Neuroimmune interactions: The bridge between inflammatory bowel disease and the gut microbiota

IF 7.9 1区 医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL
Jinxia Zhai, Yingjie Li, Jiameng Liu, Cong Dai
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引用次数: 0

Abstract

Background

The multidimensional regulatory mechanism of the gut–brain–immune axis in the context of inflammatory bowel disease (IBD) has garnered significant attention, particularly regarding how intestinal microbiota finely regulates immune responses through immune cells and sensory neurons.

Main Body

Metabolites produced by intestinal microbiota influence the phenotype switching of immune cells via complex signalling pathways, thereby modulating their anti-inflammatory and pro-inflammatory functions during intestinal inflammation. Furthermore, sensory neurons exhibit heightened sensitivity to microbial-derived signals, which is essential for preserving intestinal balance and controlling pathological inflammation by integrating peripheral environmental signals with local immune responses. The dynamic equilibrium between immune cells and the neuroimmunoregulation mediated by sensory neurons collectively sustains immune homeostasis within the intestine. However, this coordination mechanism is markedly disrupted under the pathological conditions associated with IBD.

Conclusion

An in-depth exploration of the interactions among immune cells, gut microbiota and sensory neurons may yield significant insights into the pathological mechanisms underlying IBD and guide the creation of new treatment approaches.

Key points

  • The gut microbiota regulates the gut-brain-immune axis, modulating neuroimmune interactions in IBD.
  • Microbiota-derived metabolites influence immune cells, thereby affecting neurons.
  • Neurons secrete mediators, enabling bidirectional neuroimmune communication essential for intestinal homeostasis.
  • Disruptions contribute to IBD, offering therapeutic targets.
神经免疫相互作用:炎症性肠病和肠道微生物群之间的桥梁
炎症性肠病(IBD)背景下肠-脑-免疫轴的多维调节机制已经引起了人们的广泛关注,特别是肠道微生物群如何通过免疫细胞和感觉神经元精细调节免疫反应。肠道微生物群产生的代谢物通过复杂的信号通路影响免疫细胞的表型转换,从而调节其在肠道炎症期间的抗炎和促炎功能。此外,感觉神经元对微生物来源的信号表现出更高的敏感性,这对于通过整合外周环境信号和局部免疫反应来维持肠道平衡和控制病理性炎症至关重要。免疫细胞与感觉神经元介导的神经免疫调节之间的动态平衡共同维持肠道内的免疫稳态。然而,在与IBD相关的病理条件下,这种协调机制明显中断。结论深入探索免疫细胞、肠道微生物群和感觉神经元之间的相互作用,可能对IBD的病理机制有重要的认识,并指导新的治疗方法的建立。肠道微生物群调节肠-脑-免疫轴,调节IBD中的神经免疫相互作用。微生物衍生的代谢物影响免疫细胞,从而影响神经元。神经元分泌介质,实现肠道内稳态所必需的双向神经免疫通讯。破坏有助于IBD,提供治疗靶点。
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来源期刊
CiteScore
15.90
自引率
1.90%
发文量
450
审稿时长
4 weeks
期刊介绍: Clinical and Translational Medicine (CTM) is an international, peer-reviewed, open-access journal dedicated to accelerating the translation of preclinical research into clinical applications and fostering communication between basic and clinical scientists. It highlights the clinical potential and application of various fields including biotechnologies, biomaterials, bioengineering, biomarkers, molecular medicine, omics science, bioinformatics, immunology, molecular imaging, drug discovery, regulation, and health policy. With a focus on the bench-to-bedside approach, CTM prioritizes studies and clinical observations that generate hypotheses relevant to patients and diseases, guiding investigations in cellular and molecular medicine. The journal encourages submissions from clinicians, researchers, policymakers, and industry professionals.
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