Journal
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
Volume 12, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fcimb.2022.1022603
Keywords
anastomosis leak; gut microbiota; pathogen colonization; extracellular matrix; adhesin; collagen degradation
Categories
Funding
- Ningbo Clinical Research Center for Digestive System Tumors
- National Natural Science Foundation of China
- [2019A21003]
- [NSFC81970466]
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This review focuses on the role of gut microbiota in the occurrence of anastomotic leak (AL) following colorectal surgery. It discusses the changes in gut microbiota profiles in patients with AL, the colonization and tissue breakdown effects of AL-specific pathogenic or collagenase bacteria at the anastomosis site, and the potential mechanisms of pathogen-induced impaired anastomotic healing.
Anastomotic leak (AL) is a life-threatening postoperative complication following colorectal surgery, which has not decreased over time. Until now, no specific risk factors or surgical technique could be targeted to improve anastomotic healing. In the past decade, gut microbiota dysbiosis has been recognized to contribute to AL, but the exact effects are still vague. In this context, interpretation of the mechanisms underlying how the gut microbiota contributes to AL is significant for improving patients' outcomes. This review concentrates on novel findings to explain how the gut microbiota of patients with AL are altered, how the AL-specific pathogen colonizes and is enriched on the anastomosis site, and how these pathogens conduct their tissue breakdown effects. We build up a framework between the gut microbiota and AL on three levels. Firstly, factors that shape the gut microbiota profiles in patients who developed AL after colorectal surgery include preoperative intervention and surgical factors. Secondly, AL-specific pathogenic or collagenase bacteria adhere to the intestinal mucosa and defend against host clearance, including the interaction between bacterial adhesion and host extracellular matrix (ECM), the biofilm formation, and the weakened host commercial bacterial resistance. Thirdly, we interpret the potential mechanisms of pathogen-induced poor anastomotic healing.
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