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Background Growing evidences indicate that the alterations in gut microbiota are associated with the efficacy of glucocorticoids (GCs) in the treatment of systemic lupus erythematosus (SLE). However, there is no evidence to prove whether gut microbiota directly mediates the effects of GCs. Methods Using the MRL/lpr mice, this study firstly addressed the effects of three doses of prednisone on gut microbiota. Then, this study used fecal microbiota transplantation (FMT) to transfer the gut microbiota of prednisone-treated MRL/lpr mice into the blank MRL/lpr mice to reveal whether the gut microbiota regulated by prednisone had similar therapeutic efficiency and side effects as prednisone. Results The effects of prednisone on gut microbiota were dose-dependent in the treatment of MRL/lpr mice. After transplantation into MRL/lpr mice, prednisone-regulated gut microbiota could alleviate lupus, which might be due to decreasing Ruminococcus and Alistipes and retaining the abundance of Lactobacillus . However, prednisone-regulated gut microbiota did not exhibit side effects as prednisone. The reason might be that the pathogens upregulated by prednisone could not survive in the MRL/lpr mice as exogenous microbiota, such as Parasutterella , Parabacteroides , and Escherichia-Shigella . Conclusions These data demonstrated that the transplantation of gut microbiota may be an effective method to obtain the therapeutic effects of GCs and avoid the side effects of GCs.

Wound care is a major healthcare expenditure. Treatment of burns, surgical and trauma wounds, diabetic lower limb ulcers and skin wounds is a major medical challenge with current therapies largely focused on supportive care measures. Successful wound repair requires a series of tightly coordinated steps including coagulation, inflammation, angiogenesis, new tissue formation and extracellular matrix remodelling. Zinc is an essential trace element (micronutrient) which plays important roles in human physiology. Zinc is a cofactor for many metalloenzymes required for cell membrane repair, cell proliferation, growth and immune system function. The pathological effects of zinc deficiency include the occurrence of skin lesions, growth retardation, impaired immune function and compromised would healing. Here, we discuss investigations on the cellular and molecular mechanisms of zinc in modulating the wound healing process. Knowledge gained from this body of research will help to translate these findings into future clinical management of wound healing.

Hydrogels, comprising 3D hydrophilic polymer networks, have emerged as promising biomaterial candidates for emulating the structure of biological tissues and delivering drugs through topical administration with good biocompatibility. Nanozymes can catalyze endogenous biomolecules, thereby initiating or inhibiting biological processes. A nanozyme-hydrogel composite inherits the biological functions of hydrogels and nanozymes, where the nanozyme serves as the catalytic core and the hydrogel forms the structural scaffold. Moreover, the composite can concentrate nanozymes in targeted lesions and catalyze the binding of a specific group of substrates, resulting in pathological microenvironment remodeling and drug-penetrating barrier impairment. The composite also shields nanozymes to prevent burst release during catalytic production and reduce related toxicity. Currently, the application of these composites has been extended to antibacterial, anti-inflammatory, anticancer, and tissue repair applications. In this review, we elucidate the preparation methods for nanozyme-hydrogel composites, provide compelling evidence of their advantages in drug delivery and provide a comprehensive overview of their biological application.

Background The assessment and characterization of the gut microbiome has become a focus of research in the area of human autoimmune diseases. Ankylosing spondylitis is an inflammatory autoimmune disease and evidence showed that ankylosing spondylitis may be a microbiome-driven disease. Results To investigate the relationship between the gut microbiome and ankylosing spondylitis, a quantitative metagenomics study based on deep shotgun sequencing was performed, using gut microbial DNA from 211 Chinese individuals. A total of 23,709 genes and 12 metagenomic species were shown to be differentially abundant between ankylosing spondylitis patients and healthy controls. Patients were characterized by a form of gut microbial dysbiosis that is more prominent than previously reported cases with inflammatory bowel disease. Specifically, the ankylosing spondylitis patients demonstrated increases in the abundance of Prevotella melaninogenica , Prevotella copri , and Prevotella sp. C561 and decreases in Bacteroides spp. It is noteworthy that the Bifidobacterium genus, which is commonly used in probiotics, accumulated in the ankylosing spondylitis patients. Diagnostic algorithms were established using a subset of these gut microbial biomarkers. Conclusions Alterations of the gut microbiome are associated with development of ankylosing spondylitis. Our data suggest biomarkers identified in this study might participate in the pathogenesis or development process of ankylosing spondylitis, providing new leads for the development of new diagnostic tools and potential treatments.

Background Cancer cells develop resistance to chemotherapeutic intervention by excessive formation of stress granules (SGs), which are modulated by an oncogenic protein G3BP2. Selective control of G3BP2/SG signaling is a potential means to treat non-small cell lung cancer (NSCLC). Methods Co-immunoprecipitation was conducted to identify the interaction of MG53 and G3BP2. Immunohistochemistry and live cell imaging were performed to visualize the subcellular expression or co-localization. We used shRNA to knock-down the expression MG53 or G3BP2 to test the cell migration and colony formation. The expression level of MG53 and G3BP2 in human NSCLC tissues was tested by western blot analysis. The ATO-induced oxidative stress model was used to examine the effect of rhMG53 on SG formation. Moue NSCLC allograft experiments were performed on wild type and transgenic mice with either knockout of MG53, or overexpression of MG53. Human NSCLC xenograft model in mice was used to evaluate the effect of MG53 overexpression on tumorigenesis. Results We show that MG53, a member of the TRIM protein family (TRIM72), modulates G3BP2 activity to control lung cancer progression. Loss of MG53 results in the progressive development of lung cancer in mg53 -/- mice. Transgenic mice with sustained elevation of MG53 in the bloodstream demonstrate reduced tumor growth following allograft transplantation of mouse NSCLC cells. Biochemical assay reveals physical interaction between G3BP2 and MG53 through the TRIM domain of MG53. Knockdown of MG53 enhances proliferation and migration of NSCLC cells, whereas reduced tumorigenicity is seen in NSCLC cells with knockdown of G3BP2 expression. The recombinant human MG53 (rhMG53) protein can enter the NSCLC cells to induce nuclear translation of G3BP2 and block arsenic trioxide-induced SG formation. The anti-proliferative effect of rhMG53 on NSCLC cells was abolished with knockout of G3BP2. rhMG53 can enhance sensitivity of NSCLC cells to undergo cell death upon treatment with cisplatin. Tailored induction of MG53 expression in NSCLC cells suppresses lung cancer growth via reduced SG formation in a xenograft model. Conclusion Overall, these findings support the notion that MG53 functions as a tumor suppressor by targeting G3BP2/SG activity in NSCLCs.

Background Humidity was an unfavorable factor for patients with rheumatoid arthritis (RA). RA disease activity was severe in high humidity conditions. However, there is no evidence to demonstrate the effects of humidity on arthritis in the animal experiments and explore its relevant mechanism. Methods Using the DBA/1 mice, this study addressed the effects of a high humidity (80 ± 5%) on arthritis in collagen-induced arthritis (CIA) mice. Then, this study used the gas chromatography-mass spectrometer (GC-MS) to explore alterations in serum metabolome caused by the high humidity. Furthermore, xylitol and L-pyroglutamic acid, which were both significantly upregulated by the high humidity, were selected to further study their effects on arthritis in the CIA mice. Results The high humidity (80 ± 5%) could aggravate arthritis variables including increasing arthritis score and swelling, serum autoantibodies (anti-COII and anti-CCP), and proinflammatory cytokines (IL-6, IL-17A, and G-CSF). In addition, the high humidity could cause significant alterations in serum metabolome in the CIA mice. Xylitol and L-pyroglutamic acid were the representative serum metabolites that were significantly upregulated by the high humidity. Further experiments demonstrated that the supplementation of 0.4 mg/mL xylitol in drinking water after inducing the CIA model and 2.0 mg/mL in drinking water before inducing the CIA model could both aggravate arthritis in the CIA mice. Conclusions These data demonstrated that high humidity was not beneficial for arthritis development and its mechanism might be associated with xylitol and L-pyroglutamic acid.

Oxygen deficiency after myocardial infarction (MI) leads to massive cardiac cell death. Protection of cardiac cells and promotion of cardiac repair are key therapeutic goals. These goals may be achieved by re-introducing oxygen into the infarcted area. Yet current systemic oxygen delivery approaches cannot efficiently diffuse oxygen into the infarcted area that has extremely low blood flow. In this work, we developed a new oxygen delivery system that can be delivered specifically to the infarcted tissue, and continuously release oxygen to protect the cardiac cells. The system was based on a thermosensitive, injectable and fast gelation hydrogel, and oxygen releasing microspheres. The fast gelation hydrogel was used to increase microsphere retention in the heart tissue. The system was able to continuously release oxygen for 4 weeks. The released oxygen significantly increased survival of cardiac cells under the hypoxic condition (1% O 2 ) mimicking that of the infarcted hearts. It also reduced myofibroblast formation under hypoxic condition (1% O 2 ). After implanting into infarcted hearts for 4 weeks, the released oxygen significantly augmented cell survival, decreased macrophage density, reduced collagen deposition and myofibroblast density, and stimulated tissue angiogenesis, leading to a significant increase in cardiac function.

Objective This meta-analysis aims to explore the potential link between vaccines and systemic lupus erythematosus (SLE). Methods We systematically searched PubMed, Cochrane Library, and Embase for observational studies from inception to September 3, 2023, using medical subject headings (MeSH) and keywords. Study quality was assessed using the NOS scale. Statistical analyses were conducted using STATA software (version 14.0). Publication bias was evaluated using funnel plots and Egger’s regression. Results The meta-analysis incorporated 17 studies, encompassing 45,067,349 individuals with follow-up periods ranging from 0.5 to 2 years. The pooled analysis revealed no significant association between vaccinations and an increased risk of SLE [OR = 1.14, 95% CI (0.86–1.52), I 2  = 78.1%, P  = 0.348]. Subgroup analyses indicated that HBV vaccination was significantly associated with an elevated risk of SLE [OR =2.11, 95% CI (1.11-4.00), I 2  = 63.3%, P  = 0.02], HPV vaccination was slightly associated with an increased risk of SLE [OR = 1.43, 95% CI (0.88–2.31), I 2  = 72.4%, P  = 0.148], influenza vaccination showed no association with an increased risk of SLE [OR = 0.96, 95% CI (0.82–1.12), I 2  = 0.0%, P  = 0.559], and COVID-19 vaccine was marginally associated with a decreased risk of SLE [OR = 0.44, 95% CI (0.18–1.21), I 2  = 91.3%, P  = 0.118]. Conclusions This study suggests that vaccinations are not linked to an increased risk of SLE. Our meta-analysis results provide valuable insights, alleviating concerns about SLE risk post-vaccination and supporting further vaccine development efforts.

Rheumatoid arthritis (RA) and chronic obstructive pulmonary disease (COPD) are prevalent and incapacitating conditions, sharing common pathogenic pathways such as tobacco use and pulmonary inflammation. The influence of respiratory conditions including COPD on RA has been observed, meanwhile RA may constituting one of the risk factors for COPD. It unclear that whether a bidirectional associate between RA and COPD. Our study aims to explore the bidirectional relationship between RA and COPD. We systematically searched PubMed, Cochrane Library, and Embase for observational studies from the databases inception to February 20, 2024, utilizing medical subject headings (MeSH) and keywords. We included studies in which RA and COPD were studied as either exposure or outcome variables. Statistical analyses were conducted employing STATA software (version 14.0). The relationship was reported as odds ratios (OR) and corresponding 95% confidence intervals (CI). Publication bias was assessed using funnel plots and Egger's regression. Nineteen studies with 1,549,181 participants were included. Risk of bias varied from low to moderate, with evidence levels rated as low or very low. Pooled analysis revealed a significant association between RA and increased COPD risk (OR=1.41, 95%CI 1.13 to 1.76, I = 97.8%, =0.003). Subgroup analyses showed similar COPD risk elevations in both of genders, seropositive/seronegative RA, cohort and case control studies. Additionally, there was a significant RA risk increase among those with COPD (OR=1.36, 95%CI 1.05 to 1.76, I = 55.0%, =0.022), particularly among females and seropositive RA, and cohort studies. The meta-analysis identifies a significant bidirectional association between RA and COPD, emphasizing mutually increased risk. Recognizing this connection may can inform proactive approaches to disease prevention and management, potentially reducing the public health burden and improving quality of life. https://www.crd.york.ac.uk/PROSPERO/, identifier CRD42024518323.

Hyperuricemia (HUA) is a metabolic disorder characterized by elevated serum uric acid (UA) level, which would trigger inflammatory processes contributing to kidney damage. Acupuncture stimulation of BL23, a therapeutic strategy in traditional Chinese medicine (TCM), has been reported to promote diuresis and suppress the immune system and seems to be efficacious in HUA. In this study, we aimed to investigate the effect of electroacupuncture (EA) at BL23 on HUA and HUA‐induced kidney inflammation and dysfunction in mice. Mice received EA once daily after being given intragastric potassium oxonate (500 mg/kg) and adenine (100 mg/kg). EA administration not only decreased the levels of serum UA, creatinine, blood urea nitrogen, urinary UA, and protein, along with increased urinary CREA excretion, but also decreased the inflammatory cytokines productions (IL‐1 β , IL‐6, and TNF‐ α ) in serum. scRNA‐seq of treated kidneys revealed that EA at BL23 suppressed the NLRP3 inflammasome complex, the IL‐6/JAK/STAT3 signaling pathway, and the production of IL‐6 and IL‐1 β in HUA mice. Western blot analyses verified that EA suppressed the HUA‐induced NLRP3 inflammasome activation by promoting autophagy. In conclusion, the study demonstrated that EA at BL23 exhibited anti‐HUA and nephroprotective effects by inhibiting both the NLRP3 inflammasome and the IL‐6/JAK/STAT3 signaling pathway, reducing renal inflammation and supporting its therapeutic potential for HUA‐associated kidney injury.