Colorectal cancer (CRC) is a leading cause of global cancer incidence and mortality, with rising prevalence among younger individuals. Accumulating evidence reveals a critical pathological axis linking intestinal barrier disruption, gut microbial dysbiosis, and chronic inflammation, collectively driving CRC initiation. Early colorectal lesions exhibit microbial shifts—reduced α-diversity with clear β-diversity separation, enrichment of oral-origin/pathobiont taxa and depletion of butyrate producers—alongside impaired mucus and tight junction integrity. Concurrent chemical barrier drifts, with decreased short-chain fatty acids and increased secondary bile acids, enhance epithelial stress and vulnerability. The resultant permeability facilitates the translocation of microbial products, triggering inflammation and tumorigenesis. This paper focuses on a review of the relationship between gut microbiota, intestinal barrier, inflammatory signaling pathways, and tumor initiation, sorting out its potential role in developing, diagnosing, and treating CRC. Collectively, this cascade axis offers theoretical and empirical support for the early pathological detection and intervention of CRC, indicating promising directions for future precision screening and stratified management strategies.

Acute pancreatitis (AP) is a prevalent clinical condition of the digestive system, with a growing frequency each year. Approximately 20% of patients suffer from severe acute pancreatitis (SAP) with local consequences and multi-organ failure, putting a significant strain on patients’ health insurance. According to reports, the lungs are particularly susceptible to SAP. Acute respiratory distress syndrome, a severe type of acute lung injury (ALI), is the primary cause of mortality among AP patients. Controlling the mortality associated with SAP requires an understanding of the etiology of AP-associated ALI, the discovery of biomarkers for the early detection of ALI, and the identification of potentially effective drug treatments. Exosomes are a class of extracellular vesicles with a diameter of 30–150 nm that are actively released into tissue fluids to mediate biological functions. Exosomes are laden with bioactive cargo, such as lipids, proteins, DNA, and RNA. During the initial stages of AP, acinar cell-derived exosomes suppress forkhead box protein O1 expression, resulting in M1 macrophage polarization. Similarly, macrophage-derived exosomes activate inflammatory pathways within endothelium or epithelial cells, promoting an inflammatory cascade response. On the other hand, a part of exosome cargo performs tissue repair and anti-inflammatory actions and inhibits the cytokine storm during AP. Other reviews have detailed the function of exosomes in the development of AP, chronic pancreatitis, and autoimmune pancreatitis. The discoveries involving exosomes at the intersection of AP and acute lung injury (ALI) are reviewed here. Furthermore, we discuss the therapeutic potential of exosomes in AP and associated ALI. With the continuous improvement of technological tools, the research on exosomes has gradually shifted from basic to clinical applications. Several exosome-specific non-coding RNAs and proteins can be used as novel molecular markers to assist in the diagnosis and prognosis of AP and associated ALI.