European Journal of Inflammation欧洲炎症杂志

European Journal of Inflammation(英文缩写 EUR J INFLAMM),ISSN 1721-727X,eISSN 2058-7392,中文译名:欧洲炎症杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。

2026 年数据 · 影响因子
1.100
JCR 分区
Q4
CAS 分区
B4
近一年发文量
0
本站 PubMed 收录统计

发文量统计区间:2025-10-01 至 2026-09-30,按本站收录文献的发表日期统计。

ISSN: 1721-727X · eISSN: 2058-7392 · 缩写: EUR J INFLAMM ·中文: 欧洲炎症杂志

期刊介绍

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期刊简介

《European Journal of Inflammation》是一本聚焦炎症基础与临床研究的国际英文期刊,涵盖免疫机制、炎症介质、慢性炎症疾病及相关治疗探索。读者群包括免疫学、病理学、药学及临床医学研究者,尤其关注炎症在感染、自身免疫和代谢疾病中的作用。该刊为开放获取平台,强调跨学科对话,适合展示实验与临床观察成果。

研究方向

主要方向包括炎症信号通路、细胞因子与趋化因子、固有免疫与适应性免疫、炎症相关疾病模型及抗炎药物研究。论文类型涵盖原创研究、综述、短篇报告和病例观察,鼓励从分子到临床的多层次探讨,尤其欢迎转化医学和新型生物标志物研究。

期刊特色

研究取向偏重机制探索与临床相关性,论文需有明确实验设计和数据支撑。特点在于兼顾基础免疫学与临床炎症疾病,适合从事免疫、药理、风湿病学及感染病学的研究人员。对阴性结果或重复性研究接受度有限,更青睐有新发现或新方法的工作。

投稿难度

投稿难度中等偏下,但并非仅因分区低而容易录用。期刊对创新性和方法严谨性有一定要求,建议准备充分的前期数据、清晰的统计分析和规范的英文写作。若研究仅描述现象而缺乏机制解释,可能需补充实验或改投更合适的专科期刊。

历年影响因子趋势

JCR 数据年份影响因子JCR 分区
20210.424Q4
20220.700Q4
20230.600Q4
20240.800Q4
20251.100Q4

European Journal of Inflammation 最新收录文献

  1. JCR分区: Q4 CAS分区: B4 影响因子: 1.1

    1. A primary role for kinin B1 receptor in inflammation, organ damage, and lethal thrombosis in a rat model of septic shock in diabetes.

    作者:
    N Tidjane, A Hachem, Y Zaid, Y Merhi, L Gaboury, J-P Girolami, R Couture
    日期:
    2015-04-01

    Diabetes mellitus and septic shock increase the incidence of mortality by thrombosis. Although kinin B1 receptor (B1R) is involved in both pathologies, its role in platelet function and thrombosis remains unknown. This study investigates the expression, the inflammatory, and pro-thrombotic effects of B1R in a model of septic shock in diabetic rats. Sprague-Dawley rats were made diabetic with streptozotocin (STZ) (65 mg/kg, i.p.). Four days later, control and STZ-diabetic rats were injected with lipopolysaccharide (LPS) (2 mg/kg, i.p.) or the vehicle. B1R antagonist (SSR240612, 10 mg/kg by gavage) was given either acutely (12 and 24 h prior to endpoint analysis) or daily for up to 7 days. Moreover, a 7-day treatment was given either with cyclooxygenase (COX)-2 inhibitor (niflumic acid, 5 mg/kg, i.p.), non-selective COX-1 and COX-2 inhibitor (indomethacin, 10 mg/kg, i.p.), non-selective nitric oxide synthase (NOS) inhibitor (L-NAME, 50 mg/kg by gavage), iNOS inhibitor (1400W, 5 mg/kg, i.p.), or heparin (100 IU/kg, s.c.). The following endpoints were measured: edema and vascular permeability (Evans blue dye), B1R expression (qRT-PCR, western blot, flow cytometry), aggregation in platelet-rich plasma (optical aggregometry), and organ damage (histology). Rats treated with STZ, LPS, and STZ plus LPS showed significant increases in edema and vascular permeability (heart, kidney, lung, and liver) and increased expression of B1R in heart and kidney (mRNA) and platelets (protein). Lethal septic shock induced by LPS was enhanced in STZ-diabetic rats and was associated with lung and kidney damage, including platelet micro-aggregate formation. SSR240612 prevented all these abnormalities as well as STZ-induced hyperglycemia and LPS-induced hyperthermia. Similarly to SSR240612, blockade of iNOS and COX-2 improved survival. Data provide the first evidence that kinin B1R plays a primary role in lethal thrombosis in a rat model of septic shock in diabetes. Pharmacological rescue was made possible with B1R antagonism or by inhibition of iNOS and COX-2, which may act as downstream mechanisms.

  2. JCR分区: Q4 CAS分区: B4 影响因子: 1.1

    2. IMPACT OF AGE AND AUTOANTIBODY STATUS ON THE GENE EXPRESSION OF SCLERODERMA FIBROBLASTS IN RESPONSE TO SILICA STIMULATION.

    作者:
    Y Yang, P Wei, X J Guo, D Zhou, W Z Zhang, S Assassi, X D Zhou
    日期:
    2013-09

    Environmental factors are believed to play an important role in the pathogenesis of systemic sclerosis (SSc). Silica exposure has been implicated as potentially hazardous in epidemiological studies of SSc. It can activate fibroblasts to express profibrotic genes at certain conditions. The aim of this study is to examine whether the fibroblasts of SSc patients respond to silica particles with specific gene expressions differentially from normal control fibroblasts. The fibroblasts obtained from skin biopsies of 96 SSc patients and 104 controls were examined. Silica particles were used to perturb the cultures of the fibroblasts in time-course and dose-response assays. The transcript levels of COL1A2, COL3A1, MIVIP1, MMP3, TIMP3 and CTGF genes of the fibroblasts were measured with quantitative RT-PCR. The results showed that the expressions of all six genes in SSc fibroblasts under silica perturbation appeared significantly different from normal control fibroblasts. In age stratified analysis, compared to control fibroblasts, SSc fibroblasts from patients at age 30-40 years and 50-60 years displayed significantly decreased expressions of MMP1 gene in all dosage assays and increased expression of COL3A1 genes started at low dosages perturbation of silica particles, respectively. In autoantibody stratified analysis, specific gene expression patterns were significantly associated with autoantibody-subgroups of fibroblasts. A common feature of SSc fibroblasts was unstable and a wide range of gene expression changes in response to silica perturbation. Our studies may suggest an altered intrinsic dynamic control in SSc fibroblasts. In addition, sensitivity and specificity of SSc fibroblasts to potentially hazardous environmental trigger is age and autoantibody-subgroup-dependent. The fibroblasts of SSc patients at age 30-60 years may be more sensitive to silica perturbation toward a profibrotic gene expression.

  3. JCR分区: Q4 CAS分区: B4 影响因子: 1.1

    3. INDOLE-3-CARBINOL EXERTS SEX-SPECIFIC EFFECTS IN MURINE COLITIS.

    作者:
    J M Benson, C A Beamer, B P Seaver, D M Shepherd
    日期:
    2012-09

    Due to the severe adverse effects that can accompany conventional therapies for Crohn's disease, the search for natural complementary therapies has increased dramatically in recent years. Indole-3-carbinol (I3C), a constituent of cruciferous vegetables, possesses anti-inflammatory properties; however, its effects on intestinal inflammation have yet to be evaluated. To test the hypothesis that I3C dampens intestinal inflammation, C57Bl/6 mice were treated with I3C and exposed to 2,4,6-trinitrobenzenesulfonic acid (TNBS) to induce colitis. Several parameters of disease severity and inflammation were subsequently evaluated. I3C dampened the disease severity, as indicated by decreased body weight loss and decreased severity of clinical signs. Interestingly, this effect was observed in female but not male mice, which displayed a trend towards exacerbated colitis. Differential effects were observed in the profiles of cytokine production, as the production of pro-inflammatory cytokines was increased in males. The sex-specific effect of I3C in TNBS-induced colitis is a novel finding and warrants further investigation since this is a common dietary compound and is also available commercially.

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