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关键词： Cutaneous wound healing   Bone marrow mesenchymal stem cells (BMSCs)   Exosomes   IL-1 beta-BMSC-exos   SIRT6   NLRP3  

摘要： Cutaneous wound healing is a complex process of tissue repair and remodeling that includes inflammation, proliferation, and regeneration. Mesenchymal stem cell (MSCs) therapy has emerged as a widely studied therapeutic approach, demonstrating promising therapeutic potential. The purpose of this work is to examine the function and mechanism of exosomes produced from bone marrow mesenchymal stromal cells (BMSCs) pretreatment with IL-1(3 in the healing of skin injuries. Exosomes were extracted from both untreated BMSCs and those treated with IL-1(3. HUVEC proliferation, migration, angiogenesis, and apoptosis were assessed through CCK-8, Transwell, tube formation, qPCR, western blot, and flow cytometry. Wound healing in mice was evaluated using H&E staining, Masson's staining, and immunofluorescence. IL-1(3-BMSC-exos significantly enhance the proliferation, migration, and angiogenesis of HUVECs. LPS treatment induces the expression of NLRP3 and SIRT6 in HUVECs and the acetylation of NLRP3, but these effects are mitigated by treatment with IL-1(3-BMSC-exos. Knockdown of SIRT6 reverses the pro-angiogenic and anti-inflammatory effects of IL-1(3-BMSC-exos by inhibiting NLRP3-mediated inflammation. Furthermore, IL-1(3-BMSC-exos reduce skin wound area, increase collagen deposition, promote neovascularization, and accelerate wound healing in a mouse model of skin injury. IL-1(3-BMSC-exos have been shown to effectively promote cutaneous wound healing, primarily through the modulation of the SIRT6/NLRP3 signaling pathway, thereby accelerating the repair process of skin trauma. This suggests that IL-1(3-BMSC-exos hold therapeutic potential as a future treatment strategy for cutaneous wound healing.

关键词： Rheumatoid arthritis   FLS   BMP9   Inflammatory response  

摘要： Rheumatoid arthritis (RA) represents a chronic autoimmune disease in which fibroblast-like synoviocytes (FLS) are pivotal contributors to disease pathogenesis. Reportedly, BMP9 inhibits the proliferation and migration of FLS in adjuvant-induced arthritis (AIA). Herein, we examined whether BMP9 suppresses the inflammatory response of RA FLS. The experimental results demonstrated a significant downregulation of BMP9 in RA synovial tissues, exhibiting an inverse correlation with TNF-alpha expression patterns. BMP9 silencing exacerbated TNF alpha-mediated inflammatory responses in RA FLS, leading to substantial upregulation of IL-1 beta, IL-6, CXCL2, CXCL3, and CXCL5 expression levels. Conversely, BMP9 overexpression attenuated the inflammatory responses following stimulation with TNF-alpha and blocked the expression of IL-1 beta, IL-6, CXCL2, CXCL3, and CXCL5. Furthermore, BMP9 overexpression differentially regulated Smad signaling pathways by downregulating p-Smad2/3 while enhancing p-Smad1/5/9 activation. These findings demonstrate that BMP9 exerts anti-inflammatory effects in RA FLS by modulating Smad-dependent signaling pathways.

关键词： Acute liver injury   Autoimmune hepatitis   IL-23/JAK2/STAT3 signaling pathway   Th17 differentiation   Tubuloside B  

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关键词： Psoriatic arthritis   Anti-TNF alpha therapy   Nailfold videocapillaroscopy   Early scleroderma pattern   Drug-induced autoimmunity   Microvascular changes  

摘要： Tumor necrosis factor-alpha (TNF alpha) inhibitors have profoundly transformed the therapeutic landscape of psoriatic arthritis (PsA), offering effective control of synovitis, enthesitis, and axial disease, while preventing progressive joint destruction. However, emerging evidence suggests that TNF alpha blockade may be temporally associated with autoimmune phenomena, including vasculitis, drug-induced lupus erythematosus, and systemic sclerosis-like manifestations. The potential impact of vascular homeostasis and endothelial function changes secondary to TNF alpha inhibition has emerged as a topic of considerable clinical interest. Through a detailed case presentation and comprehensive literature review, we examine the case of a 30-year-old male with PsA who, during maintenance therapy with adalimumab, developed a capillaroscopic pattern characterized by megacapillaries and microhemorrhages, consistent with early systemic sclerosis (SSc) features, despite the absence of overt connective tissue disease manifestations. Comprehensive immunological screening excluded specific autoantibodies typically associated with SSc, and extensive instrumental evaluations ruled out internal organ involvement. This clinical observation, analyzed within the context of current literature, highlights the need for understanding the potential temporal relationship between long-term TNF alpha inhibition and microvascular changes, while supporting the prospective use of nailfold videocapillaroscopy (NVC) as a valuable surveillance tool in biologic-treated cohorts. Early recognition of subclinical vascular abnormalities may enhance risk stratification and guide tailored monitoring strategies in selected patients.

关键词： Biomarker   Cytokine   Hodgkin lymphoma   IL-18   Inflammation   Prognosis  

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