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关键词： 甲型流感病毒   免疫球蛋白M抗体   铁路职工   胶体金法   影响因素  

摘要： 目的 本研究基于血清流行病学调查方法,对上海铁路地区客运乘务人员甲型流感病毒特异性免疫球蛋白M(IgM)抗体阳性率及其影响因素进行系统分析,旨在为制定铁路甲型流感病毒防控策略提供科学依据.方法 基于目的抽样原则,综合考虑工作地点分散化和工作时间差异性,于2025年春运前选取上海地区三个乘务员出勤点的在岗客运乘务人员作为研究样本,发放标准化网络问卷,并对完成问卷填写的受试者实施静脉血样本采集.采用胶体金法检测血清甲型流感病毒IgM抗体水平,并运用SPSS 26.0进行数据分析.结果 血清甲型流感病毒IgM抗体检测结果阳性81份,阳性率为16.46%.研究结果表明,人口学特征(年龄、性别)、职业暴露因素(乘务类型)以及免疫预防措施(流感疫苗接种情况)与甲型流感IgM抗体阳性率在统计学存在显著关联(P＜0.05).结论 492 名上海铁路地区客运乘务人员中,＜25 岁、女性、高铁乘务服务人员以及未接种季节性流感疫苗的人群表现出更高的血清甲型流感病毒IgM抗体阳性率(P＜0.05).铁路客运单位应加强客运乘务人员在密闭值乘环境中的健康防护,有效降低职业暴露风险;鼓励客运乘务人员在没有接种禁忌的情况下进行甲型流感疫苗接种,多措并举,构建有效的防控屏障.

关键词： Fraxetin   Rheumatoid arthritis   Collagen-induced arthritis   Fibroblast-like synoviocytes   MAPKs   MEK inhibitor  

摘要： Rheumatoid arthritis (RA) is a chronic autoimmune disease that profoundly affects patients' lives. Developing new treatments by screening small molecule compounds targeting RA-related signaling pathways is a key area of research. This study employs bioinformatics analysis, Western blotting, and cellular thermal shift assay (CETSA) to demonstrate, for the first time, that fraxetin may function as a novel natural MEK inhibitor, modulating RA pathogenesis via the MEK/ERK signaling pathway. We further evaluated fraxetin's therapeutic effects on collagen-induced arthritis (CIA) in rats in vivo and its inhibitory effects on TNF alpha-induced arthritic fibroblast-like synoviocytes (FLSs) in vitro. The results showed that fraxetin significantly alleviated ankle joint inflammation and bone destruction in CIA rats and markedly suppressed TNF alpha-induced proliferation, migration, and cytokine secretion (IL-1(3, IL-6, and TNF alpha) in arthritic FLSs. These findings highlight fraxetin's potential as a promising therapeutic agent for RA.

关键词： NSCLC   Sarcopenia   Immunometabolism   Muscle degradation   IL-6  

摘要： Non-small cell lung cancer (NSCLC) is the most prevalent subtype of lung cancer and a leading cause of cancerrelated mortality worldwide. Literature evidences indicates a strong association between systemic inflammation, driven by cytokines such as Interleukin-6 (IL-6), and the development of NSCLC-associated sarcopenia. However, the immuno-metabolic underpinnings that link tumor-derived IL-6 signaling to skeletal muscle degradation remain incompletely understood. We developed a comprehensive immuno-metabolic mathematical model to investigate how IL-6 signaling influences branched-chain amino acids (BCAA) metabolism and redox homeostasis in the context of NSCLC-induced sarcopenia by understanding two key causes of sarcopenia which are malnutrition and redox homeostasis. Our model proposes that IL-6 alters tumor metabolism by activating the STAT3 pathway. Elevated IL-6 impairs protein synthesis, proteolysis, and muscle atrophy by interfering with insulin signaling, inhibiting mTORC1 activation, and increasing oxidative stress. Additionally, it reveals a central role for IL-6-driven metabolic rewiring, particularly BCAA utilization and redox imbalance, in promoting NSCLCinduced sarcopenia. These findings underscore the dual impact of IL-6 on tumor progression and systemic muscle degradation, and provide a framework for evaluating therapeutic strategies that target IL-6/STAT3 signaling and amino acid metabolism via STAT3 and acetyl-CoA cross talk to mitigate NSCLC-induced sarcopenia.

关键词： Colorectal cancer   NF-kappa B p65/RelA   NLRP3 inflammasome   Lipid droplets   Metformin   Monocyte subsets   Tumor microenvironment   Tumor-conditioned medium  

摘要： Background: Colorectal cancer (CRC) generates a complex tumor microenvironment (TME) known to profoundly alter the function and phenotype of immune cells, including monocytes. Key aspects of this environment can be mimicked by tumor-conditioned medium (TCM). Metformin has emerged as a promising candidate to counteract TCM-induced immune and inflammatory dysregulation. Therefore, this study aimed to evaluate the effects of metformin on NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome expression, monocyte subset distribution, and lipid droplet (LD) accumulation upon exposure to colorectal TCM. Methods: Assays were performed on primary human monocytes exposed to colorectal TCM in the presence or absence of metformin. Results: TCM significantly increased nitric oxide (NO, p < 0.001) and hydrogen peroxide (H2O2, p < 0.001) production, intracellular free calcium ions (Ca-if(2+)) (p < 0.001) levels, expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B p65/RelA, p < 0.001), NLRP3 (p < 0.01), and interleukin-1 beta (IL-1 beta, p < 0.0001), as well as intracellular triacylglycerols ((i)TAGs, p < 0.05), total cellular cholesterol content (tccCHOL, p < 0.001), and lipid droplet accumulation (p < 0.05). It also impaired phagocytic activity (p < 0.05) and altered monocyte phenotype, along with a shift toward a CD14(low), CD16(high) phenotype (p < 0.0001 for both markers). Notably, metformin treatment exerted broad and significant reversing effects, specifically on respiratory burst (NO, p < 0.05;H2O2, p < 0.01), Ca-if(2+) levels (p < 0.01), NF-kappa B p65/RelA and NLRP3 expression, and IL-1 beta production (p < 0.0001 for all), and the lipid droplet accumulation (p < 0.0001), (i)TAGs (p < 0.001), and tccCHOL (p < 0.01). Metformin also significantly restored CD14 expression (p < 0.05) and increased CD14(+) monocyte frequency (p < 0.01), while reducing CD16 expression (p < 0.05) and CD16(+) monocyte frequency (p < 0.01). Ho

关键词： Gut macrophages   IL-10   IL-1 beta   IL-1receptor   Intestinal homeostasis   Inflammatory bowel disease  

摘要： Inflammatory bowel disease (IBD) is a chronic condition characterized by intestinal immune imbalance. Gut macrophages help maintain homeostasis by producing interleukin-10 (IL-10), which prevents excessive immune responses. However, the mechanism of IL-10 production remains unclear. This study hypothesized that an IL-1 receptor (IL-1R)-dependent pathway, independent of gut microbes, contributes to IL-10 production in gut macrophages. We compared Il10 expression in gut macrophages from germ-free (GF) and specific-pathogen-free (SPF) wildtype mice and SPF MyD88 knockout (KO) mice. Il1r1 expression was assessed, and IL-1 beta stimulation was tested on murine gut macrophages and RAW 264.7 cells overexpressing IL-1R1. We analyzed the involvement of MyD88, p38, ERK, and CREB in IL-1R1 signaling using small interfering RNA (siRNA). Il10 expression did not differ between GF and SPF wild-type mice but decreased in MyD88 KO mice. Il1r1 expression was higher in gut macrophages than in other macrophage types. IL-1 beta stimulation induced Il10 expression and IL-10 production in IL-1R1-overexpressing RAW 264.7 cells, activating p38, ERK, and CREB. Suppression of MyD88 or CREB reduced Il10 expression and IL-10 production. These findings suggest that the IL-1 beta/IL-1R-MyD88-CREB pathway, involving p38 and ERK, functions as a microbe-independent IL-10 production mechanism in gut macrophages, sharing signaling cascades with bacterial lipopolysaccharide pathways. Further studies using human gut macrophages are needed to explore their relevance to IBD pathogenesis.

关键词： Regulatory B cells   STING   IRF3   IL-35   Hemozoin   TLR9  

摘要： Augmented regulatory B cell (Breg) responses are commonly observed in malaria;however, the specific parasite components and Breg subtypes involved remain unclear. In this study, we investigated C57BL/6 mice infected with Plasmodium berghei ANKA, which induces cerebral malaria pathology, in comparison to P. yoelii YM, which does not. We found that distinct Breg types differentiated in response to these infections, driven by hemozoinmediated Toll-like receptor 9 activation. Interleukin-35-positive (IL-35+) Breg expansion occurred in P. yoelii YM-infected mice but not in those infected with P. berghei ANKA. We demonstrated that stimulator of interferon genes (STING)-mediated interferon regulatory factor 3 (IRF3) phosphorylation suppressed IL-35+ Breg differentiation, potentially contributing to experimental cerebral malaria (ECM). In contrast, P. yoelii YM infection activated IRF3 in a STING-independent manner, promoting IL-35+ Breg expansion. These findings highlight IL-35+ Bregs as key modulators in malarial immunopathology.

关键词： 猪流行性腹泻病毒   兔多抗   中和活性  

摘要： 为了探究兔多克隆抗体在猪流行性腹泻病毒检测和鉴定中的有效性。本研究通过Vero细胞大量培养了猪流行性腹泻病毒（PEDV），并利用蔗糖密度梯度离心法对其进行了浓缩纯化。以纯化后的PEDV免疫新西兰白兔四次，采集收获了大量PEDV兔血清，用饱和硫酸铵沉淀法对其进行粗提，再用亲和层析法纯化得到PEDV兔多抗。ELISA检测结果显示，PEDV兔多抗的ELISA效价为1∶32000。间接免疫荧光试验结果表明，PEDV兔多抗能够识别PEDV-XD（G2a型）株、PEDV G1型CV777株，但不与猪其他易感病原猪瘟病毒C株（CSFV-C）、猪伪狂犬病毒K61株（PRVbartha-K61）发生反应，这提示，本研究制备的PEDV兔多抗具有检测的广谱性和特异性。Western blot鉴定结果显示，PEDV兔多抗能够与PEDV G2a和G1型的核衣壳蛋白N、刺突蛋白S、膜蛋白M发生特异性识别，其中，对N蛋白识别信号最强。此外，PEDV兔多抗具有体外中和活性，对PEDV-XD（G2a型）株的中和IC50为1.418μg/mL，对G1型CV777株的中和IC50为5.524 μg/mL，这表明PEDV兔多抗具有治疗潜力。综上，本研究为PEDV检测和鉴定提供了经济高效的多抗试剂，为PEDV治疗性抗体开发奠定了基础。

关键词： 栀子苷   溃疡性结肠炎   结肠黏膜损伤   IL/6/JAK2/STAT3信号通路   肠道微生物群  

摘要： 目的 探讨栀子苷对溃疡性结肠炎(UC)的缓解作用及其潜在作用机制。方法 使用5%硫酸葡聚糖钠(DSS)诱导UC小鼠模型,并随机分为6组(n=8):正常对照组、模型组、柳氮磺吡啶组[100 mg/(kg·d)]、栀子苷低剂量组[10 mg/(kg·d)]、栀子苷中剂量组[20 mg/(kg·d)]、栀子苷高剂量组[40 mg/(kg·d)],灌胃给药,持续10 d。测量结肠长度和小鼠体质量,评分结肠黏膜损伤指数(CMDI)和疾病活动指数(DAI);采用苏木精-伊红(HE)染色观察结肠组织病理变化;试剂盒检测结肠组织丙二醛(MDA)、髓过氧化物酶(MPO)、过氧化氢酶(CAT)和谷胱甘肽(GSH)水平;采用酶联免疫吸附试验(ELISA)分析结肠组织肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-6和IL-1β表达水平;采用蛋白质印迹(Western blot)检测结肠组织黏蛋白1(MUC-1)、occlucdin、IL-6、p-JAK2、p-STAT3蛋白表达。结果 与正常对照组相比,模型组小鼠体质量、结肠长度下降(P<0.01);MUC-1、occludin蛋白表达降低(P<0.01);CAT、SOD活性降低(P<0.01);DAI评分、CMDI评分升高(P<0.01);TNF-α、IL-6和IL-1β表达水平升高(P <0.01);MPO、MDA含量升高(P <0.01);IL-6、p-JAK2、p-STAT3蛋白表达升高(P <0.01)。与模型组相比,柳氮磺吡啶组和栀子苷中、高剂量组小鼠体质量、结肠长度增加(P <0.05或P <0.01),MUC-1、occludin蛋白表达及CAT、SOD活性升高(P <0.05或P<0.01),DAI评分、CMDI评分降低(P <0.05或P<0.01),TNF-α、IL-6和IL-1β表达水平减少(P <0.05或P<0.01),MPO、MDA含量降低(P <0.05或P<0.01);IL-6、p-JAK2、p-STAT3蛋白表达降低(P<0.05或P<0.01)。结论 栀子苷通过调节肠道菌群结构维持肠道稳态,并通过抑制IL-6/JAK2/STAT3通路激活,改善UC小鼠结肠炎损伤。

关键词： 3型固有淋巴细胞(ILC3)   肾脏纤维化(RF)   作用机制   研究进展   跨器官调控   综述  

摘要： 3型固有淋巴细胞（ILC3）是一类由转录因子维甲酸受体相关孤儿受体γt（RORγt）调控的固有免疫细胞，主要分布于肠道黏膜及淋巴组织中，其通过分泌白细胞介素17（IL-17）、IL-22和粒细胞-巨噬细胞集落刺激因子（GM-CSF）等细胞因子，在维持肠道黏膜稳态、抵御病原体侵袭及调节免疫反应中发挥重要作用。肾脏纤维化（RF）是由创伤、感染、炎症或代谢异常等致病因素引发的病理过程，表现为肾脏固有细胞受损、细胞外基质（ECM）异常沉积及肾实质渐进性硬化，最终导致肾功能不可逆的丧失。最新研究揭示，ILC3不仅在维持肠道平衡方面发挥作用，还参与了RF的进程。因此，本文综述了ILC3在RF中跨器官调控作用机制的研究进展，旨在为RF的防治提供新的视角。

关键词： 支原体肺炎   体液免疫   炎症因子   免疫球蛋白   临床诊断  

摘要： 目的:系统探究支原体肺炎患儿血清体液免疫检测指标的变化规律及其与疾病发生发展的关联性,为临床评估患儿免疫功能状态、疾病的监测及判断预后提供可靠的依据。方法:选取2023年5月-2024年5月确诊的67例支原体肺炎患儿纳入观察组,选取同一时间段67例健康儿童纳入对照组。采集所有研究对象的空腹静脉血,对2组血清中炎症细胞因子和免疫球蛋白水平进行检测,并比较分析2组数据差异。结果:经检测,观察组患儿血清中的炎症细胞因子白细胞介素-6(IL-6)、白细胞介素-8(IL-8)及肿瘤坏死因子-α(TNF-α)水平均高于对照组,观察组患儿血清IgG、IgA、IgM水平高于对照组,差异具有统计学意义(P<0.05)。结论:支原体肺炎患儿存在的体液免疫激活与炎症因子网络失衡,这些指标的变化可能参与了支原体肺炎的病理生理过程,对其检测可作为病情评估及疗效监测的重要辅助手段,为个体化治疗提供免疫学分型的依据。