Protective effect of Pediococcus pentosaceus Li05 on diarrhea-predominant irritable bowel syndrome in rats.

Pediococcus pentosaceus Li05 (Li05) has demonstrated potential benefits in various intestinal and liver diseases, but its potential and mechanisms in relieving diarrhea have not been understood. The objective of this research was to examine the effects and mechanisms of Li05 in rats with diarrhea-predominant irritable bowel syndrome (IBS-D) induced by wrap restrain stress (WRS) and 4% acetic acid. The results demonstrated that Li05 effectively alleviated weight loss, visceral sensitivity and diarrhea in rats with IBS-D. It also improved intestinal and systemic inflammation by reducing the levels of chemokines and proinflammatory cytokines (GRO/KC, RANTES, IL-1ß, IL-7, and IL-18). The 5-hydroxytryptamine (5-HT) signaling pathway is involved in regulating excessive intestinal motility and secretion in IBS-D. Li05 effectively reduced the expression levels of the 5-HT3B receptor (5-HT3BR) (p < 0.01) in the intestine. Additionally, Li05 intervention had a regulatory effect on the gut composition, with a decrease in the abundance of [Ruminococcus] gauvreauii group, Dubosiella, Erysipelatoclostridium and Blautia, and an increase in the abundance of Alloprevotella, Anaerotruncus and Mucispirillum. Furthermore, Li05 induced significant changes in fatty acid and amino acid metabolism in the gut of rats with IBS-D. These findings indicate that Li05 exhibits an effective improvement in IBS-D symptoms by reducing inflammation and modulating gut microbiota and metabolism. Based on the above results, Li05 holds promise as a potential probiotic for managing IBS-D.

Longitudinal gut fungal alterations and potential fungal biomarkers for the progression of primary liver disease.

Liver disease, a major health concern worldwide, is a serious and progressive disorder. Herein, we not only established a mouse model of DEN+CCl4-induced primary liver disease but also collected clinical human samples to investigate longitudinal alterations in the gut mycobiome. As liver disease advanced, gut integrity was disrupted, and the mycobiota was disturbed in the mouse models. The metabolites associated with hepatocellular carcinoma (HCC) differed from those associated with the cirrhotic phase as follows: levels of stercobilin and aflatoxin B1 dialcohol were reduced, while levels of triterpenoids, bafilomycin A1, and DHEA were increased in the HCC group. The abundance of the phylum Chytridiomycota increased as the chronic liver disease progressed and was then replaced by the phylum Ascomycota in HCC. Based on the results from clinical human samples, the genus Candida (Ascomycota) (in humans) and the genus Kazachstania (Ascomycota) (in mice) occupied a dominant position in the HCC group, while other fungi were depleted. The increased abundance of C. albicans and depletion of S. cerevisiae may be hallmarks of the progression of liver cirrhosis to early HCC. Moreover, the administration of C. albicans and S. cerevisiae in the LC-HCC progression could accelerate or retard the progression of HCC. Therefore, gut fungi have the potential to serve as a noninvasive clinical biomarker and even a treatment method.

Foodborne and airborne polyethersulfone nanoplastics respectively induce liver and lung injury in mice: Comparison with microplastics.

Micro/nanoplastics (MNP) are ubiquitous in the environment and multiple living organisms. The toxicity of some common types of MNP, e.g., polyethersulfone (PES) MNP, remains poorly understood. Multi-omics approaches were used in this study to determine the effects of foodborne and airborne PES MNP on liver and lung, respectively. Foodborne MNP were capable of inducing gut microbial dysbiosis, gut and serum metabolic disruption, and liver transcriptomic dysregulation, and affecting serum antioxidant activity and liver function, resulting in liver injury. As for the airborne MNP, they were found to induce nasal and lung microbial dysbiosis, serum and lung metabolic disruption, and liver transcriptome disturbance, and cause disrupted serum antioxidant activity and lung injury. Foodborne and airborne PES NP were found to respectively induce greater liver and lung toxicity than MP, which could be associated with the differences between NP and MP exposures. The relevant results suggest that foodborne PES MNP could disrupt the "gut microbiota-gut-liver" axis and induce hepatic injury, while airborne PES MNP could affect the "airborne microbiota-lung" axis and cause lung injury. The findings could benefit the diagnoses of liver and lung injury respectively induced by foodborne and airborne PES MNP, as well as the proper use of PES in human living environment.

Multi-omics analysis of the effects of dietary changes and probiotics on diet-induced obesity.

The consumption of a healthy diet is critical for maintaining and promoting human health. In the context of the rapid transformation from a high-fat diet (HFD) to a Mediterranean diet (MD) leading to major systemic changes, we explored the necessity of a transitional standard diet (TSD) between these two varied diets and the adjuvant effect of probiotics. HFD-fed mice were used for studying the changes and benefits of a dietary intervention and probiotic treatment. By measuring multiple systemic alterations such as weight (group B vs. group E, P < 0.05), liver function (AST, group C vs. group E, P < 0.001), and histopathology, we found that an MD, TSD and Bifidobacterium longum all contribute to alleviating lipid deposition and liver injury. The downregulation of IL-17 (group B vs. group E, P < 0.01) and MIP-1α (group B vs. group E, P < 0.001) also demonstrated the anti-inflammatory effects of the TSD. Moreover, we performed multi-omics analysis combined with the 16S sequencing, transcriptome and metabolome results and found that the TSD increased the abundance of the Lactobacillus genus (group C vs. group E, P < 0.01) and effectively lowered lipid accumulation and systemic inflammation. Furthermore, B. longum played an important role in the synergistic effect. The results showed that a TSD might be useful for HFD-induced obesity before drastic dietary changes, and probiotics were also beneficial.

T-cell infiltration, contribution and regulation in the central nervous system post-traumatic injury.

T cells participate in the repair process and immune response in the CNS post-traumatic injury and play both a beneficial and harmful role. Together with nerve cells and other immune cells, they form a microenvironment in the CNS post-traumatic injury. The repair of traumatic CNS injury is a long-term process. T cells contribute to the repair of the injury site to influence the recovery. Recently, with the advance of new techniques, such as mass spectrometry-based flow cytometry, modern live-cell imaging, etc, research focusing on T cells is becoming one of the valuable directions for the future therapy of traumatic CNS injury. In this review, we summarized the infiltration, contribution and regulation of T cells in post-traumatic injury, discussed the clinical significance and predicted the future research direction.

New Insight of Circular RNAs' Roles in Central Nervous System Post-Traumatic Injury.

The central nervous system (CNS) post-traumatic injury can cause severe nerve damage with devastating consequences. However, its pathophysiological mechanisms remain vague. There is still an urgent need for more effective treatments. Circular RNAs (circRNAs) are non-coding RNAs that can form covalently closed RNA circles. Through second-generation sequencing technology, microarray analysis, bioinformatics, and other technologies, recent studies have shown that a number of circRNAs are differentially expressed after traumatic brain injury (TBI) or spinal cord injury (SCI). These circRNAs play important roles in the proliferation, inflammation, and apoptosis in CNS post-traumatic injury. In this review, we summarize the expression and functions of circRNAs in CNS in recent studies, as well as the circRNA-miRNA-mRNA interaction networks. The potential clinical value of circRNAs as a therapeutic target is also discussed.

Mitochondrial Unfolded Protein Response and Its Roles in Stem Cells.

The mitochondrial unfolded protein response (UPRmt) is a mitochondrial protein quality control mechanism that is involved in many pathophysiological activities and maintains cellular homeostasis. The UPRmt signaling pathway in both Caenorhabditis elegans and mammals has gained much attention in recent years. Many studies have reported the general function of UPRmt, including the relationship between UPRmt and longevity, survival, apoptosis, innate immunity, cancer growth, and neurodegenerative diseases. Stem cells are capable of self-renewing and differentiating, thus playing an important role in maintaining tissue homeostasis and tissue regeneration. Although the role and regulation of UPRmt in somatic cells have been widely studied, the regulatory mechanism of UPRmt in stem cells is not fully known. Thus, in this article, the regulatory role of UPRmt in stem cell proliferation, cellular differentiation, and aging is reviewed. This review aims to provide novel insights for UPRmt promoting stem cell rejuvenation and improving life span in mammals.