Journal of Inflammation-London炎症杂志（伦敦）
Journal of Inflammation-London(英文缩写 J INFLAMM-LOND),ISSN 1476-9255,eISSN 1476-9255,中文译名:炎症杂志（伦敦） 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。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 6.283 | Q2 |
| 2022 | 5.100 | Q2 |
| 2023 | 4.400 | Q2 |
| 2024 | 4.100 | Q2 |
| 2025 | 5.800 | Q1 |
Journal of Inflammation-London 最新收录文献
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1. Differences in systemic inflammation and prethrombotic biomarkers between AECOPD patients with and without pulmonary hypertension.
1. AECOPD合并和不合并肺动脉高压患者全身炎症和血栓前生物标志物的差异PMID:日期:2026-07-15The relationship between inflammatory cytokines and prothrombotic markers with PH during the acute phase of acute exacerbation of chronic obstructive pulmonary disease (AECOPD) remains unclear. This study aims to compare the profiles of peripheral blood biomarkers in AECOPD patients with and without Pulmonary Hypertension(PH), and to evaluate their diagnostic significance. We conducted a case-control study enrolling 148 patients admitted to the Department of Respiratory Medicine at Fuyang First People's Hospital in Hangzhou, Zhejiang Province, China, between January 2023 and April 2025. The patients were categorized into three groups: a control group (n = 49), an AECOPD group (n = 59), and an AECOPD with PH group (n = 40). The clinical characteristics and the relationships between inflammatory cytokines and prothrombotic markers were compared among the three groups. Logistic regression analysis was employed to identify inflammatory biomarkers and prothrombotic markers with independent predictive value. The predictive accuracy of these risk factors was assessed using receiver operating characteristic (ROC) curves. Compared with healthy volunteers, AECOPD patients showed elevated levels of PIV, SII, IL-8, CRP, NLR, and PLR (p < 0.0001) based on quartile comparisons. Levels of these inflammatory markers were significantly elevated in both AECOPD and AECOPD + PH groups compared to controls (p < 0.0001). However, no significant differences were found between the AECOPD and AECOPD + PH groups. Among the prethrombotic markers, D-dimer and TAT were elevated in AECOPD patients with PH. ROC curve analysis identified PIV, SII, IL-8, CRP, NLR, and PLR as significant predictors of AECOPD. Among the inflammatory markers, SII exhibited the highest area under the curve (AUC) of 0.834 (95% CI: 0.748-0.905). The combination of SII and IL-8 yielded the highest AUC among inflammatory markers, at 0.926 (95% CI: 0.876-0.967). Furthermore, the combination of D‑dimer and TAT resulted in a higher AUC than either marker alone, with an AUC of 0.919 (95% CI: 0.865-0.966) for identifying PH in AECOPD patients. AECOPD patients with PH exhibit a distinct biomarker pattern characterized by a plateau in systemic inflammation alongside progressive coagulation activation. We speculate that this may be attributed to a regionalized redistribution of the inflammatory response or functional exhaustion of the immune system. The combination of inflammatory markers (SII and IL-8) and prothrombotic markers (D-dimer and TAT) provides excellent discriminative ability for diagnosing AECOPD and identifying concomitant PH, respectively. These findings support the use of combined biomarker panels for individualized risk assessment and early detection of PH in AECOPD patients. Not suitable.
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2. Administration of human macrophage colony-stimulating factor-mFc fusion protein increases macrophage phagocytic capacity and stimulates liver regeneration in mice.
PMID:日期:2026-06-25Acute and chronic liver diseases are rising contributors of the worldwide healthcare burden. Inflammation plays a key role in progression of both acute and chronic disease, and effective treatments are limited. Macrophages, a diverse population of professional phagocytes, are required for the timely resolution of tissue injury and are an emerging target to treat acute and chronic liver disease. Colony stimulating factor 1 (CSF1), promotes differentiation and survival of macrophages, which are essential in epithelial regeneration, but the CSF1 protein is rapidly eliminated in vivo. We therefore fused human CSF1 genetically to a modified mouse IgG2a Fc region and transiently expressed this in HEK293-6E cells. The protein was purified from culture supernatant to obtain > 97% monomeric purity, suitable for in vivo testing. The nascent hCSF1-Fc fusion proteins were evaluated in vitro and in murine models of health and liver disease. hCSF1-mFc is pharmacologically active in healthy mice, resulting in increases in liver and spleen mass closely reflecting changes in tissue macrophage content. In an acetaminophen-induced acute liver injury model, hCSF1-mFc treatment increased hepatic macrophage accumulation at necrotic sites, reduced serum ALT activity, and serum IL-1β levels, and restored white blood cell counts within 72 h. Furthermore, hCSF1-mFc treatment also increased hepatic macrophage numbers in a carbon tetrachloride (CCl)-induced liver fibrosis model corresponding with a striking 3.5-fold increased uptake of a soluble phagocytic label, indicating improved hepatic clearance capacity. hCSF1-mFc was also tested in a model of acute on chronic liver injury, which included a bolus delivery of proinflammatory E. coli-coated bioparticles to pre-existing fibrosis. Here, hCSF1-mFc treatment restored body weight, induced hepatomegaly, and reduced several plasma pro-inflammatory cytokines, suggesting reduction of systemic inflammation. Finally, immunofluorescence staining showed hCSF1-mFc treatment induced significant hepatocyte proliferation in healthy and all liver disease models. This report demonstrates that hCSF1-mFc treatment increases liver macrophage populations, improves phagocytic capacity, and stimulates hepatocyte proliferation in experimental liver disease models. hCSF1-based fusion protein therapy might represent a novel immune-based strategy to treat acute and chronic liver disease in the clinic. Not applicable.
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4. FOXD2-AS1/miR-185-5p/CDC42 axis in chronic obstructive pulmonary disease: clinical significance and mechanistic insights.
PMID:日期:2026-05-16Long non-coding RNA (lncRNA), a key molecule within gene expression regulatory network, is important in various respiratory diseases. This study assessed the expression changes and regulatory mechanism of lncRNA FOXD2-AS1 in chronic obstructive pulmonary disease (COPD). Two hundred COPD patients were enrolled, comprising 100 with AECOPD and 100 with stable COPD. 16HBE cells were exposed to cigarette smoke extract (CSE) to simulate disease conditions in vitro. Relative mRNA levels were measured via RT-qPCR. Cell function, including cell proliferation, apoptosis and inflammation, was assessed. Target binding genes were predicted using online tools, with their functions annotated via GO and KEGG analysis. Both stable COPD patients and AECOPD patients had significantly higher serum FOXD2-AS1 levels than healthy controls, with the highest values in AECOPD. It can differentiate stable COPD from healthy controls and AECOPD, and increased gradually with COPD stage progression. Silencing FOXD2-AS1 afforded protection against apoptotic and inflammatory phenotype induced by CSE in 16HBE cells. FOXD2-AS1 sponges miR-185-5p, which were downregulated in clinical serum samples and cell models. miR-185-5p downregulation reversed the effects of FOXD2-AS1 silencing on cell apoptosis and inflammation. CDC42, a downstream target of miR-185-5p, was upregulated in COPD patients and cell models, and negatively related to serum miR-185-5p levels. CDC42 reversed the role of FOXD2-AS1/ miR-185-5p in CSE-exposed 16HBE cells. Serum FOXD2-AS1 was markedly upregulated in COPD patients, with close correlation to disease severity. The FOXD2-AS1/miR-185-5p/CDC42 axis may contribute to COPD pathogenesis by mediating bronchial epithelial cell apoptosis and inflammation.
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5. A spotlight on the inflammatory role of uremic toxins in the dysbiosis-CKD axis: a review.
PMID:日期:2026-05-11There is growing evidence that gut-derived metabolites activate specific signaling pathways that lead to renal inflammation and injury, suggesting that the gut-kidney axis plays a significant role in the inflammatory processes that underlie chronic kidney disease (CKD). Alterations in the gut microbiota in CKD patients known as dysbiosis increases the production of uremic toxins such as p-cresyl sulfate, indoxyl sulfate and Trimethylamine N-oxide. These toxins trigger pro-inflammatory signaling pathways in renal tubular cells by initiating a series of inflammatory events, such as immune dysregulation, oxidative stress, and endotoxemia. As a result, cytokines like TNF-α, IL-6, and IL-1β are expressed more frequently, creating a chronic inflammatory environment that increase kidney damage and the progression of CKD. Emerging therapeutic strategies that alter gut microbiota composition, such as prebiotics, probiotics, dietary fiber, and fecal microbiota transplantation, have demonstrated promise in decreasing the burden of inflammation-inducing toxins. As research reveals new linkages between microbial metabolites and inflammatory signaling in CKD, addressing uremic toxin-mediated inflammation could revolutionize disease management. Understanding these interrelated signaling systems provides a more detailed understanding of how gut microbes influence renal inflammation at the molecular level. The aim of this review is to investigate the underlying signaling pathways by which gut-renal dysbiosis induces inflammation in CKD. The review attempts to guide the development of targeted treatment approaches that can reduce the inflammatory load and slow the progression of CKD by examining the mechanisms in which gut-derived uremic toxins alter oxidative stress, immunological responses, and inflammatory cascades.
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6. Myeloperoxidase regulates hypoxia-induced inflammation and oxidative stress in liver-spleen axis.
PMID:日期:2026-05-02High-altitude hypobaric hypoxia induces inflammation and oxidative stress, yet the role of myeloperoxidase (MPO) in this pathology remains incompletely understood. This study aimed to investigate whether MPO mediates injury to the liverspleen axis under hypoxic conditions. Using a 3day murine hypoxia model, we unexpectedly found that MPO deficiency exacerbated, rather than mitigated, damage to the liverspleen axis. Compared with hypoxic wildtype mice, MPO mice displayed aggravated histopathological injury, accompanied by excessive phagocyte recruitment and elevated expression of key chemokines (KC, MCP1, MIP2) and proinflammatory mediators (TNFα, IL1β, IL17A). At the molecular level, MPO absence increased splenic protein expression of NFκB, NLRP3, and iNOS, while dysregulating the antioxidant response via the NRF2/HO1 pathway. These results reveal a novel protective role for MPO during hypoxic stress, where it functions to moderate the innate immune response and limit collateral tissue damage in the liverspleen axis. The study provides new insights into the complex immunomodulatory functions of MPO and suggests its activity is essential for maintaining immune homeostasis during acute hypoxia.
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7. Resolvin D1 attenuates senescence-associated secretory phenotype independently of TGF-β-driven cardiac fibroblasts differentiation to myofibroblast.
PMID:日期:2026-04-29Cardiac fibroblasts (CF) are key regulators of myocardial inflammation through their ability to acquire senescent phenotypes and secrete inflammatory mediators. Although transforming growth factor-β (TGF-β) signaling is a central driver of myofibroblast differentiation, its contribution to inflammation-induced senescence and the senescence-associated secretory phenotype (SASP) remains poorly understood. In this study, we examined whether inflammatory stress induces senescence in adult rat CF independently of TGF-β signaling and evaluated the ability of Resolvin D1 (RvD1) to modulate the established SASP. Adult rat CF were treated with the ALK5 inhibitor SB431542 from isolation to prevent spontaneous myofibroblast differentiation. Cells were exposed to lipopolysaccharide (LPS, 1 μg/mL) under high (10%) serum conditions for 3 or 7 days. Senescence was assessed by cellular hypertrophy and SA-β-galactosidase activity. Following LPS stimulation, culture media were replaced and CF were treated with RvD1 for 48 h. Secreted cytokines, chemokines were quantified in conditioned media. LPS induced a robust senescent phenotype in CF, characterized by increased cell size and SA-β-galactosidase activity, regardless of TGF-β pathway inhibition or serum concentration. Inhibition of TGF-β signaling prevented myofibroblast differentiation but did not attenuate senescence induction. Importantly, RvD1 treatment significantly reshaped the SASP of senescent CF, reducing pro-inflammatory mediators including IL-1β, IL-6, TNF-α, and MCP-1, while preserving anti-inflammatory cytokines. These findings identify inflammatory stress as a driver of TGF-β–independent senescence in cardiac fibroblasts and highlight RvD1 as a potent modulator of senescence-associated inflammation.
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8. Dihydromyricetin exerts neuroprotective effects in acute spinal cord injury by inhibiting NLRP3/Caspase-1 inflammasome through gut microbiome modeling.
PMID:日期:2026-04-18BACKGROUND: The gut microbiota is closely associated with spinal cord injury (SCI). Dihydromyricetin (DHM), a potent anti-inflammatory compound with neuroprotective properties, has been shown to improve outcomes in various diseases. However, the role of gut microbiota mediating the mechanism neuroprotective effects of DHM in SCI is unknown. METHODS: Male Sprague-Dawley rats were randomly divided into three groups: SHAM, SCI, and DHM group. Motor function was assessed using the cylinder rearing test, and alterations in gut microbiota composition and metabolites were analyzed via 16S rRNA sequencing. Subsequently, Western blotting and immunofluorescence staining were employed to evaluate intestinal barrier integrity, as well as changes in proteins associated with the TLR4/NF-κB pathway and NLRP3/Caspase-1. Finally, fecal microbiota transplantation experiments were conducted to elucidate the necessity of gut microbiota in mediating the anti-inflammatory effects of DHM. RESULTS: DHM exhibits a therapeutic effect by attenuating the severity of pathological SCI and promoting motor function recovery. Notably, DHM restored a balanced microbiota pattern by increasing the relative abundance of Actinobacteria and Bacteroidetes, while concurrently decreasing that of Proteobacteria. Furthermore, DHM promoted intestinal barrier recovery, reduced blood lipopolysaccharide (LPS) levels, and suppressed the activation of the TLR4/NF-κB pathway and reduced the activity of the NLRP3/Caspase-1 inflammasome, thereby effectively decreasing the subsequent release of inflammatory factors in spinal cord tissue. Furthermore, the results from the two FMT groups demonstrated that the gut microbiota serves as a critical target for DHM to exert its anti-inflammatory effects. CONCLUSION: The results of this study demonstrate that restoring microbial balance, repairing intestinal barrier integrity, reducing serum LPS levels, and suppressing the TLR4/NF-κB pathway as well as NLRP3/Caspase-1 inflammasome activity constitute the key regulatory mechanisms underlying the neuroprotective effects of DHM following SCI, thereby opening up possibilities for a novel microbiome-directed therapeutic approach to SCI.
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9. WWC1 deficiency exacerbates sepsis-induced lung injury by promoting NETosis, M1 and M2b macrophage recruitment, and pyroptosis via YAP1 and STING pathways.
PMID:日期:2026-04-17BACKGROUND: Our recent investigations have shown that WWC1 loss leads to sepsis-induced lung injury (SiLI) by reducing activation of Yes-associated protein 1 (YAP1) and stimulator of interferon genes (STING) pathways. This study further explores the involvements of pyroptosis, NETosis, and macrophage recruitment in the associated events. METHODS: Wild-type (wt) C57BL/6 mice, or mice with WWC1 gene knockout (WWC1-ko) or knock-in (WWC1-ki), were subjected to cecal ligation and puncture for SiLI modeling. Immunofluorescence staining and western blot (WB) were employed to analyze NETosis-related markers in lung tissues. Flow cytometry was employed to analyze the proportions of neutrophils and macrophages in bronchoalveolar lavage fluid (BALF). Immunohistochemistry and WB were applied to analyze pyroptosis markers. Histological staining was performed to analyze inflammatory responses in the lung tissues. Specific antagonists or agonists were utilized to analyze the involvements of YAP1 and STING in the inflammatory cascades. RESULTS: WWC1-ko mice showed more pronounced NETosis in the lung, accompanied by increased recruitment of neutrophils and macrophages, particularly M1 and M2b subtype macrophages, in the BALF. The pro-pyroptotic cascade was also activated in the lung of WWC1-ko mice. Administration of specific antagonists of NLRP3, YAP1, STING, and IRF3 reduced pyroptosis, alleviated NETosis, reduced abundance of macrophages, and mitigated inflammatory damage in the lung of WWC1-ko mice. By contrast, WWC1-ki mice were more resistant to these inflammatory cascades, which were, however, diminished upon the artificial activation of YAP1 or STING. CONCLUSION: The activation of pyroptosis, YAP1, and STING cascades upon WWC1 deficiency contributes to NETosis and accumulation of pro-inflammatory immune cells in SiLI.
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10. Hypoxia synergizes cGAS-STING activation and AKT1 phosphorylation to drive pulmonary inflammation in one-lung ventilation: therapeutic attenuation by RU.521 and MK2206.
PMID:日期:2026-04-13To explore the mechanisms involved in hypoxia-induced acute lung injury (ALI) and oxidative stress during one-lung ventilation (OLV) in order to find pharmacological interventions that can attenuate OLV injury. An OLV model was established in Sprague-Dawley (SD) rats. Lung tissue damage was assessed via histological staining and by quantifying inflammatory factors (TNF-α, IL-6, IL-1β) using qPCR. High-throughput transcriptome sequencing of left lung tissues from the OLV group and the two-lung ventilation (TLV) group screened for differentially expressed genes (DEGs) in pathways and biological functions associated with lung injury. Furthermore, a hypoxia reoxygenation (H/R) model was established using the mouse lung epithelial cell line (MLE-12) for further mechanism mapping and validation in vitro. Transcriptomic analysis revealed upregulated gene signatures linked to DNA damage, mitochondrial membrane permeabilization, oxidative stress, and innate immune activation. KEGG enrichment identified innate immune pathways, specifically cytosolic DNA sensing. Subsequent in vivo and in vitro studies confirmed cGAS-STING pathway activation, characterized by increased expression and enhanced phosphorylation of downstream components. Genetic knockdown of cGAS or AKT1 (a kinase required for downstream phosphorylation of key cGAS-STING downstream effectors) suppressed cGAS-STING pathway signaling. This study highlights that innate immunity contributes to lung tissue damage during OLV. Hypoxia-induced DNA damage activates the cytoplasmic DNA-sensing cGAS-STING pathway. Subsequently, AKT1 modulates the downstream phosphorylation of TBK1, IRF3, and NF-κB, thereby promoting DNA damage-associated inflammation in alveolar epithelial cells. Pharmacologically, both the cGAS inhibitor RU.521 and AKT1 inhibitor MK2206 attenuated cGAS-STING-mediated inflammation and mitigated hypoxia-induced oxidative stress in alveolar epithelia. Not applicable.