Gomes Juliana Assis Silva, Molica Andreia Maria, Keesen Tatjana Souza Lima, Morato Maria José Ferreira, de Araujo Fernanda Fortes, Fares Rafaelle Christine Gomes, Fiuza Jacqueline Araujo, Chaves Ana Thereza, Pinheiro Vladimir, Nunes Maria do Carmo Pereira, Correa-Oliveira Rodrigo, da Costa Rocha Manoel Otávio
Department of Morphology, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 31270-901, Brazil; School of Medicine, Postgraduate Program in Health Sciences: Infectology in Tropical Medicine, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 30130-100, Brazil; René Rachou Research Center, FIOCRUZ, Belo Horizonte, Minas Gerais 30190-002, Brazil.
School of Medicine, Postgraduate Program in Health Sciences: Infectology in Tropical Medicine, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 30130-100, Brazil; René Rachou Research Center, FIOCRUZ, Belo Horizonte, Minas Gerais 30190-002, Brazil.
Hum Immunol. 2014 Jan;75(1):20-8. doi: 10.1016/j.humimm.2013.09.009. Epub 2013 Sep 24.
Exposure to Trypanosoma cruzi parasites induces monocytes and macrophages to produce various endogenous mediators, including prostaglandins and cytokines. To clarify the involvement of monocytes as an important source of inflammatory mediators in Chagas disease patients, we evaluated PBMC before and after depletion of adherent cells (monocytes) from patients with indeterminate (IND) and cardiac (CARD) clinical forms and from non-infected individuals (NI). We demonstrated that after the partial depletion of adherent cells, production of PGE2 was slightly decreased in patients with Chagas disease. Inhibition of the cells by indomethacin increased the proliferation in PBMC cells from patients after antigen stimulation. Pro-inflammatory cytokines as IL-2 and IFN-γ also had a greater decrease after partial depletion of adherent cells in both clinical forms of Chagas disease. IL-10 and IL-5 levels were also reduced after partial depletion of adherent cells both in IND and CARD patients. In addition, we evaluated the APC potential of B cells and observed that the MHCII and CD80 molecules had an increased expression after partial depletion of most monocytes in all groups. Thus, inflammatory mediators produced by monocytes seem to be important to modulate immune responses in Chagas disease by regulating the processes of inflammation and antigen presentation.
感染克氏锥虫寄生虫会诱导单核细胞和巨噬细胞产生多种内源性介质，包括前列腺素和细胞因子。为了阐明单核细胞作为恰加斯病患者炎症介质重要来源的作用，我们评估了来自不确定型（IND）和心脏型（CARD）临床类型的恰加斯病患者以及未感染个体（NI）的外周血单核细胞（PBMC）在去除贴壁细胞（单核细胞）前后的情况。我们发现，在部分去除贴壁细胞后，恰加斯病患者中前列腺素E2（PGE2）的产生略有减少。用吲哚美辛抑制细胞后，抗原刺激后患者PBMC细胞的增殖增加。在恰加斯病的两种临床类型中，贴壁细胞部分去除后，促炎细胞因子如白细胞介素-2（IL-2）和干扰素-γ（IFN-γ）的减少也更为明显。在IND和CARD患者中，贴壁细胞部分去除后，IL-10和IL-5水平也降低。此外，我们评估了B细胞的抗原呈递细胞（APC）潜能，发现所有组中大多数单核细胞部分去除后，主要组织相容性复合体II类分子（MHCII）和CD80分子的表达增加。因此，单核细胞产生的炎症介质似乎通过调节炎症和抗原呈递过程，对调节恰加斯病的免疫反应很重要。
