Linna Zhao

The co-morbidity of psoriasis (PsO) and metabolic syndrome (MetS) is prevalent. While the mechanisms causing PsO in MetS remain unknown, it is understood that gut microbiota plays a critical role in maintaining immune and metabolic balance. However, the specific mechanisms and whether biomarkers are involved in the pathophysiological process of PSO in MetS patients have yet to be elucidated. This study involved 29 patients with PSO and MetS (PM) and 29 with MetS (M). It analyzed their clinical parameters, microbial composition, function, diagnostic, and predictive performance. The results unveiled significant differences between the two groups concerning microbial diversity and community composition. Most of the differential microbiota in the PM group exhibited a negative correlation with high-density lipoprotein (HDL) and a positive correlation with serum uric acid (SUA). In contrast, the opposite was observed in the M group. Sixteen MetaCyc pathways showed significance in the PM group, encompassing peptidoglycan biosynthesis II (staphylococci), the super pathway of L-arginine and L-ornithine degradation, teichoic acid (poly-glycerol) biosynthesis, and palmitic biosynthesis II (bacteria and plants). Six KEGG pathways were enriched in the M group, such as flavone, flavonol biosynthesis, and carotenoid biosynthesis. Most importantly, we determined that eight biomarkers, represented by Akkermansia, demonstrated robust diagnostic predictive power. This study elucidates the potential mechanism through which metabolic disorders impact the onset and progression of psoriasis via intestinal microbiota. Furthermore, it offers novel strategies for preventing, diagnosing, and treating PsO in MetS.

Psoriasis is an immune-mediated chronic inflammatory skin disease that affects 2% to 3% of the world’s population. It is widely assumed that immune cells and cytokines acting together play a crucial part in the pathophysiology of psoriasis by promoting the excessive proliferation of skin keratinocytes and inflammatory infiltration. Interleukins (ILs), as a critical component of cytokines, have been closely associated with the pathogenesis and progression of psoriasis. This review summarizes the current contribution of ILs to psoriasis and describes the role each IL performs in psoriasis. Furthermore, the paper presents the therapeutic effects and application prospects of biologics developed for ILs in clinical treatment and experiments. The study aims to further the research on ILs in the treatment of psoriasis.

There are complex interactions between the gut and the brain. With increasing research on the relationship between gut microbiota and brain function, accumulated clinical and preclinical evidence suggests that gut microbiota is intimately involved in the pathogenesis of neurodegenerative diseases (NDs). Increasingly studies are beginning to focus on the association between gut microbiota and central nervous system (CNS) degenerative pathologies to find potential therapies for these refractory diseases. In this review, we summarize the changes in the gut microbiota in Alzheimer's disease, Parkinson's disease, multiple sclerosis, and amyotrophic lateral sclerosis and contribute to our understanding of the function of the gut microbiota in NDs and its possible involvement in the pathogenesis. We subsequently discuss therapeutic approaches targeting gut microbial abnormalities in these diseases, including antibiotics, diet, probiotics, and fecal microbiota transplantation (FMT). Furthermore, we summarize some completed and ongoing clinical trials of interventions with gut microbes for NDs, which may provide new ideas for studying NDs.

Background: Stroke is not only a major cause of disability but also the third leading cause of death, following heart disease and cancer. It has been established that stroke causes permanent disability in 80% of survivors. However, current treatment options for this patient population are limited. Inflammation and immune response are major features that are well‐recognized to occur after a stroke. The gastrointestinal tract hosts complex microbial communities, the largest pool of immune cells, and forms a bidirectional regulation brain‐gut axis with the brain. Recent experimental and clinical studies have highlighted the importance of the relationship between the intestinal microenvironment and stroke. Over the years, the influence of the intestine on stroke has emerged as an important and dynamic research direction in biology and medicine.Aims: In this review, we describe the structure and function of the intestinal microenvironment and highlight its cross‐talk relationship with stroke. In addition, we discuss potential strategies aiming to target the intestinal microenvironment during stroke treatment.Conclusion: The structure and function of the intestinal environment can influence neurological function and cerebral ischemic outcome. Improving the intestinal microenvironment by targeting the gut microbiota may be a new direction in treating stroke.