Idaho Veterans Research & Education Foundation (IVREF) - Boise VA Medical Center (BVAMC), Boise, Idaho, USA.
Curr Opin Infect Dis. 2019 Jun;32(3):204-209. doi: 10.1097/QCO.0000000000000550.
Despite modern advances in medicine, nonhealing wounds are the number one cause of nontraumatic, lower-limb amputation. Nonhealing wounds are characterized by a healing process stalled between inflammation and tissue remodel/repair, a stage characterized by a shift in macrophage functional phenotype. Characterization of diversity in macrophage functional phenotype in wounds and metabolic contributions to macrophage polarization are discussed.
Macrophage functional diversity in phenotype has recently evolved from duality (classically activated, pro-inflammatory M1 and alternatively activated, anti-inflammatory M2) to include an additional four alternately activated subphenotypes (M2a, M2b, M2c and M2d). Metabolic pathway utilization shifts characterize macrophage polarization with resulting metabolic and immune outcomes impacting host-pathogen interactions during wound healing.
Recognition of the key role macrophage diversity plays in wound healing, along with better characterization of diverse macrophage phenotypes, will inform our understanding of pathogenicity in wound healing. Comprehensive profiling of the metabolism regulating macrophage polarization and host-pathogen interaction creates opportunity of discovery for innovative new diagnostics and therapeutics for treating nonhealing wounds.
尽管现代医学取得了进步，但非愈合性伤口仍是导致非创伤性下肢截肢的首要原因。非愈合性伤口的特点是炎症和组织重塑/修复之间的愈合过程停滞不前，这一阶段的特征是巨噬细胞功能表型发生转变。本文讨论了伤口中巨噬细胞功能表型的多样性特征以及代谢对巨噬细胞极化的贡献。
巨噬细胞功能表型的多样性已从二元性（经典激活、促炎 M1 和替代激活、抗炎 M2）演变为包括另外四个替代激活亚表型（M2a、M2b、M2c 和 M2d）。代谢途径的利用转变特征描述了巨噬细胞的极化，由此产生的代谢和免疫结果影响着宿主-病原体相互作用在伤口愈合过程中的作用。
认识到巨噬细胞多样性在伤口愈合中所起的关键作用，以及对不同巨噬细胞表型的更好描述，将有助于我们了解伤口愈合过程中的发病机制。对调节巨噬细胞极化和宿主-病原体相互作用的代谢进行全面分析，为治疗非愈合性伤口的创新型新诊断和治疗方法提供了发现的机会。
