Myeloid cell dysfunction and the pathogenesis of the diabetic chronic wound.

Kate Wicks, Tanja Torbica, Kimberly Mace

Research output: Contribution to journalArticlepeer-review


Diabetes can promote a state of chronic inflammation associated with serious complications that are difficult to treat, including ulceration of the lower extremities and chronic wounds. Chronic wounds are often incurable and contribute to both a reduced quality of life for patients and an enormous burden for healthcare services. In diabetes, the inflammatory response early in wound healing is inappropriately amplified and prolonged, leading to the persistent presence in the wound of vastly elevated numbers of dysfunctional, hyperpolarised macrophages that fail to transition to a pro-healing phenotype. Recent evidence suggests that systemic chronic inflammation induces intrinsic defects in monocytes via chromatin modifications that may pre-programme monocytes to a pro-inflammatory phenotype, while the local wound environment inhibits differentiation to a pro-healing phenotype. Current understanding remains incomplete, and careful dissection of how local and systemic inflammation combine to negatively influence myeloid cell development will be key to developing effective therapies aimed at healing the diabetic wound.
Original languageEnglish
Pages (from-to)341–353
JournalSeminars in Immunology
Issue number4
Publication statusPublished - Aug 2014


  • Chromatin regulation
  • Chronic inflammation
  • Chronic wound
  • Diabetes
  • Macrophage polarisation
  • Myeloid cell


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