Levy D A, Frondoza C
Fed Proc. 1983 Apr;42(6):1750-5.
Nippostrongylus brasiliensis infection of rats and mice is a model for studying immunity at mucosal surfaces. Adult worms are spontaneously expelled from the intestine at the end of the second week of infection. Expulsion from the jejunum requires the presence of immune T lymphocytes and IgG antibodies. Mucosal mast cells (MMCs) are a prominent part of the jejunal inflammatory response. They are derived from a hematopoietic stem cell, possibly the same precursor as basophils. Their differentiation is not absolutely T dependent but their accumulation at the site of infection is. The possible involvement of IgE antibodies and intestinal MMCs through a "leak lesion" is still uncertain. Increased mucus secretion from epithelial goblet cells is also a prominent feature of the inflammatory reaction at the site of infection. Goblet cell numbers increase two to four times at the onset of worm expulsion; this increase is regulated by T lymphocytes and possibly immune serum. The mechanism of mucus secretion in these infections is not clear; it may be a response to mast cell mediators. Together with antiworm antibodies, intestinal mucus may trap worms and prevent them from surviving in the intervillous spaces of the jejunum. Thus, expulsion of this intestinal parasite may occur through a nonspecific process that is induced by specific immune mechanisms.
巴西日圆线虫感染大鼠和小鼠是研究黏膜表面免疫的一种模型。感染第二周结束时，成虫会自发从肠道排出。从空肠排出需要免疫T淋巴细胞和IgG抗体的存在。黏膜肥大细胞（MMCs）是空肠炎症反应的一个显著部分。它们来源于造血干细胞，可能与嗜碱性粒细胞有相同的前体。它们的分化并非绝对依赖T细胞，但它们在感染部位的聚集是依赖T细胞的。IgE抗体和肠道MMCs通过“渗漏病变”的可能参与情况仍不确定。上皮杯状细胞黏液分泌增加也是感染部位炎症反应的一个显著特征。在蠕虫排出开始时，杯状细胞数量增加两到四倍；这种增加由T淋巴细胞调节，可能还受免疫血清调节。这些感染中黏液分泌的机制尚不清楚；它可能是对肥大细胞介质的一种反应。连同抗蠕虫抗体一起，肠道黏液可能捕获蠕虫并阻止它们在空肠绒毛间隙存活。因此，这种肠道寄生虫的排出可能通过由特定免疫机制诱导的非特异性过程发生。
