Mukherjee Sandip, Mukherjee Budhaditya, Mukhopadhyay Rupkatha, Naskar Kshudiram, Sundar Shyam, Dujardin Jean-Claude, Roy Syamal
Department of Infectious Diseases and Immunology, Council of Scientific and Industrial Research-Indian Institute of Chemical Biology, Kolkata 700032, India;
Institute of Medical Sciences, Benaras Hindu University, Varanasi 221005, India; and.
J Immunol. 2014 Oct 15;193(8):4083-94. doi: 10.4049/jimmunol.1400710. Epub 2014 Sep 12.
The efflux of antimony through multidrug resistance protein (MDR)-1 is the key factor in the failure of metalloid treatment in kala-azar patients infected with antimony-resistant Leishmania donovani (Sb(R)LD). Previously we showed that MDR-1 upregulation in Sb(R)LD infection is IL-10-dependent. Imipramine, a drug in use for the treatment of depression and nocturnal enuresis in children, inhibits IL-10 production from Sb(R)LD-infected macrophages (Sb(R)LD-Mϕs) and favors accumulation of surrogates of antimonials. It inhibits IL-10-driven nuclear translocation of c-Fos/c-Jun, critical for enhanced MDR-1 expression. The drug upregulates histone deacetylase 11, which inhibits acetylation of IL-10 promoter, leading to a decrease in IL-10 production from Sb(R)LD-Mϕs. It abrogates Sb(R)LD-mediated p50/c-Rel binding to IL-10 promoter and preferentially recruits p65/RelB to IL-12 p35 and p40 promoters, causing a decrease in IL-10 and overproduction of IL-12 in Sb(R)LD-Mϕs. Histone deacetylase 11 per se does not influence IL-12 promoter activity. Instead, a imipramine-mediated decreased IL-10 level allows optimal IL-12 production in Sb(R)LD-Mϕs. Furthermore, exogenous rIL-12 inhibits intracellular Sb(R)LD replication, which can be mimicked by the presence of Ab to IL-10. This observation indicated that reciprocity exists between IL-10 and IL-12 and that imipramine tips the balance toward an increased IL-12/IL-10 ratio in Sb(R)LD-Mϕs. Oral treatment of infected BALB/c mice with imipramine in combination with sodium stibogluconate cleared organ Sb(R)LD parasites and caused an expansion of the antileishmanial T cell repertoire where sodium stibogluconate alone had no effect. Our study deciphers a detailed molecular mechanism of imipramine-mediated regulation of IL-10/IL-12 reciprocity and its impact on Sb(R)LD clearance from infected hosts.
通过多药耐药蛋白1(MDR-1)排出锑是抗锑利什曼原虫(Sb(R)LD)感染的黑热病患者中金属类药物治疗失败的关键因素。此前我们发现,Sb(R)LD感染中MDR-1的上调是依赖白细胞介素10(IL-10)的。丙咪嗪是一种用于治疗抑郁症和儿童夜间遗尿症的药物,它可抑制受Sb(R)LD感染的巨噬细胞(Sb(R)LD-Mϕs)产生IL-10,并有利于锑剂替代物的蓄积。它抑制IL-10驱动的c-Fos/c-Jun核转位,而这对于增强MDR-1表达至关重要。该药物上调组蛋白脱乙酰基酶11,后者抑制IL-10启动子的乙酰化,导致Sb(R)LD-Mϕs产生的IL-10减少。它消除了Sb(R)LD介导的p50/c-Rel与IL-10启动子的结合,并优先将p65/RelB募集至IL-12 p35和p40启动子,导致Sb(R)LD-Mϕs中IL-10减少而IL-12过量产生。组蛋白脱乙酰基酶11本身并不影响IL-12启动子活性。相反,丙咪嗪介导的IL-10水平降低使得Sb(R)LD-Mϕs中IL-12得以最佳产生。此外,外源性重组IL-12抑制细胞内Sb(R)LD复制,这可通过存在抗IL-10抗体来模拟。这一观察结果表明IL-10和IL-12之间存在相互作用,并且丙咪嗪使Sb(R)LD-Mϕs中的IL-12/IL-10比值朝着增加的方向倾斜。用丙咪嗪联合葡萄糖酸锑钠口服治疗受感染的BALB/c小鼠,清除了器官中的Sb(R)LD寄生虫,并导致抗利什曼原虫T细胞库扩增,而单独使用葡萄糖酸锑钠则没有效果。我们的研究阐明了丙咪嗪介导的IL-10/IL-12相互作用调节及其对从受感染宿主清除Sb(R)LD的影响的详细分子机制。