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首页> 外文期刊>Infection and immunity >Coinfection with the Intestinal Nematode Heligmosomoides polygyrus Markedly Reduces Hepatic Egg-Induced Immunopathology and Proinflammatory Cytokines in Mouse Models of Severe Schistosomiasis
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Coinfection with the Intestinal Nematode Heligmosomoides polygyrus Markedly Reduces Hepatic Egg-Induced Immunopathology and Proinflammatory Cytokines in Mouse Models of Severe Schistosomiasis

机译：与肠道线虫Helicomosomoides polygyrus的共感染显着降低严重血吸虫病小鼠模型中肝卵诱导的免疫病理和促炎细胞因子。

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Infection with the trematode helminth Schistosoma mansoni results in a parasite egg-induced, CD4 T-cell-mediated, hepatointestinal granulomatous and fibrosing inflammation that varies greatly in severity, with a higher frequency of milder forms typically occurring in regions where the disease is endemic. One possible explanation for this is that in these regions the degree of inflammation is lessened by widespread concurrent infection with gastrointestinal nematodes. We tested this hypothesis by establishing a murine coinfection model in which mice were infected with the intestinal nematode parasite Heligmosomoides polygyrus prior to infection with S. mansoni. In CBA mice that naturally display a severe form of schistosomiasis, preinfection with H. polygyrus resulted in a marked reduction in schistosome egg-induced hepatic immunopathology, which was associated with significant decreases in the levels of interleukin-17 (IL-17), gamma interferon, tumor necrosis factor alpha, IL-23, IL-6, and IL-1β and with increases in the levels of IL-4, IL-5, IL-10, and transforming growth factor β in mesenteric lymph node cells, purified CD4 T cells, and isolated liver granuloma cells. There also were increases in liver Ym1 and forkhead box P3 transcription factor expression. In another model of high-pathology schistosomiasis induced in C57BL/6 mice by immunization with schistosome egg antigens in complete Freund's adjuvant, coinfection with the nematodes also resulted in a marked inhibition of hepatic immunopathology accompanied by similar shifts in cytokine production. These findings demonstrate that intestinal nematodes prevent Th1- and Th17-cell-mediated inflammation by promoting a strong Th2-polarized environment associated with increases in the levels of alternatively activated macrophages and T regulatory cells, which result in significant amelioration of schistosome-induced immunopathology.
机译：感染吸虫的蠕虫曼氏血吸虫会导致寄生虫卵诱导的，CD4 T细胞介导的肝肠肉芽肿和纤维化炎症，其严重程度差异很大，通常发生于中等水平的温和形式的频率更高该病为地方病的地区。对此的一种可能解释是，在这些区域中，由于广泛并发感染胃肠道线虫而减轻了炎症程度。我们通过建立鼠共感染模型来检验该假设，在该模型中，小鼠在感染 S之前先感染了肠道线虫寄生虫 Heligmosomoides polygyrus 。 mansoni 。在自然表现出严重形式的血吸虫病的CBA小鼠中，预先感染了 H。 polygyrus 导致血吸虫卵诱导的血吸虫病的肝免疫病理学显着降低，这与白介素17（IL-17），γ干扰素，肿瘤坏死因子α，IL-23，IL的水平显着降低有关-6和IL-1β以及肠系膜淋巴结细胞，纯化的CD4 T细胞和分离的肝肉芽肿细胞中IL-4，IL-5，IL-10和转化生长因子β的水平增加。肝脏Ym1和叉头盒P3转录因子表达也增加。在另一种通过在完全弗氏佐剂中用血吸虫卵抗原免疫C57BL / 6小鼠中诱发的高病理性血吸虫病模型中，线虫的共感染还导致肝免疫病理学受到明显抑制，并伴随着类似的细胞因子产生变化。这些发现表明，肠道线虫通过促进与交替激活的巨噬细胞和T调节细胞水平升高相关的强Th2极化环境来预防Th1和Th17细胞介导的炎症，从而显着改善了血吸虫病诱导的免疫病理学。

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