Darabniya Ali
Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, 13145-784, Iran.
Inflammopharmacology. 2025 Sep 24. doi: 10.1007/s10787-025-01968-8.
Fosfomycin, a broad-spectrum bactericidal antibiotic, has recently gained interest for its potential anti-inflammatory and immunomodulatory effects beyond its well-established antimicrobial activity. Emerging evidence from preclinical studies demonstrates that fosfomycin suppresses key pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6, while enhancing anti-inflammatory mediators such as IL-10. It modulates essential intracellular pathways by inhibiting NF-κB and MAPK signaling and reducing NLRP3 inflammasome activation. Fosfomycin also influences immune cell function by limiting neutrophil migration and activation, suppressing T-cell proliferation, and decreasing B-cell immunoglobulin production. In addition, it promotes tissue regeneration through enhanced collagen deposition, angiogenesis, and improved wound healing in experimental models. These combined effects suggest a dual therapeutic role for fosfomycin, both in controlling infection and modulating inflammatory responses. Despite promising preclinical results, clinical evidence on its immunomodulatory effects remains limited, with most human studies primarily addressing its antibacterial efficacy. This review summarizes current knowledge on fosfomycin's non-antibacterial properties, highlights its therapeutic potential in inflammatory and infectious diseases, and identifies research gaps that warrant further investigation. Overall, fosfomycin emerges as a promising adjunctive agent, particularly in conditions such as sepsis, chronic wounds, and sterile surgical inflammation, where excessive immune activation impairs recovery.
磷霉素是一种广谱杀菌抗生素,最近因其除了已确立的抗菌活性外还具有潜在的抗炎和免疫调节作用而受到关注。临床前研究的新证据表明,磷霉素可抑制关键的促炎细胞因子,包括肿瘤坏死因子-α、白细胞介素-1β和白细胞介素-6,同时增强抗炎介质如白细胞介素-10。它通过抑制核因子-κB和丝裂原活化蛋白激酶信号传导以及减少NLRP3炎性小体活化来调节重要的细胞内途径。磷霉素还通过限制中性粒细胞迁移和活化、抑制T细胞增殖以及减少B细胞免疫球蛋白产生来影响免疫细胞功能。此外,在实验模型中,它通过增强胶原蛋白沉积、血管生成和改善伤口愈合来促进组织再生。这些综合作用表明磷霉素在控制感染和调节炎症反应方面具有双重治疗作用。尽管临床前结果很有前景,但其免疫调节作用的临床证据仍然有限,大多数人体研究主要关注其抗菌疗效。本综述总结了目前关于磷霉素非抗菌特性的知识,强调了其在炎症和感染性疾病中的治疗潜力,并确定了值得进一步研究的研究空白。总体而言,磷霉素是一种有前途的辅助药物,特别是在脓毒症、慢性伤口和无菌手术炎症等情况下,过度的免疫激活会影响恢复。