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摘要： Innate immunity is the first line of host defense and contributes to pain. However, how innate immune system interacts with sensory neurons to govern pain remains poorly understood. Here, we report that interleukin 33(IL-33) initiates pain hypersensitivity that requires chemokine (C-C motif) ligand 2 (CCL2) secretion from infiltrated macrophages and neutrophils and activation of transient receptor potential vanilloid 1 (TRPV1) and transient receptor potential melastatin 8 (TRPM8) channels in sensory neurons. Blocking CCL2 receptor (CCR2) attenuates IL-33- induced and Complete Freund's adjuvant (CFA)-induced thermal hyperalgesia and blocking TRPV1 and TRPM8 attenuates IL-33-induced mechanical and thermal hypersensitivity and cold allodynia respectively. Furthermore, depletion of macrophages reduces IL-33-induced pain and expression of CCL2 and suppression of tumorigenicity 2 (ST2) in hindpaw skin and inhibition of CCR2 prevents recruitment of macrophages and neutrophils. Our findings reveal an unrecognized neuroimmune crosstalk of IL-33-CCL2 signaling from infiltrated immune cells with TRPV1/TRPM8 in sensory neurons to facilitate pain states.

关键词： post-COVID-19 condition   long-COVID-19   vitamin D-3 supplementation   cholecalciferol   interleukin-6   glutathione peroxidase activity   respiratory symptoms   anxiety   depression  

摘要： Coronavirus disease 2019 (COVID-19) presents with various symptoms, and some patients develop post-COVID-19 condition (PCC). Vitamin D has shown therapeutic potential in COVID-19 and may offer benefits for PCC. The aim of this study was to evaluate the differences associated with two supplementation strategies (bolus and daily) on interleukin-6 (IL-6) levels, glutathione peroxidase (GPx) activity, and clinical outcomes in PCC patients, regardless of whether target 25 (OH) D levels reached the ideal range. We conducted a self-controlled study in which 54 participants with PCC were supplemented with vitamin D-3 (n = 28 bolus and n = 26 daily) for 2 months. Blood samples were collected to measure IL-6 levels and GPx activity using spectrophotometric methods. The Hospital Anxiety and Depression Scale (HADS) was used to assess mental function. Both bolus and daily vitamin D supplementation were significantly associated with increased GPx activity and decreased IL-6 levels. Daily supplementation was additionally associated with a significant reduction in anxiety and depression scores. However, neither regimen was associated with improvements in cough, dyspnea, or fatigue. These findings suggest a potential association between vitamin D supplementation and improvements in antioxidant and neuropsychiatric parameters in PCC, possibly mediated by its immunomodulatory and antioxidant properties. Further placebo-controlled trials are warranted to determine whether these observed associations reflect causal relationships.

关键词： IL-34   IL-35   gastric cancer   TAMs   prognosis  

摘要： Gastric cancer (GC) remains a major challenge due to its high mortality and morbidity, despite extensive research. Dysregulated host immunity plays a critical role in carcinogenesis, particularly among susceptible cohorts. In the gastric mucosa of GC patients, a reduction in IL-34 and TAM1, accompanied by an increase in TAM2 via M-CSF, enhances Th2 cell function, reduces pro-inflammatory activity, and elevates anti-inflammatory responses. Consequently, TAM2 acts in both paracrine and autocrine manners to polarize and boost TAM2, creating a tumour-favourable microenvironment that supports GC progression. High levels of TAM2, observed during advanced GC stages, suppress gastric IL-34 production, further promoting GC development. In contrast, IL-35, a cytokine involved in immune regulation and suppression, is produced by activated T cells and/or B cells in the affected gastric mucosa. Persistent H. pylori infection in GC tissues is associated with significant infiltration of IL-35-producing B cells and regulatory T cells (Tregs), which enhance the immunosuppressive and pro-tumour microenvironment by disrupting the local immune balance. Upregulated mucosal IL-35 promotes the polarization of TAM2 and Tregs while suppressing TAM1 cells, fostering a tumour-friendly environment that allows transformed gastric mucosal cells to evade immune surveillance, particularly in chronic H. pylori-infected patients. This cascade enhances proliferation and invasion while suppressing differentiation and apoptosis of GC cells. Together, the differential regulation of these cytokines creates an environment that supports cancer progression and resistance to therapy. Targeting the IL-34 and IL-35 pathways may offer a novel therapeutic strategy for improving outcomes in GC patients.

关键词： 急性淋巴细胞白血病   移植   口腔黏膜炎   护理干预  

摘要： 探讨和分析儿童急性淋巴细胞白血病移植后口腔黏膜炎的护理干预策略。方法 选取50例儿童急性淋巴细胞白血病移植后口腔黏膜炎患儿随机分成参考组与研究组,分别提供常规护理与综合护理;对比护理干预效果。结果 研究组的VAS评分更低,愈合时间更短;患儿的依从性与患儿家长满意度均高于参考组,P<0.05。结论 为接受造血干细胞移植后出现口腔年结膜炎的急性淋巴细胞白血病患儿提供综合护理干预,能够有效改善患儿疼痛,缩短愈合时间,提高患儿的依从性和家长的满意度。

关键词： 肝脏再生   IL-6   TGF-β   IL-1β   炎症反应   免疫调节  

摘要： 促炎细胞因子在肝再生过程中发挥着重要作用,通过调节免疫反应和细胞增殖,为肝再生提供了新的药物作用靶点。其中,肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)和白介素-1β(IL-1β)这些促炎细胞因子在肝再生中发挥重要作用。TNF-α 可以诱导肝细胞凋亡和炎症反应,但其在肝再生中的作用是复杂的,既可能促进也可能抑制肝再生,具体取决于其浓度和作用时间。IL-6 通过激活 STAT3 信号通路,促进肝细胞增殖和肝再生。IL-1β 在急性肝损伤中通过清除坏死组织和激活 STAT3 通路,显著促进肝再生,但在慢性肝病或衰老模型中,其持续释放则会导致炎症和纤维化,抑制其促增殖作用。因此,这些促炎细胞因子在肝再生中的作用具有双重性,既可促进肝再生,也可通过诱导炎症和纤维化抑制肝再生。深入研究这些细胞因子的作用机制,将有助于开发新的治疗策略,促进肝再生并抑制肝纤维化。

关键词： Trophoblast Retrieval and Isolation from the Cervix (TRIC)   Fluorescence-activated cell sorting (FACS) Prenatal testing   Extravillous Trophoblast   Human Leukocyte Antigen (HLA)   Preeclampsia.  

摘要： Introduction Maternal-fetal HLA compatibility influences pregnancy outcome, including preeclampsia risk. Cervical extravillous trophoblasts (EVT) in early pregnancy provide a non-invasive source for fetal genome acquisition, potentially enabling fetal HLA typing for obstetric risk assessment. This study aimed to achieve fetal HLA typing through EVT isolation using HLA-G-coupled nanoparticle immunomagnetic separation (TRIC) and fluorescence-activated cell sorting (FACS).Method Cervical samples from 32 pregnant women were collected by cytobrush. Saliva and umbilical cord blood (n=13) served as maternal and fetal HLA genotype controls, respectively. Cervical samples from non-pregnant women, primary cultured EVT, and cryo-sectioned term placentas served as controls for cell phenotype, protein expression, and effect of fixation. FACS and TRIC were applied to isolate EVT from maternal cells, followed by RSSO-PCR for HLA typing. EVT presence pre- and post-isolation was determined through HLA-G, beta-hCG, and Cytokeratin-7 (CK-7) expression. TRIC was optimized by improving antibody-binding-efficiency, and comparing three (nano)beads types and two *** Purity and yield of HLA-G+beta-hCG+CK-7+ cells after TRIC failed to match pre-isolation HLA-G+ cell counts, despite protocol optimization. FACS revealed a fetal HLA genotype. In contrast, only the maternal HLA genotype was detected in TRIC-isolated *** EVT counts and maternal cell contamination limit reliable fetal HLA typing from cervical samples. Refining non-invasive EVT isolation techniques may enable fetal HLA typing to be included in risk assessment of pregnancy complications.

关键词： 子宫内膜异位症   分子机制   生育能力   细胞因子   激素受体  

摘要： 探讨子宫内膜异位症的分子机制及其对女性生育能力的影响。方法 选取2023年1月至12月在我院就诊的80例子宫内膜异位症患者和80例健康女性作为对照组。于月经周期黄体期进行子宫内膜活检及静脉血采集,采用甲基化特异性PCR、ELISA和实时荧光定量PCR等技术检测分子标志物,同时监测排卵情况、检查输卵管通畅性并评估免疫功能。结果 子宫内膜异位症组目标基因甲基化率、TNF-α和IL-6水平显著高于对照组(P<0.05),而ER和PR表达水平显著低于对照组(P<0.05)。子宫内膜异位症组排卵障碍和输卵管粘连或阻塞发生率显著高于对照组(P<0.05),且T淋巴细胞、B淋巴细胞和NK细胞比例显著升高(P<0.05),而免疫球蛋白和补体水平无显著差异(P>0.05)。结论 子宫内膜异位症的发生与DNA甲基化、细胞因子和激素受体等分子机制密切相关,其通过影响排卵、输卵管功能和免疫调节等多方面显著降低女性生育能力。

关键词： 乙型肝炎   血清免疫球蛋白   临床检验价值  

摘要： 以乙型肝炎患者为例,予血清免疫球蛋白,探析价值。方法 以2023.01~2023.12为研究背景时间,以80例乙型肝炎患者(轻症、重症例数比38:42)、50例健康者作为本次研究的分析对象。前者、后者分别视为试验组、健康组。均行血清免疫球蛋白检测,结果 予以比对。结果 疾病组IgA、IgG、IgM、TBIL水平,>健康组,PTA水平,<健康组(P<0.05);重症组IgA、IgG、IgM、TBIL水平,>轻症组,PTA水平,<轻症组(P<0.05)。结论 乙型肝炎可用血清免疫球蛋白诊断和病情评估,应用价值极高,值得推广和借鉴。

关键词： autoimmune hepatitis (AIH)   liver cirrhosis   cytokines   CD38   interleukin-22 (IL-22)   biomarkers  

摘要： Background Autoimmune hepatitis (AIH) is a chronic inflammatory disease that can progress to cirrhosis and liver failure. While various biomarkers have been associated with AIH progression and prognosis, their specific roles in diagnosing, predicting, and managing cirrhosis, particularly in compensated cirrhosis, remain unclear. Accurately predicting 2-year survival and clinical outcomes for patients with compensated cirrhosis is a critical *** This study analyzed clinical data from non-cirrhotic and cirrhotic AIH patients to identify factors influencing cirrhosis development and prognosis. Serum and nutritional indices were compared between groups with differing prognoses. The diagnostic efficacy of TSP-1, Gal-3, Cys-C, AIb, and PA was evaluated in compensated cirrhosis patients, and their prognostic value was validated using linear regression and Cox proportional hazards *** No significant differences in gender, age, BMI, hypertension, diabetes history, or AMA positivity were observed between the non-cirrhotic AIH and cirrhotic AIH groups. However, TBil levels were significantly higher, and CD38 and IL-22 levels were significantly lower in the cirrhosis group. Multivariate logistic regression identified elevated TBil and reduced CD38 and IL-22 levels were associated with increased cirrhosis risk. Prognosis analysis revealed that patients with good outcomes had significantly lower TSP-1, Gal-3, and Cys-C levels and higher AIb and PA levels than those with poor outcomes. Cox proportional hazards modeling identified TSP-1, Gal-3, and Cys-C as independent risk factors and AIb and PA as protective factors influencing 2-year *** This study underscores the critical roles of TBil, CD38, and IL-22 in cirrhosis development among AIH patients and validates the diagnostic and prognostic significance of TSP-1, Gal-3, Cys-C, AIb, and PA in compensated cirrhosis. These biomarkers facilitate early risk identification and inform clinical de