课程文献中心 更多>>

关键词： 纹带棒杆菌   生物膜   纹带棒杆菌毒力   菌毛组装蛋白D   多克隆抗体  

摘要： 目的：制备纹带棒杆菌（C. striatum）生物膜形成相关蛋白菌毛组装蛋白D （SpaD）多克隆抗体，分析其抑制C. striatum强产膜株生物膜形成的作用和潜在应用价值。方法：选取2011-2021年内蒙古医科大学附属医院住院患者临床标本中分离的117株C. striatum为研究对象。采用结晶紫染色法检测各菌株生物膜形成能力，实时荧光定量PCR （RT-qPCR）法检测SpaD编码基因spaD在C. striatum强产膜株中的分布。将C. striatum强产膜株分为对照组和蛋白酶K组，采用结晶染色法检测蛋白酶对C. striatum强产膜株生物膜形成能力的抑制作用。蛋白重组技术构建C. striatum SpaD重组蛋白，实验分为对照组和5及10 mg·L-1SpaD重组蛋白组，采用结晶染色法检测SpaD重组蛋白对C. striatum强产膜株生物膜形成能力的抑制作用。并通过动物免疫获得兔抗SpaD多克隆抗体实验分为对照组和1∶400、1∶200及1∶100 SpaD多克隆抗体组，采用结晶紫染色法检测SpaD多克隆抗体对C. striatum强产膜临床株生物膜形成能力的抑制作用。结果：结晶紫染色法检测，强产膜株、中等产膜株和弱产膜株占比分别为47.9%（56/117）、29.0%（34/117）及23.1%（27/117）。RT-qPCR法，所有强产膜株均携带spaD基因。与对照组比较，5和10 mg·L-1SpaD重组蛋白组13株强产膜菌生物膜形成能力均明显降低（P<0.05）。与对照组比较，1∶100和1∶200倍数稀释SpaD兔多克隆抗体组中分别有61.5%（8/13）及7.7%（1/13）的强产膜菌株生物膜形成能力明显降低（P<0.05）。结论：spaD基因在***强产膜株中呈高表达状态。SpaD多克隆抗体可明显抑制C. striatum强产膜株生物膜形成，其抑制效应呈浓度依赖性。SpaD可作为防治C. striatum产膜株感染的新靶点。

关键词： span id="cetext0002">OCTretinal parameterschoroidal vascular indexIBDregressionbiological treatment responseOCToptical coherence tomographyIBDinflammatory bowel diseaseRNFLretinal nerve fiber layerGCIPLganglion cell inner plexiform layerCMTcentral macular thicknessCVIchoroidal vascular distribution indexCC-VDchoroidal capillary vascular densitySF-CTchoroidal thickness in the macular central sulcusUCUlcerative colitisCDCrohn’s diseaseEIMsextraintestinal manifestationsBMIbody mass indexFBGfasting blood glucoseHbAlcglycated hemoglobin  

关键词： Periodontitis   Single-cell sequencing   Fibroblasts   Macrophages  

摘要： ObjectivesTo reveal the cellular composition and molecular environment of the inflammatory infiltrates in residual deep pockets of severe periodontitis following non-surgical periodontal therapy (NSPT). This may provide critical insights for targeted therapy in managing severe ***-cell RNA-seq (scRNA-seq) and bulk RNA-seq of periodontal tissues from patients with severe periodontitis following NSPT and healthy donors were performed. Eligible public datasets of scRNA-seq and bulk RNA-seq were also used for analysis. Multiplex immunohistochemical immunofluorescence was used to validate the identified cell subtypes *** identified a diverse inflammatory microenvironment landscape in the residual deep pockets of severe periodontitis after NSPT, in which IL-6+ fibroblasts were enriched in the deep pocket granulation tissue of severe periodontitis. The hypoxic microenvironment orchestrated by IL-6+ fibroblasts was closely associated with the persistent inflammation in severe periodontitis after NSPT. The infiltration of IL-6+ fibroblasts and FCN1+ macrophages exhibited a strong correlation, suggesting a potential crosstalk between the two cell subtypes. The coexistence of IL-6+ fibroblasts and FCN1+ macrophages was associated with sustained inflammatory responses, response to hypoxia and oxidative stress, osteoclast differentiation, and bone resorption in severe periodontitis after *** study unveiled the presence of a fibroblast-mediated network localized in the hypoxic region of the severe periodontitis that functionally linked macrophages and fibroblasts, which collaborate to exacerbate the periodontal inflammation microenvironment. These findings may offer a new perspective for the targeted treatment of severe periodontitis, especially the targeted treatment against IL-6+ fibroblasts.

关键词： Tau   Microglia   Tau spread   LRP1   Endo-lysosomal dysfunction   Inflammation  

摘要： Microglia are the tissue resident macrophages of the brain and their contribution to tau pathology progression remains to be fully understood. In this study, we developed a quantitative platform to elucidate the processing of extracellular tau within human induced pluripotent stem cell (iPSC)-derived microglia. We show that iPSCderived microglia internalize monomeric and fibrillar tau through different cellular mechanisms and with different clearance kinetics. Acute inflammatory activation of microglia alters tau endocytosis, but surprisingly does not impact tau clearance. These results highlight the importance of the microglial endo-lysosome system as a regulator of tau pathology that is decoupled from acute microglial activation.

关键词： Chronic periodontitis   Interleukin-6   Oral squamous cell carcinoma   Saliva  

摘要： Periodontal disease is an inflammatory disease that affects periodontal tissue, such as the gingiva, periodontal ligament and alveolar bone. Recently, a link between periodontal disease, oral cancer and inflammation has been suggested. In this study, the concentration of the inflammatory cytokine salivary IL-6 was measured to determine its role in the inflammatory process of periodontitis and oral squamous cell carcinoma. An analytical cross-sectional study was conducted at the Khartoum Dental Teaching Hospital, Sudan. Three study groups were enrolled with their consent: patients diagnosed with chronic periodontitis with at least two interproximal sites showing clinical attachment loss > 4 mm and pocket depth > 5 mm. (n = 32); patients with chronic periodontitis and oral squamous cell carcinoma (OSCC) pathology reports of OSCC at the time of saliva collection (n = 22); and matched healthy controls (n = 30). Patients were excluded if they had any chronic inflammatory condition or disease; had a history of recent trauma, acute infection, burns, laceration, previous surgery, chemotherapy, or radiotherapy; had used antibiotics within the previous three months; had a history of periodontal treatment within the previous three months; were pregnant or lactating; were taking drugs that induce hyposalivation; or had a history of previous radiation therapy to the head and neck area. A trained dentist clinically examined the participants. Periodontal parameters (plaque index, bleeding on probing, probable pocket depth and clinical attachment level) were measured, and the IL-6 concentration in the saliva samples was measured via enzyme-linked immunosorbent assay. A statistically significant difference in periodontal parameters was observed between the OSCC patient group and the other groups. OSCC patients had significantly greater IL-6 concentrations in their saliva (log 2.40 ± 0.37) pg/ml) than did chronic periodontitis patients (CP) (log 1.42 ± 0.418 pg/ml) and healthy contro

关键词： IKK   MMPP   NF-κB   ROS   Skin inflammation  

摘要： Keratinocytes play a significant role in regulating skin immune homeostasis, and their dysregulation is central to chronic inflammatory disorders such as atopic dermatitis and psoriasis. Inflammatory mediators such as tumor necrosis factor alpha (TNF-α) and interferon-gamma (IFN-γ) can disrupt this balance, inducing abnormal cytokine and chemokine expression that promotes immune cell infiltration and chronic inflammation in the skin. While (E)-2,4-bis(p-hydroxyphenyl)-2-butenal (BHPB) has shown anti-inflammatory effects, its clinical potential is limited due to poor stability and lack of drug-like properties. To overcome these limitations, (E)-2-Methoxy-4-(3-(4-methoxyphenyl)prop-1-en-1-yl)phenol (MMPP), a stable BHPB analog, was synthesized as a potential therapeutic candidate. This study examined the antioxidant and anti-inflammatory effects of MMPP in TNF-α/IFN-γ-stimulated human HaCaT keratinocytes, assessing its impact on reactive oxygen species (ROS) production and proinflammatory signaling pathways. MMPP significantly reduced ROS levels and inhibited proinflammatory cytokine and chemokine expression by interacting with IKKα/β and suppressing the main downstream IκBα and NF-κB, with additional effects on MAPK, AP-1, and STAT1 pathways. These findings highlight the promise of MMPP as a stable, drug-like agent with therapeutic potential for skin inflammation and oxidative stress by modulating keratinocyte-mediated immune responses.

关键词： cardiac magnetic resonance   constrictive pericarditis   recurrent pericarditis   rilonacept   steroid-sparing therapy   systemic lupus erythematosus   CMR   cardiac magnetic resonance   CRP   C-reactive protein   dsDNA   double-stranded DNA   ESR   erythrocyte sedimentation rate   IL   interleukin   LGE   late gadolinium enhancement   SLE   systemic lupus erythematosus  

摘要：

关键词： Diabetic nephropathy   Interleukin-6   Nicotinamide mononucleotide   Podocyte injury   Proximal tubular epithelial cell   Rab5 signaling  

摘要： BACKGROUND:Diabetic nephropathy (DN) is a leading cause of chronic kidney disease and end-stage renal disease, and is a significant global healthcare burden. Although proximal tubular epithelial cells (PTECs) and podocytes are involved in DN progression, the specific molecular interactions between these cells are not well understood. AIM:To elucidate the role of interleukin-6 (IL-6)/Rab5 signaling in mediating crosstalk between PTECs and podocytes, and to evaluate the protective effects of nicotinamide mononucleotide (NMN) against DN progression. METHODS:We utilized and models to investigate the pathogenesis of DN. , human PTECs and murine podocytes were cultured under high-glucose conditions, and IL-6 neutralizing antibodies or NMN treatments were applied. Podocyte injury was assessed by measurements of nephrin endocytosis, Rab5 activity, cytoskeletal organization, cell adhesion, and cell-spreading assays. , DN was induced in mice using streptozotocin, and mice then received NMN, insulin, or both treatments over an 8-week period. Renal tissues were analyzed histologically, ultrastructurally, and immunochemically, and urinary albumin excretion was measured to assess renal function. Statistical analyses were conducted using one-way ANOVA and Tukey's test. RESULTS:High-glucose conditions induced the epithelial-mesenchymal transition (EMT) in PTECs, increased IL-6 secretion, and activated Rab5 signaling in podocytes, leading to increased nephrin endocytosis and podocyte injury. Blocking IL-6 significantly attenuated these effects. NMN treatment of diabetic mice markedly reduced podocyte injury, glomerular hypertrophy, foot-process effacement, and urinary albumin excretion. Mechanistically, NMN suppressed the EMT and IL-6 secretion by PTECs, inhibited Rab5 activation in podocytes, and prevented nephrin endocytosis, thereby preserving the cytoskeletal integrity and function of podocytes. CONCLUSION:Our findings reveal a novel pathogenic mechanism of DN in which IL-6 re

摘要： Interleukin(IL)-15 is critical for intestinal homeostasis, but the precise origin and functions of IL-15 involved in inflamed mucosal healing are not fully understood. This study demonstrated that IL-15/IL-15Rα signaling was up-regulated during wound healing in 5-fluorouracil(5-FU)-induced intestinal mucositis. Moreover, a subset of podoplanin + stromal cells located adjacent to crypts were the primary cellular source of IL-15 following gut damage. Stroma-specific IL-15 proved to be crucial for the regeneration of damaged intestine. The deletion of IL-15Rα in intestinal epithelial cells compromised the recovery from intestinal injury. Moreover, compared with IL-15, IL-15/IL-15Rα complex can more efficiently promote intestinal epithelial repair. When stimulating human-derived ileal organoids, IL-15/IL-15 complex induced epithelial proliferation through an STAT3-HIF-1α signaling axis and afforded protection against 5-FU-induced epithelial damage. These findings innovatively demonstrated that stroma-specific IL-15 coordinates epithelial IL-15Rα to accelerate wound healing in response to gut damage.