From Microbiota Correction to Host Protection: A New Therapeutic Target for the Prevention and Treatment of Postoperative Complications
Zelimkhan Berikkhanov, Miroslava Pilipenko, Elizaveta Ermakova, Maria Sukhanova, Milena Ivanova, Aleksey Kotelnikov, Andrey Nikolaev, Vadim Razumovsky, Vladislav Rakintsev, Alexey Shestakov, Evgeniy Tarabrin, Sergey MuravievBackground/Objectives. The intestinal microbiota is a key contributor to postoperative complications, yet direct interventions targeting dysbiosis—antibiotics, probiotics, and synbiotics—have produced inconsistent results. This paradox indicates a fundamental gap in understanding host–microbiota interactions under surgical stress. We aimed to re-examine the causal role of dysbiosis in postoperative pathogenesis and propose a revised therapeutic paradigm centered on host barrier protection. Methods. A narrative literature review was conducted, searching PubMed/MEDLINE, Scopus, and Web of Science for articles published between 2009 and 2025. Reference lists of included publications were additionally screened. Studies in English and Russian were eligible; 107 references were included. Results. We hypothesize that dysbiosis in surgical patients may, at least in part, represent a predictable ecological response to systemic hypoperfusion, pharmacological burden, and ischemia–reperfusion injury, rather than acting solely as an independent pathogenic agent. Microbial shifts, characterized by the depletion of short-chain fatty acid-producing commensals and the expansion of pathobionts, frequently accompany epithelial injury; however, available human data are predominantly observational and do not permit definitive determination of the temporal sequence. This hypothesis provides the conceptual foundation for the proposed therapeutic reorientation. Conclusions. The present findings support the rationale for transitioning from microbiome manipulation to a “host-first” strategy, which prioritizes the restoration of intestinal barrier integrity through the administration of cytoprotective agents and targeted metabolic substrates (glutamine and butyrate). We propose the Gut Resilience Index (GRI) as a theoretical construct to identify patients approaching a critical threshold necessitating rescue therapy. It must be emphasized that both the “host-first” strategy and the GRI remain hypothetical frameworks requiring prospective validation. The most critical next steps include the development and validation of the GRI in prospective cohort studies, as well as randomized controlled trials directly comparing barrier-oriented strategies with standard care.