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Semin Immunol. 2014 Aug;26(4):341-53. doi: 10.1016/j.smim.2014.04.006. Epub 2014 Jun 18.

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

Author information

1
The Healing Foundation Centre, Faculty of Life Sciences, University of Manchester, Manchester M13 9PT, United Kingdom.
2
The Healing Foundation Centre, Faculty of Life Sciences, University of Manchester, Manchester M13 9PT, United Kingdom. Electronic address: kimberly.mace@manchester.ac.uk.

Abstract

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.

KEYWORDS:

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

PMID:
24954378
DOI:
10.1016/j.smim.2014.04.006
[Indexed for MEDLINE]

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