberg School of Medicine Northwestern University  Chicago Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seok J.","family":"Hong","sequence":"additional","affiliation":[{"name":"Division of Plastic Surgery Feinberg School of Medicine Northwestern University  Chicago Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew R.","family":"Geringer","sequence":"additional","affiliation":[{"name":"Division of Plastic Surgery Feinberg School of Medicine Northwestern University  Chicago Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ping","family":"Xie","sequence":"additional","affiliation":[{"name":"Division of Plastic Surgery Feinberg School of Medicine Northwestern University  Chicago Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kai P.","family":"Leung","sequence":"additional","affiliation":[{"name":"Microbiology Branch US Army Dental and Trauma Research Detachment Institute of Surgical Research  Fort Sam Houston Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas A.","family":"Mustoe","sequence":"additional","affiliation":[{"name":"Division of Plastic Surgery Feinberg School of Medicine Northwestern University  Chicago Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert D.","family":"Galiano","sequence":"additional","affiliation":[{"name":"Division of Plastic Surgery Feinberg School of Medicine Northwestern University  Chicago 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