da Silva Ferreira Ana R, Wardill Hannah R, Tissing Wim J E, Harmsen Hermie J M
Department of Medical Microbiology.
Department of Pediatrics Oncology, Beatrix Children's Hospital, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Curr Opin Support Palliat Care. 2020 Jun;14(2):127-134. doi: 10.1097/SPC.0000000000000497.
There is a growing number of studies implicating gut dysbiosis in mucositis development. However, few studies have shed light on the causal relationship limiting translational potential. Here, we detail the key supportive evidence for microbial involvement, candidate mechanisms by which the microbiome may contribute to mucositis and emerging approaches to model host-microbe interactions with clinical relevance and translational potential.
Synthesis of existing clinical data demonstrate that modulating the microbiome drastically alters the development and severity of mucositis, providing a strong rationale for its involvement. Review of the literature revealed potential microbiome-dependent mechanisms of mucosal injury including altered drug metabolism, bile acid synthesis and regulation of the intestinal barrier. Current studies are limited in their mechanistic insight due to cross-sectional and would benefit from longitudinal analyses and baseline phenotyping.
The causative role of the microbiome in mucositis development remains unclear. Future studies must adopt comprehensive microbial analyses with functional assessment, and utilize emerging ex-vivo models to interrogate host-microbe interactions in mucositis.
越来越多的研究表明肠道微生物群失调与粘膜炎的发生有关。然而，很少有研究阐明这种因果关系，限制了其转化潜力。在此，我们详细阐述了微生物参与的关键支持证据、微生物群可能导致粘膜炎的候选机制，以及模拟具有临床相关性和转化潜力的宿主-微生物相互作用的新方法。
现有临床数据的综合分析表明，调节微生物群会显著改变粘膜炎的发生和严重程度，这为其参与提供了有力的理论依据。文献综述揭示了潜在的微生物群依赖性粘膜损伤机制，包括药物代谢改变、胆汁酸合成和肠道屏障调节。由于目前的研究是横断面的，其机制洞察力有限，纵向分析和基线表型分析将有助于这些研究。
微生物群在粘膜炎发生中的因果作用仍不清楚。未来的研究必须采用全面的微生物分析和功能评估，并利用新出现的体外模型来研究粘膜炎中的宿主-微生物相互作用。
