Sampaio E P, Moraes M O, Nery J A, Santos A R, Matos H C, Sarno E N
Leprosy Laboratory, Oswaldo Cruz Institute, Rio de Janeiro, Brazil.
Clin Exp Immunol. 1998 Feb;111(2):300-8. doi: 10.1046/j.1365-2249.1998.00510.x.
Increasing evidence has implicated TNF-alpha as a pivotal molecule involved in the systemic inflammatory manifestations of ENL, an acute inflammatory complication that may occur in the chronic course of leprosy. In the present study, the mechanism of action of pentoxifylline (PTX) as an alternative therapy for management of leprosy reactions has been evaluated. The effect of PTX on TNF-alpha production was examined in leprosy patients at the protein level and at the transcriptional level as well. Treatment of ENL patients with PTX (1200 mg daily) ameliorated the systemic symptoms and favoured the evolution of reactional leprosy lesions. Serum TNF-alpha was assayed before and during treatment with PTX in 15 patients. The increased TNF-alpha levels seen in the circulation during the reaction were dramatically reduced within 3-7 days of therapy. No significant effect on serum IL-6 was noted. In vitro TNF-alpha production was assayed upon culture stimulation with Mycobacterium leprae. A reduction of inducible TNF-alpha in peripheral blood mononuclear cells (PBMC) was seen after 1-2 weeks of in vivo administration of PTX. Furthermore, no effect of the drug on IL-10 secretion was detected in these cultures. A kinetic analysis of the expression of TNF-alpha and IL-6 mRNA at the site of leprosy lesion was performed in six reactional patients by semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR). The amount of TNF-alpha mRNA was increased in the tissue during ENL compared with before the reaction, and decreased thereafter following treatment for reaction (either PTX or thalidomide). These data suggest that PTX inhibits TNF-alpha production in ENL patients both in vivo and in vitro, and it may be useful in the treatment of leprosy patients undergoing ENL.
越来越多的证据表明,肿瘤坏死因子-α(TNF-α)是结节性红斑(ENL)全身炎症表现所涉及的关键分子,ENL是一种可能发生在麻风病慢性病程中的急性炎症并发症。在本研究中,已对己酮可可碱(PTX)作为麻风反应管理替代疗法的作用机制进行了评估。还在蛋白质水平和转录水平上研究了PTX对麻风病患者TNF-α产生的影响。用PTX(每日1200毫克)治疗ENL患者可改善全身症状,并有利于反应性麻风病变的演变。对15例患者在PTX治疗前和治疗期间测定血清TNF-α。反应期间循环中升高的TNF-α水平在治疗3-7天内显著降低。未观察到对血清白细胞介素-6有显著影响。在用麻风杆菌进行培养刺激后,测定体外TNF-α的产生。在体内给予PTX 1-2周后,外周血单核细胞(PBMC)中可诱导的TNF-α减少。此外,在这些培养物中未检测到该药物对白细胞介素-10分泌有影响。通过半定量逆转录聚合酶链反应(RT-PCR)对6例反应性患者麻风病变部位TNF-α和白细胞介素-6 mRNA的表达进行了动力学分析。与反应前相比,ENL期间组织中TNF-α mRNA的量增加,反应治疗(PTX或沙利度胺)后随后减少。这些数据表明,PTX在体内和体外均抑制ENL患者TNF-α的产生,并且它可能对正在经历ENL的麻风病患者的治疗有用。