Clindamycin (hydrochloride hydrate) is a lincosamide antibiotic used to treat severe infections caused by susceptible anaerobes, streptococci, staphylococci, and pneumococci. Clindamycin primary clinical applications include osteomyelitis, respiratory tract infections, biliary tract infections, endocarditis, otitis media, skin and soft tissue infections, and sepsis[1-2]. Clindamycin exerts its antibacterial effect by binding to the bacterial 50S ribosomal subunit, thereby inhibiting protein synthesis and exhibiting bacteriostatic or bactericidal activity[3]. However, Clindamycin can also induce adverse reactions in the host, including triggering arthritis[4].
In vitro, Clindamycin(0.25–2.0μg/mL) co-cultured with McCoy cells post-infection with Chlamydia trachomatis significantly inhibited chlamydial inclusion formation. This inhibitory effect was further enhanced when combined with gentamicin (2–16μg/mL), as evidenced by a sustained reduction in inclusion numbers and morphological abnormalities (shrinkage, decreased staining, irregular shape)[5]. Clindamycin (30–1000μg/mL) treatment of human dental pulp stem cells (DPSCs) and human umbilical vein endothelial cells (HUVECs) demonstrated that concentrations of 30–100μg/mL significantly enhanced cell viability and proliferation while promoting angiogenic capacity[6].
In vivo, Clindamycin (1, 3, and 1.5mg/g feed) administered via oral mixed-feed to mouse models of acute and chronic toxoplasmosis (starting immediately post-infection) effectively prevented acute infection-related mortality across all three doses, significantly reduced mortality rates, and decreased the number of Toxoplasma cysts in liver and spleen tissues of chronically infected mice[7]. Clindamycin (250mg/kg) administered by gavage for 14 consecutive days established an antibiotic-associated diarrhea (AAD) model in male C57BL/6 mice. Clindamycin significantly reduced intestinal glutamine levels, disrupted gut microbiota diversity, caused fecal butyrate deficiency, and increased intestinal permeability. Concurrently, Clindamycin downregulated colonic tight junction proteins occludin and ZO-1 while upregulating pro-inflammatory cytokines IL-6 and TNF-α, ultimately leading to intestinal barrier dysfunction and diarrhea symptoms[8].
References:
[1] Klainer AS. Clindamycin. Med Clin North Am. 1987 Nov;71(6):1169-75.
[2] Guay D. Update on clindamycin in the management of bacterial, fungal and protozoal infections. Expert Opin Pharmacother. 2007 Oct;8(14):2401-44.
[3] Warner GT, Plosker GL. Clindamycin/benzoyl peroxide gel: a review of its use in the management of acne. Am J Clin Dermatol. 2002;3(5):349-60.
[4] Fransen M, Verstraeten VLRM. Cutaneous Vasculitis Caused by Clindamycin. Dermatitis. 2021 Nov-Dec 01;32(6):e100-e101.
[5] Pearlman MD, Faro S, Riddle GD, et al. In vitro synergy of clindamycin and aminoglycosides against Chlamydia trachomatis. Antimicrob Agents Chemother. 1990 Jul;34(7):1399-401.
[6] Dubey N, Xu J, Zhang Z, et al. Comparative Evaluation of the Cytotoxic and Angiogenic Effects of Minocycline and Clindamycin: An In Vitro Study. J Endod. 2019 Jul;45(7):882-889.
[7] Araujo FG, Remington JS. Effect of clindamycin on acute and chronic toxoplasmosis in mice. Antimicrob Agents Chemother. 1974 Jun;5(6):647-51.
[8] Mao J, Yan Y, Li H, et al. Glutamine deficiency links clindamycin-induced dysbiosis and intestinal barrier dysfunction in mice. Br J Nutr. 2021 Aug 14;126(3):366-374.
Clindamycin (hydrochloride hydrate)是一种林可酰胺类抗生素，用于治疗由敏感厌氧菌、链球菌、葡萄球菌和肺炎球菌引起的严重感染，主要用于骨髓炎、呼吸系统感染、胆道感染、心内膜炎、中耳炎、皮肤软组织感染及败血症等[1-2]。Clindamycin通过结合细菌50S核糖体亚基抑制蛋白质合成，表现为抑菌或杀菌作用[3]，但是Clindamycin也会引起机体的不良反应，包括诱发关节炎等[4]。
在体外，Clindamycin（0.25–2.0μg/mL）与McCoy细胞共培养后感染沙眼衣原体（Chlamydia trachomatis），Clindamycin显著抑制了衣原体包涵体的形成，且联合庆大霉素（2–16μg/mL）时抑制作用进一步增强，表现为包涵体数量持续减少及形态异常（缩小、染色减弱、形状不规则）[5]。Clindamycin（30μg/mL-1000μg/mL）处理人牙髓干细胞（DPSCs）和人脐静脉内皮细胞（HUVEC），Clindamycin（30μg/mL-100μg/mL）显著增强细胞活性和增殖能力，同时促进细胞血管形成能力[6]。
在体内，Clindamycin（1、3和1.5mg/g饲料）通过口服混饲给药，用于治疗急性及慢性弓形虫感染的小鼠模型，给药时间为感染后立即开始。Clindamycin在所有三个剂量下均能有效预防急性感染导致的死亡，显著降低死亡率，并减少慢性感染小鼠肝、脾组织中的弓形虫包囊数量[7]。Clindamycin（250mg/kg）通过灌胃给药，用于构建抗生素相关性腹泻（AAD）的雄性C57BL/6小鼠模型，给药时间为连续14天。Clindamycin显著降低小鼠肠道谷氨酰胺水平，破坏肠道菌群多样性，导致粪便丁酸缺乏，并增加肠道通透性。同时，Clindamycin下调结肠紧密连接蛋白occludin和ZO-1表达，并升高促炎因子IL-6和TNF-α水平，最终引发肠道屏障功能障碍和腹泻症状[8]。