微粒子吸附 LPS 在克罗恩病患者中诱导不同免疫反应的初步证据

P Ashwood
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摘要

在现代西方饮食中,无机微粒作为食品添加剂无处不在,并被覆盖在人体肠道淋巴聚集体上的微褶(M)细胞积极清除。在克罗恩病(CD)中,炎症是由于肠道粘膜无法维持对包括细菌及其副产品在内的肠腔因子的耐受性而引起的。膳食颗粒的表面积大、带电能力强,能与脂多糖(LPS)等生物大分子紧密结合。本文旨在研究二氧化钛(TiO2)这种食物微粒是否会改变 CD 患者外周血单核细胞(PBMC)与健康对照组相比对 LPS 的不同细胞免疫反应。我们的数据显示,无论在健康还是疾病状态下,外周单核细胞摄取颗粒后,LPS 相关颗粒主要刺激 IL-1β 的释放,并同时诱导细胞死亡。此外,与对照组相比,CD 患者在颗粒刺激后 IL-1β 的释放增加得更多。总之,膳食微粒中的 LPS 吸附为刺激吞噬性单核细胞提供了一种机制,并可能通过增加促炎细胞因子的产生来介导免疫引物,从而加重肠道炎症(如 CD、肠易激综合征、自闭症谱系障碍和精神分裂症相关的胃肠道疾病)的粘膜免疫反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Preliminary Evidence of Differentially Induced Immune Responses by Microparticle-adsorbed LPS in Patients with Crohn's Disease.

Inorganic microparticles are ubiquitous in the modern Western diet present as food additives and are actively scavenged by microfold (M) cells overlying human intestinal lymphoid aggregates. In Crohn's disease (CD), inflammation is caused by the inability of the intestinal mucosa to sustain tolerance to gut luminal factors including bacteria and their by-products. Having large, highly charged surface areas dietary particles can avidly bind biomolecules such as lipopolysaccharide (LPS). The aim of this paper was to examine whether the dietary particle, titanium dioxide (TiO2), modified cellular immune responses to LPS differently in peripheral blood mononuclear cells (PBMC) from CD patients compared with healthy controls. Our data showed that LPS-associated particles predominantly stimulated release of IL-1β and induced concurrent cell death in peripheral monocytes following particle uptake in both health and disease. In addition, IL-1β release was increased more in CD patients compared with controls following particle stimulation. In conclusion, LPS adsorption to dietary particulates provides a mechanism for stimulation of phagocytic mononuclear cells and may cause aggravation of mucosal immune responses in inflammatory conditions of the bowel such as CD, irritable bowel syndrome, and autism spectrum disorder and schizophrenia associated gastrointestinal conditions, by immune priming mediated through increased production of pro-inflammatory cytokines.

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