The intestinal microbiota plays a crucial role in the onset of diarrhea and can be modulated through dietary changes. Shenling Baizhu powder (SLBZ) has been shown to regulate diarrhea. Thirty Kunming mice were randomly divided into a normal group (MCN), model group (MMD), and SLBZ group (MSLBZ). Diarrhea was induced by fatigue combined with a high-fat diet. After modeling, the MSLBZ group received 145.6 g/(kg & centerdot;d) SLBZ for 7 days. Pathological examination of small intestine tissues, along with measurements of interleukin 6 (IL-6), interleukin 17 (IL-17), immunoglobulin A (sIgA), and mucin 2 (Muc2) levels, were conducted. The intestinal mucosa was extracted for high-throughput sequencing of 16S rRNA. In the MMD group, intestinal damage, lymphocyte infiltration, decreased sIgA, diarrhea, and a significant increase in Helicobacter were observed compared with the MCN group. After SLBZ treatment, the MSLBZ group exhibited improved body weight, reduced intestinal damage, decreased levels of IL-6, increased sIgA, and alleviated diarrhea. Compared with the MMD group, the abundance of Duncaniella freteri was significantly higher, while Helicobacter was markedly reduced. Correlation analysis showed that Duncaniella freteri was positively correlated with sIgA and Muc2 and negatively correlated with IL-6 and IL-17. SLBZ alleviates intestinal mucosal damage, reduces pro-inflammatory cytokines, enhances sIgA production, and restores the microbiota balance in mice with diarrhea.
In non-IgE-mediated food allergy, food protein-induced enteropathy (FPE) can be evoked by the Th2 response. Some reports show that either Th2-biased immune responses or gut microbial dysbiosis can exacerbate food-allergic gastrointestinal inflammation. Nevertheless, it remains unclear whether gut microbiota directly affect Th2-biased immune responses involving FPE. To address this issue, we used OVA23-3 & times; BALB/cA mice, which is an FPE-like model. Feeding the mice an egg-white diet (EW) induced excessive Th2-type immune responses in CD4+ T cells in the mesenteric lymph nodes (MLNs), resulting in weight loss and enteropathy. Firstly, we compared specific pathogen-free (SPF) OVA23-3 & times; BALB/cA mice with germ-free (GF) OVA23-3 & times; BALB/cA mice when fed an EW diet. Symptoms shown in SPF mice were attenuated in GF mice, suggesting that gut microbiota may contribute to exacerbating symptoms. Additionally, we orally administered broad-spectrum antibiotics (Abx) to OVA23-3 & times;BALB/cA mice and analyzed the gut microbiota. Compared with a no-Abx administration group, we found that Abx administration significantly altered the alpha and beta diversity of the gut microbiota in EW-fed mice. The presence of Alloprevotella, Bacteroides, and Muribaculaceae was reduced to approximately 10%. Both weight loss and enteropathy in EW-fed mice were ameliorated afterAbx administration. Furthermore, administration ofAbx to the EW-fed group improved the Th1/Th2 balance in MLN cells and decreased the mRNA expression of IL-33 and the aryl hydrocarbon receptor in the jejunum. These results suggest that some members of the gut microbiota disturb Th1/Th2 responses in the MLN, by affecting the small intestinal epithelium, thereby exacerbating Th2-biased responses and inducing food-allergic enteropathy.
Listeria monocytogenes is a highly lethal foodborne pathogen that exhibits strain-dependent differences in virulence. Infection begins with traversal of the intestinal barrier through a two-step process involving adhesion to intestinal epithelial cells followed by intracellular invasion. In this study, Caco-2 cells were used to investigate these early infection events in 25 Japanese L. monocytogenes isolates (9 human clinical, 14 food-derived, and 2 environmental isolates) and 1 reference clinical strain (ScottA). We examined the genetic integrity of key adhesion-and invasion-related virulence genes (lap, fbpA, inlA, and inlB) and their relationships with adhesion and invasion phenotypes. Premature stop codons (PMSCs) were identified in inlA in 11 isolates and in inlB in 15 isolates. PMSCs in inlA were absent from all clinical isolates and predominantly found in serotypes 1/2a and 1/2c, which are rarely associated with clinical listeriosis. Also, three novel inlA PMSC variants were identified. Adhesion to Caco-2 cells was relatively uniform among isolates (5.87-6.88 log(10) colony-forming units [CFU]/mL), whereas invasion varied markedly (2.74-6.27 log(10) CFU/mL). Isolates carrying PMSCs in inlA consistently showed reduced invasion (<4 log(10) CFU/mL), whereas isolates lacking PMSCs exhibited significantly higher invasion (>5 log(10) CFU/mL). Western blot analysis confirmed the absence of full-length InlA in PMSC-containing isolates. Antibody-mediated inhibition of InlA produced a dose-dependent reduction in invasion, confirming the critical role of InlA in epithelial cell invasion. These findings demonstrate that the PMSCs in inlA are a key determinant of invasion capacity and may partly explain the serotype bias observed among human clinical isolates. Our results highlight the importance of virulence factor-based risk assessment for L. monocytogenes, rather than treating all strains as
Hyperuricemia (HUA) is widespread, and since conventional long-term treatments can be toxic, safer multi-target alternatives are required. Here, we tested a naturally derived synbiotic pairing of the uricolytic probiotic Lactobacillus gasseri SYP-B4432 with a polyphenol-rich Rumex hanus by. extract in a mouse model of hyperuricemia. In just five weeks of daily treatment, the combination reduced serum uric acid by 57.86%, suppressed serum xanthine oxidase activity by 14.31%, and restored the Bacteroidetes/Firmicutes ratio while lowering pro-inflammatory cytokines and attenuating renal histopathology. Importantly, no hepatic/renal impairment or body weight abnormalities were detected, confirming the safety of this intervention. Collectively, the probiotic-herbal duo alleviates HUA through the synergy of three modes of action: curtailing uric acid synthesis (via XOD inhibition), reshaping gut microbiota (to enhance UA excretion), and resolving renal inflammation (via cytokine modulation). This natural, safe, and multi-target synbiotic provides a clinically translatable strategy that may address the side effect limitations of conventional hyperuricemia drugs.
