Tuo Deng

Rotavirus (RV), a major cause of childhood diarrhea, damages intestinal epithelium and may induce lactose intolerance in some patients. Increasing studies have emphasized the importance of dysregulated gut microbiome community in diseases. In this study, fecal samples from rotavirus-infected children (n = 48) and healthy controls (n = 29) were analyzed based on 16S rRNA gene sequencing and clinical data. The rotavirus-infected group was further stratified by lactose tolerance status to investigate the distinctive features of the gut microbial communities. Our study verified a shift in gut microbiome constitution and abundance between the feces of healthy donors and rotavirus infection children. Notably, Agathobacter, Streptococcus, Veillonella, and Roseburia were significantly increased in rotavirus infection patients, while the relative abundance of the Ruminococcus gnavus group was decreased. Analyses of alpha diversity unveiled significant differences in the abundance of gut microbiota between rotavirus infection patients with or without lactose intolerance. In particular, the abundance of Parasutterella, Lachnospiraceae NK4A136 group, Morganella, and Veillonellaceae unclassified decreased significantly in rotavirus infection patients with lactose intolerance. Further, PLR, an inflammatory hematological ratio, was significantly elevated in rotavirus infection patients with lactose intolerance. Overall, our study indicated the characteristic of change in diversity, taxonomy, and function of gut microbiota between rotavirus infection and healthy control in children, revealing the existence of dysbiosis in rotavirus infection. Further, our analysis identified the compositional uniqueness of gut microbiota between rotavirus infection patients with or without lactose intolerance, highlighting the diversity and taxonomy in gut microbiome and association with inflammatory state. • Rotavirus causing diarrhea in children worldwide, causing damage to the intestinal epithelium and lactose intolerance-related diarrhea in children. • Results demonstrated the characteristic changes of gut microbiome in rotavirus-infected children and further investigated the different gut microbiome composition between rotavirus infection-related lactose intolerance and lactose tolerance patients. • Further, the relationship between gut microbiome and inflammatory hematological ratios was explored.

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Metastasis causes most cancer-related deaths, and the role and mechanism of periostin (POSTN) in the metastasis of hepatocellular carcinoma (HCC) remain undiscovered. In this study, DEN and HTVi HCC models were performed in hepatic-specific Postn ablation and Postn knock-in mouse to reveal the role of POSTN in HCC metastasis. Furthermore, POSTN was positively correlated with circulating EPCs level and promoted EPC mobilization and tumour infiltration. POSTN also mediated the crosstalk between HCC and EPCs, which promoted metastasis ability and upregulated CD36 expression in HCC through indirect crosstalk. Chemokine arrays further revealed that hepatic-derived POSTN induced elevated CCL2 expression and secretion in EPCs, and CCL2 promoted prometastatic traits in HCC. Mechanistic studies showed that POSTN upregulated CCL2 expression in EPCs via the αvβ3/ILK/NF-κB pathway. CCL2 further induced CD36 expression via the CCR2/STAT3 pathway by directly binding to the promoter region of CD36. Finally, CD36 was verified to have a prometastatic role in vitro and to be correlated with POSTN expression, metastasis and recurrence in HCC in clinical samples. Our findings revealed that crosstalk between HCC and EPCs is mediated by periostin/CCL2/CD36 signalling which promotes HCC metastasis and emphasizes a potential therapeutic strategy for preventing HCC metastasis.

To investigate the potential of the gut microbiome as a biomarker for predicting the early recurrence of HBV‐related hepatocellular carcinoma (HCC), we enrolled 124 patients diagnosed with HBV‐associated HCC and 82 HBV‐related hepatitis, and 86 healthy volunteers in our study, collecting 292 stool samples for 16S rRNA sequencing and 35 tumor tissue samples for targeted metabolomics. We performed an integrated bioinformatics analysis of gut microbiome and tissue metabolome data to explore the gut microbial–liver metabolite axis associated with the early recurrence of HCC. We constructed a predictive model based on the gut microbiota and validated its efficacy in the temporal validation cohort. Dialister, Veillonella, the Eubacterium coprostanoligenes group, and Lactobacillus genera, as well as the Streptococcus pneumoniae and Bifidobacterium faecale species, were associated with an early recurrence of HCC. We also found that 23 metabolites, including acetic acid, glutamate, and arachidonic acid, were associated with the early recurrence of HCC. A comprehensive analysis of the gut microbiome and tissue metabolome revealed that the entry of gut microbe‐derived acetic acid into the liver to supply energy for tumor growth and proliferation may be a potential mechanism for the recurrence of HCC mediated by gut microbe. We constructed a nomogram to predict early recurrence by combining differential microbial species and clinical indicators, achieving an AUC of 78.0%. Our study suggested that gut microbes may serve as effective biomarkers for predicting early recurrence of HCC, and the gut microbial–tumor metabolite axis may explain the potential mechanism by which gut microbes promote the early recurrence of HCC.