To investigate the diversity and composition of gut fungi microbiota in patients with polycystic kidney disease (PKD) and its correlation with clinical indicators.

A total of 44 PKD patients, 44 patients with non-polycystic chronic kidney disease (NPCKD) and 22 healthy controls (HC) admitted to our hospital from February 2023 to February 2024 were recruited. ITS1 DNA sequencing was applied to analyze the gut fungal composition. Bioinformatics analysis was used to compare the diversity and structural differences of fungi among the 3 groups. Pearson correlation analysis was performed to analyze the relationship between gut fungi and clinical indicators.

There were no significant differences in baseline characteristics (gender, age, body mass index, etc.) among the 3 groups, but statistical differences were seen in terms of serum indicators (such as serum creatinine, blood urea nitrogen, uric acid, estimated glomerular filtration rate, etc.) (P < 0.01). Alpha diversity analysis showed no significant difference was seen between the PKD and HC groups, but the PKD group had significant differences to the NPCKD group (P < 0.01). Beta diversity analysis revealed significant differences among the 3 groups and in pairwise comparisons (P=0.001). Fungi composition analysis found that the abundance of Candida was significantly higher in the PKD group than the other 2 groups (P < 0.01), while the abundances of Aspergillus and Cladosporium were significantly lower in the PKD group than the HC group (P < 0.05). Linear discriminant analysis (LEFSe) indicated that Candida was significantly enriched, while Aspergillus and Cladosporium were significantly reduced in the PKD group. Correlation analysis revealed that the abundance of Cladosporium was negatively correlated with cyst diameter and immunoglobulin light chain Kappa/Lambda ratio in the PKD group (P < 0.05), while the abundance of Candida was positively correlated with liver/kidney cyst diameter (P < 0.01).

PKD patients exhibit characteristic changes in gut fungi diversity and composition. The abundances of Cladosporium and Candida are closely associated with clinical indicators of PKD patients.

Nosocomial infections in patients with severe acute pancreatitis (SAP) are frequently driven by impaired intestinal barrier function, which facilitates bacterial translocation and contributes to adverse clinical outcomes. Saccharomyces boulardii (S. boulardii) can reconstitute gut microbiota composition. We investigated whether S. boulardii combined with enteral nutrition (EN) affects the microbiome and nosocomial infections in SAP.

This study is a single centre, open-label randomized controlled trial. We included 50 patients with SAP in a Chinese gastroenterology intensive care unit (ICU), randomized to Probiotic group (S. boulardii and EN) or the Control group (EN). Throat/oropharyngeal and rectal swabs were collected from patients with SAP on days 0, 1, 3, 6, 9, 12, and 15 of ICU admission. The primary endpoints were nosocomial infection and fungemia, whereas the secondary endpoints were ICU mortality, 28-day mortality, ICU stay, and length of hospital stay. All samples were subjected to full-length 16 s rRNA and internal transcribed spacer (ITS) sequencing. Multivariate analysis was performed using normalized microbial and corresponding clinical data.

After data processing, 213 16S rRNA and 120 ITS samples were analysed. S. boulardii prevented nosocomial infections (0/27 in the Probiotic group vs 5/23 in the Control group; P < 0.05). Intestinal fungi were closely associated with nosocomial infections. Bioinformatic analysis showed that S. boulardii prevented nosocomial infections by reducing intestinal bacterial perturbation and inhibiting the proliferation of Enterococcus in the intestine, and Candida in the respiratory tract and intestines.

S. boulardii in patients with SAP may positively alter the respiratory and intestinal microbiome and decrease the incidence of nosocomial infections.

This study was approved by the Ethics Committee of Xinqiao Hospital, Army Medical University, Chongqing China (2021-yd030–01), which was retrospectively registered at the Chinese Clinical Trial Registry (ChiCTR2200056011, Date of Registration: 30/01/2022 https://www.chictr.org.cn/showproj.html?proj=151215).

To investigate the efficacy of zingerone（Zin）on dextran sodium sulfate（DSS）-induced colitis in mice and its potential immunomodulatory mechanism.

SPF C57BL/6 male mice aged 6 to 8 weeks were divided into control group（Water）, model group（DSS）, and Zin intervention group（DSS+Zin）, with 5 mice in each group. Acute ulcerative colitis model was constructed using DSS solution, and the changes in body weight, disease activity index（DAI）, colon length, and histopathological scores were compared among the groups. RT-qPCR and corresponding reagents and kits were employed to detect the mRNA and protein expression of inflammatory cytokines in the colonic tissue, respectively. The effects of Zin on T cell subsets and on the expression of transcription factor RORγt were determined by flow cytometry in vitro and in vivo. Moreover, the transcriptional activity of RORγt and activity of Rorc promoter were examined using dual-luciferase reporter system.

As compared with the control group, the mice in the DSS group showed shorter colon length, higher scores of DAI and histopathological index（P<0.05）, with increased mRNA levels of IL-17A, IL-21, IL-22, IL-6, IL-1 β and IFN-γ（P<0.05）, while decreased mRNA level of TGF-β（P<0.05）. The protein levels of IL-17A, IL-17F, IL-22, and IFN-γ were also upregulated in the DSS group（P<0.05）. However, Zin treatment significantly relieved the above clinical symptoms and reversed the expression of above inflammatory factors（P<0.05）. Flow cytometry indicated that Zin inhibited the differentiation of Th17 cells and the expression of RORγt, and promoted the differentiation of Treg cells both in vitro and in vivo（P<0.05）, but the differentiation of Th1 subset was not affected. The dual-luciferase reporter assay demonstrated that the transcriptional activity of RORγt and Rorc promoter activity were remarkably suppressed after Zin treatment（P<0.05）.

Zin alleviates DSS-induced colitis in mice by regulating the balance of Th17/Treg cells and inhibiting RORγt expression.