The mouse intestinal parasite Heligmosomoides polygyrus demonstrates adaptation to the inflammatory milieu as a result of colitis induced by dextran sulphate sodium (DSS). Nematodes from mice with colitis had different effects on dendritic cells than nematodes from mice without colitis. Immature JAWSII cells pre-exposed to L4 stage H. polygyrus from DSS-treated mice were adoptively transferred to mice with induced colitis. After two days, a higher disease activity index, macroscopic damage score and colon histology score were observed. MLN T cells isolated nine days after transfer demonstrated proinflammatory IFN-γ and IL-17 production. Transfer of JAWSII stimulated with male or female L4 larvae from a control invasion resulted in a slight improvement of colitis; in addition, dendritic cells exposed to H. polygyrus female L4 larvae, provoked migration of CD8⁺CD25⁺ T cells from MLN to the colon. Nematodes from an inflammatory environment changed cytokine production by dendritic cells. Inflammatory milieu changing nematode immunomodulatory activity affects dendritic cell functions, which offers new insight into the helminth-host relationship.

由于葡聚糖硫酸钠 (DSS) 诱导的结肠炎，小鼠肠道寄生虫Heligmosomoides polygyrus表现出对炎症环境的适应。来自结肠炎小鼠的线虫对树突状细胞的影响与来自没有结肠炎的小鼠的线虫不同。未成熟的 JAWSII 细胞预先暴露于 L4 期H. polygyrus来自 DSS 处理的小鼠的过继转移至患有诱导性结肠炎的小鼠。两天后，观察到较高的疾病活动指数、宏观损伤评分和结肠组织学评分。转移后 9 天分离的 MLN T 细胞表现出促炎性 IFN-γ 和 IL-17 的产生。用来自对照入侵的雄性或雌性 L4 幼虫刺激的 JAWSII 的转移导致结肠炎的轻微改善；此外，树突状细胞暴露于H. polygyrus雌性 L4 幼虫，引发了 CD8 ⁺ CD25 ^{+ 的}迁移从 MLN 到结肠的 T 细胞。来自炎症环境的线虫改变了树突状细胞的细胞因子产生。改变线虫免疫调节活性的炎症环境会影响树突状细胞的功能，这为了解蠕虫与宿主的关系提供了新的见解。