Dried tangerine peel polysaccharide accelerates wound healing by recruiting anti-inflammatory macrophages

IF 4.8 2区 医学 Q2 IMMUNOLOGY International immunopharmacology Pub Date : 2024-08-30 DOI:10.1016/j.intimp.2024.113036
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Abstract

Macrophage polarization is a key process involved in wound healing. The continuous release of proinflammatory cytokines by macrophages inhibits the healing process of chronic wounds, such as diabetic wounds. To promote wound healing, it is important to change the phenotype of resident macrophages to prevent inflammation. We previously reported that dried tangerine peel polysaccharide (DTPP) binds to and inhibits the TLR4/MD-2 complex, which is crucial for the inflammatory activation of macrophages, suggesting the potential of DTPP in wound healing applications. Both zebrafish and mouse models were used to evaluate the therapeutic efficacy of DTPP. Moreover, we found that DTPP recruited macrophages to the wound area and promoted their M2 repolarization. Using hyperglycaemic zebrafish and db/db mouse models, we discovered that DTPP accelerated wound healing in vivo in metabolic disorders. Our results suggest that DTPP promotes the recruitment of macrophages, shifts macrophages towards the anti-inflammatory M2 phenotype, and ultimately accelerates the wound healing process.

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干橘皮多糖通过招募抗炎巨噬细胞加速伤口愈合
巨噬细胞极化是伤口愈合的一个关键过程。巨噬细胞持续释放促炎细胞因子会抑制慢性伤口(如糖尿病伤口)的愈合过程。为了促进伤口愈合,改变常驻巨噬细胞的表型以防止炎症非常重要。我们以前曾报道过,干橘皮多糖(DTPP)能与 TLR4/MD-2 复合物结合并抑制该复合物,而 TLR4/MD-2 复合物对巨噬细胞的炎症活化至关重要,这表明 DTPP 有潜力应用于伤口愈合。我们利用斑马鱼和小鼠模型来评估 DTPP 的疗效。此外,我们还发现 DTPP 能将巨噬细胞吸引到伤口区域,并促进其 M2 再极化。通过使用高血糖斑马鱼和 db/db 小鼠模型,我们发现 DTPP 加快了代谢紊乱患者体内伤口的愈合。我们的研究结果表明,DTPP 可促进巨噬细胞的招募,使巨噬细胞向抗炎 M2 表型转变,最终加速伤口愈合过程。
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来源期刊
CiteScore
8.40
自引率
3.60%
发文量
935
审稿时长
53 days
期刊介绍: International Immunopharmacology is the primary vehicle for the publication of original research papers pertinent to the overlapping areas of immunology, pharmacology, cytokine biology, immunotherapy, immunopathology and immunotoxicology. Review articles that encompass these subjects are also welcome. The subject material appropriate for submission includes: • Clinical studies employing immunotherapy of any type including the use of: bacterial and chemical agents; thymic hormones, interferon, lymphokines, etc., in transplantation and diseases such as cancer, immunodeficiency, chronic infection and allergic, inflammatory or autoimmune disorders. • Studies on the mechanisms of action of these agents for specific parameters of immune competence as well as the overall clinical state. • Pre-clinical animal studies and in vitro studies on mechanisms of action with immunopotentiators, immunomodulators, immunoadjuvants and other pharmacological agents active on cells participating in immune or allergic responses. • Pharmacological compounds, microbial products and toxicological agents that affect the lymphoid system, and their mechanisms of action. • Agents that activate genes or modify transcription and translation within the immune response. • Substances activated, generated, or released through immunologic or related pathways that are pharmacologically active. • Production, function and regulation of cytokines and their receptors. • Classical pharmacological studies on the effects of chemokines and bioactive factors released during immunological reactions.
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