Visceral leishmaniasis is a neglected tropical disease caused by Leishmania (L.) donovani parasite in the Indian subcontinent. Macrophages (mϕ) are the harboring cells for parasite and their interactions dictate the pathogenesis of this disease. Polyunsaturated fatty acids are an integral part of the mϕ cell membrane and are derived from linoleic acid (LA), which is a principal essential fatty acid. Here, we have investigated the effect of the simultaneous presence of LA during L. donovani infection in mϕ. Treatment with LA suppresses the parasitic load in mϕ (kDNA expression) and promotes the Th-1 type immune response (IL-12, iNOS). However, no significant change in kDNA expressions was observed when L. donovani promastigotes were treated with LA. Intrigued by this observation, we explored mechanism(s) by which LA promoted the protective type immune response in infected mϕ. Interestingly, LA decreased the release of L. donovani derived extracellular vesicle later characterized as microvesicles. Moreover, these microvesicles were suppressive concerning their bias toward the Th-2 type of immune responses (IL-10, Arginase) in mϕ. We suggest that LA plays a protective role in the immune response against L. donovani infection by inhibiting the release to Leishmania derived microvesicles and thus promoting Th-1 type immune response in mϕ.

内脏利什曼病是一种被忽视的热带病，由 利什曼原虫印度次大陆的寄生虫。巨噬细胞（mϕ）是寄生虫的窝藏细胞，它们的相互作用决定了该病的发病机理。多不饱和脂肪酸是m +细胞膜不可分割的一部分，并衍生自亚油酸（LA），后者是一种主要的必需脂肪酸。在这里，我们调查了LA同时存在的影响多诺尼感染 用LA处理可抑制mϕ（kDNA表达）中的寄生虫负荷并促进Th-1型免疫应答（IL-12，iNOS）。然而，当多诺尼前鞭毛体用LA治疗。对此观察结果感兴趣的是，我们探索了LA促进被感染mϕ中保护性免疫反应的机制。有趣的是，洛杉矶减少了多诺尼衍生的细胞外囊泡后来被表征为微囊泡。而且，这些微囊泡对它们在m 3中对Th-2型免疫应答（IL-10，精氨酸酶）的偏向具有抑制作用。我们建议LA在针对以下疾病的免疫反应中起保护作用多诺尼 通过抑制释放到 利什曼原虫 衍生的微泡，从而促进m-1中的Th-1型免疫反应。