The gastrointestinal (GI) tract microbiota is an environmental factor that regulates host immunity in allo-transplantation (allo-Tx). It is required for the development of resistance against pathogens and the stabilization of mucosa-associated lymphoid tissue. The gut-microbiota axis may also precipitate allograft rejection by producing metabolites that activate host cell-mediated and humoral immunity. Here, we discuss new insights into microbial immunomodulation, highlighting ongoing attempts to affect commensal colonization in an attempt to ameliorate allograft rejection cascade. Recent progress on the use of antibiotics to modulate GI microbiota diversity and innate-adaptive immune interface are discussed. Our focus on the microbiota’s influence of endoplasmic reticulum (ER) stress and autophagy signaling through hepatic EP4/CHOP/LC3B platforms reveals a novel molecular pathway and potential biomarkers determining the progression of allo-Tx damage. Understanding and harnessing the potential of microbiome/bacteriophage therapies may offer safe and effective means for personalized treatment to reduce risks of infections and immunosuppression in allo-Tx.

胃肠道（GI）微生物群是一种环境因子，可调节同种异体移植（allo-Tx）中的宿主免疫力。它是发展对病原体的抵抗力和与黏膜相关的淋巴组织稳定的必需物质。肠道菌群轴还可以通过产生代谢物来促进同种异体移植排斥，这些代谢物可以激活宿主细胞介导的体液免疫。在这里，我们讨论了对微生物免疫调节的新见解，突出了影响共生定殖的正在进行的尝试，以试图改善同种异体移植排斥反应的级联。讨论了使用抗生素调节胃肠道微生物群和先天自适应免疫界面的最新进展。我们对微生物群对内质网（ER）应激和通过肝EP4 / CHOP / LC3B平台进行自噬信号转导的影响的研究揭示了一种新颖的分子途径和潜在的生物标志物，其决定了异体Tx损伤的进展。了解和利用微生物/噬菌体疗法的潜​​力可为个性化治疗提供安全有效的方法，以减少异体Tx感染和免疫抑制的风险。