Does the failure to acquire helminthic parasites predispose to Crohn's disease?
Does the failure to acquire helminthic parasites predispose to Crohn's disease?
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DOI：
10.1096/fj.99-0885hyp
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发表时间：
2000-09-01
期刊：
影响因子：
4.8
通讯作者：
Weinstock, JV
中科院分区：
文献类型：
--
作者：
Elliott, DE;Urban, JF;Weinstock, JV
细胞因子的两种极化模式（Th1和Th2）调节炎症反应。每种细胞因子模式抑制相反模式的产生。来自克罗恩病引起的发炎肠道的淋巴细胞分泌Th1型细胞因子。克罗恩病在气候温和的高度工业化国家最为流行。它很少发生在卫生条件差的热带第三世界国家。我们认为，暴露于环境因素易使个人克罗恩病。寄生虫（蠕虫）在热带气候和拥挤和卫生条件差的人群中很常见。儿童最容易受到寄生虫的侵害。许多蠕虫生活在人类肠道内或通过人类肠道迁移，在那里它们与粘膜免疫系统相互作用。宿主产生粘膜反应，包括限制蠕虫定殖的Th2细胞因子产生。蠕虫和它们的卵可能是粘膜Th2应答的最有效的刺激物。由寄生蠕虫引起的Th2应答可以调节对无关寄生虫、细菌和病毒感染的免疫反应。发达国家的许多人现在生活在越来越卫生的环境中，避免接触蠕虫。也许未能获得这些寄生虫和经历粘膜Th2调节易患克罗恩病，这是一种过度活跃的Th1炎症。
Two polarized patterns (Th1 and Th2) of cytokines regulate inflammatory responses. Each cytokine pattern inhibits production of the opposing pattern. Lymphocytes from inflamed intestine due to Crohn's disease secrete a Th1 pattern of cytokines. Crohn's disease is most prevalent in highly industrialized countries with temperate climates. It occurs rarely in tropical third world countries with poor sanitation. We propose that exposure to an environmental agent predisposes individuals to Crohn's disease. Parasitic worms (helminths) are common in tropical climates and in populations subject to crowding and poor sanitation. Children are most subject to helminthic colonization. Many helminths live within or migrate through the human gut where they interact with the mucosal immune system. The host mounts a mucosal response that includes Th2 cytokine production limiting helminthic colonization. Helminths and their eggs probably are the most potent stimulators of mucosal Th2 responses. The Th2 response provoked by parasitic worms can modulate immune reactions to unrelated parasitic, bacterial, and viral infections. Many people in developed countries now live in increasingly hygienic environments, avoiding exposure to helminths. Perhaps failure to acquire these parasites and experience mucosal Th2 conditioning predisposes to Crohn's disease, which is an overly active Th1 inflammation.