Datta Souvik, Ghosh Manab, Dewan Koushik, Banerjee Nilotpal, Saha Bibhuti, Mukhopadhyay Sumi
Department of Laboratory Medicine, Calcutta School of Tropical Medicine, Kolkata, India.
Department of Tropical Medicine, Calcutta School of Tropical Medicine, Kolkata, India.
Am J Dermatopathol. 2019 Dec;41(12):897-907. doi: 10.1097/DAD.0000000000001412.
Galectin-3, a β-galactoside-binding lectin, has been implicated in vast repertoire of inflammatory and immunomodulatory processes including skin diseases. However, galectin-3 has not been comprehensively studied in infectious diseases. This study emphasizes on fascinating aspects of galectin-3 expression in dermal infection by studying post-kala-azar dermal leishmaniasis (PKDL), an intracellular infection caused by Leishmania donovani. Indian PKDL is a well-recognized parasitic dermatosis, with a high risk of anthroponotic transmission of L. donovani in causing leishmaniasis. This study aims to investigate the levels of galectin-3 and galectin-3-binding site expression in circulation of different forms of Indian patients with PKDL. Thirty-seven confirmed untreated PKDL patients, comprising 20 polymorphic and 17 macular PKDL manifestations, were evaluated for the levels of sera galectin-3 with respect to 28 age- and sex-matched healthy controls from endemic areas. Result shows a significant increment (P < 0.001) in circulatory galectin-3 levels in PKDL variants as compared to healthy controls. In addition, there were heightened levels of galectin-3 and galectin-3-binding sites on cellular infiltrates on lesional sites. Furthermore, there was a positive correlation between frequencies of mononuclear cells and galectin-3 during microcirculation in lesions. Data were well corroborated with positive correlation of IL-10 and IFN-γ with sera galectin-3 levels. Moreover, flow cytometry demonstrated the enhanced expression levels of the galectin-3-binding site in circulation in patients with PKDL as compared to healthy controls. Taken together, elevated levels of galectin-3 reflect its involvement in PKDL pathogenesis.
半乳糖凝集素-3是一种β-半乳糖苷结合凝集素，参与了包括皮肤病在内的大量炎症和免疫调节过程。然而，半乳糖凝集素-3在传染病方面尚未得到全面研究。本研究通过研究黑热病后皮肤利什曼病（PKDL，一种由杜氏利什曼原虫引起的细胞内感染），着重探讨半乳糖凝集素-3在皮肤感染中的有趣方面。印度的PKDL是一种公认的寄生虫性皮肤病，杜氏利什曼原虫在人与人之间传播导致利什曼病的风险很高。本研究旨在调查不同类型印度PKDL患者循环中半乳糖凝集素-3及其结合位点的表达水平。对37例未经治疗的确诊PKDL患者进行了评估，其中包括20例多形性和17例斑状PKDL表现，并与28名来自流行地区的年龄和性别匹配的健康对照者比较血清半乳糖凝集素-3水平。结果显示，与健康对照相比，PKDL各型患者循环中的半乳糖凝集素-3水平显著升高（P<0.001）。此外，病变部位细胞浸润上的半乳糖凝集素-3及其结合位点水平也升高。此外，病变微循环期间单核细胞频率与半乳糖凝集素-3之间存在正相关。白细胞介素-10和干扰素-γ与血清半乳糖凝集素-3水平呈正相关，这一数据很好地证实了上述结果。此外，流式细胞术显示，与健康对照相比，PKDL患者循环中半乳糖凝集素-3结合位点的表达水平增强。综上所述，半乳糖凝集素-3水平升高反映了其参与PKDL的发病机制。
