肠道感觉和甜食：炎症性肠病和HIV感染中肠道损伤的营养解决方案

摘要(中文译文)

肠道黏膜层损伤是慢性炎症性疾病的核心特征，常导致肠道菌群失调、微生物失衡及免疫代谢紊乱。肠道功能障碍严重影响人类健康，扰乱代谢、心血管和神经系统，并引发代谢综合征。本文讨论两种看似无关但实际共享相似肠道黏膜屏障完整性改变的临床疾病：炎症性肠病（IBD）和人类免疫缺陷病毒（HIV）感染。我们以儿童IBD和HIV感染的非人灵长类模型为具体案例，比较和对比这些疾病对肠道完整性和微生物组组成的影响。我们还探讨潜在疗法，重点关注饮食干预。HIV感染和IBD均导致肠道屏障破坏，但机制不同。HIV迅速耗竭黏膜CD4 T细胞（尤其是Th17细胞），削弱上皮防御，导致紧密连接丧失（“肠漏”）、微生物易位和全身性炎症。在IBD（克罗恩病和溃疡性结肠炎）中，慢性免疫攻击肠道内壁产生溃疡和紧密连接缺陷。这些溃疡触发免疫细胞浸润并显著增加通透性。在两种情况下，黏液和上皮完整性受损导致循环脂多糖（LPS）升高、巨噬细胞活化和全身性炎症。HIV和IBD还诱导不同但有重叠的菌群失调。HIV感染与细菌多样性显著降低及潜在炎症性分类群（如变形菌门、普雷沃氏菌属）过度生长相关。同样，IBD患者多样性低，有益厚壁菌门（特别是）丢失，相对丰度过度。在两种疾病中，肠道菌群从纤维发酵共生菌转向“致病共生菌”，助长局部炎症。虽然靶向代谢产物的治疗潜力被广泛探索，但也有人推动发现非药物解决方案，特别是通过饮食和营养。我们介绍微量营养素摄入、喂养方式（ exclusive enteral nutrition，完全肠内营养）和不同饮食（高纤维、地中海、高脂肪）对疾病进展和细胞代谢的影响。作为一种低干预方法，营养通过减少炎症和相关代谢紊乱具有改善人类健康的巨大潜力。最后，我们强调使用动物模型阐明IBD和HIV疾病机制复杂性的能力。

Abstract

Damage to the mucosal layer of the gut is a central feature of chronic inflammatory diseases, often resulting in gut dysbiosis, microbial imbalances, and dysregulated immunometabolism. Gut dysfunction significantly impacts human health, disrupting metabolic, cardiovascular, and neurological systems, and leading to metabolic syndrome. Here, we discuss two clinical entities that are apparently unrelated but actually share similar alterations to gut mucosal barrier integrity: inflammatory bowel disease (IBD) and human immunodeficiency virus (HIV). We use the particular cases of pediatric IBD and nonhuman primate models of HIV infection to compare and contrast the impact of these diseases on gut integrity and microbiome composition. We also explore potential therapies, focusing on dietary interventions. Both HIV infection and IBD cause gut barrier disruption, but via different mechanisms. HIV rapidly depletes mucosal CD4 T cells (especially Th17 cells), weakening epithelial defenses, leading to a loss of tight junctions ("leaky gut"), microbial translocation, and systemic inflammation. In IBD (Crohn's disease and ulcerative colitis), chronic immune attacks on the gut lining produce ulcers and tight-junction defects. These ulcerations trigger immune-cell infiltration and markedly increase permeability. In both conditions, impaired mucus and epithelial integrity result in higher circulating lipopolysaccharides (LPS), macrophage activation, and systemic inflammation. HIV and IBD also induce distinct yet overlapping dysbioses. HIV infection is associated with markedly reduced bacterial diversity and an overgrowth of potentially inflammatory taxa (e.g., Proteobacteria, Prevotella). Similarly, IBD patients have low diversity and loss of beneficial Firmicutes (notably ) with relative overabundance. In both diseases, the gut flora shifts away from fiber-fermenting commensals to "pathobionts," fueling local inflammation. While the therapeutic potential of targeting metabolic products is widely explored, there is also a push towards discovering nondrug solutions, particularly through diet and nutrition. We present the effects of micronutrient intake, feeding mechanisms (exclusive enteral nutrition), and different diets (high fiber, Mediterranean, high fat) on disease progression and cellular metabolism. As a low-intervention approach, nutrition has enormous potential to improve human health by reducing inflammation and associated metabolic disturbances. Finally, we emphasize the capabilities of using animal models to elucidate the complexities of disease mechanics in IBD and HIV.

如何引用

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