de Souza Marques André Murilo, Soares Santiago Aguiar Espellet, do Carmo-Neto José Rodrigues, Gomes Clayson Moura, Vinaud Marina Clare, de Matos Grazzielle Guimarães, de Oliveira Milton Adriano Pelli
Instituto de Patologia Tropical e Saúde Pública, Universidade Federal de Goiás, Rua 235 S/N- Setor Universitário, Goiânia, GO, Brazil.
Pontifícia Universidade Católica de Goiás, Escola de Ciências Médicas e da Vida, Av U, Goiânia, Brazil.
World J Microbiol Biotechnol. 2025 Mar 28;41(4):115. doi: 10.1007/s11274-025-04327-5.
The development of leishmaniasis depends on the ability of Leishmania to invade and survive within macrophages. Macrophages can either promote parasite elimination or support its survival, depending on whether they are classically (M1) or alternatively (M2) activated. Mice chronically infected with Taenia crassiceps cysticerci (TC) develop a predominantly Th2 immune response, which leads to an increased number of M2 macrophages. In this study, we assessed the susceptibility of BALB/c mice previously infected with TC to Leishmania (V.) braziliensis or Leishmania (L.) major. Mice were first inoculated intraperitoneally with TC and after eight weeks infected either L. (V.) braziliensis or L. (L.) major in the paw. We evaluated footpad swelling and parasite load in different organs. We also assessed parasite load in vitro at 3 h, 3, 6, and 9 days; nitric oxide (NO) production, and arginase activity. Macrophages obtained from TC-infected mice (TcMΦ) were more susceptible to L. (V.) braziliensis infection, maintaining a stable parasite load without significant proliferation, while the parasite was killed in thioglycolate-elicited macrophages (TgMΦ). In contrast, L. (L.) major proliferated intensely in TcMΦ, leading to a higher parasite load compared to TgMΦ. In vivo, infection with L. (V.) braziliensis in TC-coinfected mice did not alter the parasite load compared to the group without cysticerci. However, mice infected with L. (L.) major exhibited greater swelling and higher parasite burdens. These findings suggest that infection with TC modulates the immune response of mice but is unable to render resistant mice susceptible to L. (V.) braziliensis.
利什曼病的发展取决于利什曼原虫侵入巨噬细胞并在其中存活的能力。巨噬细胞可促进寄生虫清除或支持其存活,这取决于它们是经典激活(M1)还是替代激活(M2)。长期感染粗头带绦虫囊尾蚴(TC)的小鼠会产生主要为Th2的免疫反应,这会导致M2巨噬细胞数量增加。在本研究中,我们评估了先前感染TC的BALB/c小鼠对巴西利什曼原虫或硕大利什曼原虫的易感性。小鼠首先腹腔接种TC,八周后在爪部感染巴西利什曼原虫或硕大利什曼原虫。我们评估了足垫肿胀和不同器官中的寄生虫负荷。我们还在3小时、3天、6天和9天体外评估了寄生虫负荷、一氧化氮(NO)产生和精氨酸酶活性。从感染TC的小鼠获得的巨噬细胞(TcMΦ)对巴西利什曼原虫感染更敏感,维持稳定的寄生虫负荷且无明显增殖,而寄生虫在巯基乙酸盐诱导的巨噬细胞(TgMΦ)中被杀死。相比之下,硕大利什曼原虫在TcMΦ中强烈增殖,导致寄生虫负荷高于TgMΦ。在体内,与未感染囊尾蚴的组相比,TC共感染小鼠感染巴西利什曼原虫并未改变寄生虫负荷。然而,感染硕大利什曼原虫的小鼠表现出更大的肿胀和更高的寄生虫负担。这些发现表明,感染TC会调节小鼠的免疫反应,但无法使抗性小鼠对巴西利什曼原虫易感。