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Decreased anti-inflammatory (M2) macrophages in a murine model of type II diabetes (T2D) impair wound healing
Danielle Horne, MD, Amrita Joshi, PhD, Anna Eliassen, MD, Tina Chen, MD, Dani Campbell, MD, Jordan Knepper, MD, Dawn Coleman, MD, Peter Henke, MD, Katherine Gallagher, MD.
University of Michigan, Ann Arbor, MI, USA.
OBJECTIVES:
Diabetic wounds are characterized by a chronic inflammatory state that is maintained by overexpression of pro-inflammatory cytokines, with a lack of “repair” or anti-inflammatory (M2) macrophages. We hypothesized that altered bone marrow in type 2 diabetic mice may contribute to the decrease in M2 macrophages seen wounds.
METHODS:
Bone marrow derived macrophages (BMDM) were grown via standard conditions from the BM of diet induced obese (DIO) and wildtype (WT) C57B/6 mice. Macrophages were then treated on day 6 with M2 skewing agents (IL-4/IL-13)(100ng/mL) and mRNA expression of M2 markers was measured via RT-PCR at 6, 24 and 48 hours post-skewing.
RESULTS:
RT-PCR demonstrated decreased transcript for M2 markers (Ym1 and FIZZ1(retn1a)) in the DIO macrophages as compared to controls. This corresponds with decreased M2 macrophages seen in diabetic wounds. (Figure 1)
CONCLUSIONS:
DIO macrophages derived from BM appear to result in decreased Ym1 and FIZZ1, markers of the M2, anti-inflammatory phenotype, important for wound healing. Manipulation of macrophage phenotypes could allow for development of new therapies to prevent chronic inflammation and non-healing in diabetic wounds.
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