Institute for Maternal and Child Health-IRCCS Burlo Garofolo, 65/1 Via dell'Istria, 34137 Trieste, Italy.
Department of Medicine, Surgery and Health Sciences, University of Trieste, Strada di Fiume 447, 34149 Trieste, Italy.
Int J Mol Sci. 2024 Oct 2;25(19):10611. doi: 10.3390/ijms251910611.
Type 1 Diabetes Mellitus (T1DM) is a chronic autoimmune disease that results in the destruction of pancreatic β cells, leading to hyperglycaemia and the need for lifelong insulin therapy. Although genetic predisposition and environmental factors are considered key contributors to T1DM, the exact causes of the disease remain partially unclear. Recent evidence has focused on the relationship between the gut, the oral cavity, immune regulation, and systemic inflammation. In individuals with T1DM, changes in the gut and oral microbial composition are commonly observed, indicating that dysbiosis may contribute to immune dysregulation. Gut dysbiosis can influence the immune system through increased intestinal permeability, altered production of short chain fatty acids (SCFAs), and interactions with the mucosal immune system, potentially triggering the autoimmune response. Similarly, oral dysbiosis may contribute to the development of systemic inflammation and thus influence the progression of T1DM. A comprehensive understanding of these relationships is essential for the identification of biomarkers for early diagnosis and monitoring, as well as for the development of therapies aimed at restoring microbial balance. This review presents a synthesis of current research on the connection between T1DM and microbiome dysbiosis, with a focus on the gut and oral microbiomes in pediatric populations. It explores potential mechanisms by which microbial dysbiosis contributes to the pathogenesis of T1DM and examines the potential of microbiome-based therapies, including probiotics, prebiotics, synbiotics, and faecal microbiota transplantation (FMT). This complex relationship highlights the need for longitudinal studies to monitor microbiome changes over time, investigate causal relationships between specific microbial species and T1DM, and develop personalised medicine approaches.
1 型糖尿病（T1DM）是一种慢性自身免疫性疾病，导致胰腺β细胞破坏，导致高血糖和需要终身胰岛素治疗。尽管遗传易感性和环境因素被认为是 T1DM 的关键因素，但该病的确切病因仍部分不清楚。最近的证据集中在肠道、口腔、免疫调节和全身炎症之间的关系上。在 T1DM 患者中，肠道和口腔微生物组成的变化很常见，表明肠道菌群失调可能导致免疫失调。肠道菌群失调可以通过增加肠道通透性、改变短链脂肪酸（SCFAs）的产生以及与黏膜免疫系统相互作用来影响免疫系统，从而可能引发自身免疫反应。同样，口腔菌群失调可能导致全身炎症的发展，从而影响 T1DM 的进展。全面了解这些关系对于识别早期诊断和监测的生物标志物以及开发旨在恢复微生物平衡的治疗方法至关重要。本综述介绍了当前关于 T1DM 与微生物组失调之间联系的研究综述，重点关注儿科人群的肠道和口腔微生物组。它探讨了微生物失调导致 T1DM 发病机制的潜在机制，并研究了基于微生物组的治疗方法的潜力，包括益生菌、益生元、合生菌和粪便微生物移植（FMT）。这种复杂的关系强调需要进行纵向研究来监测微生物组随时间的变化，研究特定微生物物种与 T1DM 之间的因果关系，并开发个性化医学方法。
