Journal of Inflammation-London最新文献

{"title":"Retraction Note: Ginsenoside Rg3 alleviates septic liver injury by regulating the lncRNA TUG1/miR-200c-3p/SIRT1 axis.","authors":"Pan Wu, Xiao Yu, Yue Peng, Qian-Lu Wang, Long-Tian Deng, Wei Xing","doi":"10.1186/s12950-025-00435-z","DOIUrl":"10.1186/s12950-025-00435-z","url":null,"abstract":"","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"10"},"PeriodicalIF":4.4,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11837600/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143450977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unfractionated heparin attenuated histone-induced pulmonary endothelial glycocalyx injury through Ang/Tie2 pathway.","authors":"Jia Yin, Yawen Chi, Danyan Liu, Xinghua Li, Xu Li","doi":"10.1186/s12950-025-00437-x","DOIUrl":"10.1186/s12950-025-00437-x","url":null,"abstract":"<p><strong>Purpose: </strong>This study aimed to investigate the involvement of angiopoietin (Ang)/Tie2 pathway in mediating pulmonary endothelial glycocalyx injury in histone-induced acute lung injury in mice, and the protective mechanism of unfractionated heparin (UFH).</p><p><strong>Methods: </strong>Twenty-four male C57BL/6 mice (20-25 g), 8-12 weeks old, were randomly divided into control, histone, and histone + UFH groups. The histone (50 mg/kg) was administered via tail vein. UFH (400 U/kg) was administered 1 h after histone injection. The control group was administered by an equal amount of sterile saline solution. The lungs of all groups were harvested 4 h after the injection of histones or sterile saline.</p><p><strong>Results: </strong>UFH attenuated histone-induced lung histopathological changes and edema. UFH alleviated pulmonary endothelial injury and glycocalyx shedding by reducing histone-induced low expression of thrombomodulin (TM) and decreased lung syndecan-1 levels. UFH improved histone-induced low mRNA expression of TM, syndecan-1, Ang-1, Tie2 and high expression of heparinase (HPA), Ang-2.</p><p><strong>Conclusion: </strong>UFH may attenuate histone-induced lung injury and pulmonary endothelial glycocalyx degradation via the Ang/Tie2 pathway.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"9"},"PeriodicalIF":4.4,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11834598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143442997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Sodium pyruvate exerts protective effects against cigarette smoke extract-induced ferroptosis in alveolar and bronchial epithelial cells through the GPX4/Nrf2 axis.","authors":"Ziwen Zhao, Zhao Xu, Jingwen Chang, Liwei He, Zijin Zhang, Xiaoyu Song, Xianbang Hou, Fangtian Fan, Zhijun Jiang","doi":"10.1186/s12950-025-00436-y","DOIUrl":"10.1186/s12950-025-00436-y","url":null,"abstract":"","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"8"},"PeriodicalIF":4.4,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11834554/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143442996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Auto-antibodies against carbonyl-modified vimentin in COPD: potential role as a biomarker.","authors":"L Heinemann, I Adcock, K F Chung, W Lollinga, M N Hylkema, A Papi, G Caramori, P A Kirkham","doi":"10.1186/s12950-025-00434-0","DOIUrl":"10.1186/s12950-025-00434-0","url":null,"abstract":"<p><p>COPD has many hallmarks of autoimmune dysfunction. Driving this autoimmune response are self-antigens, such as highly abundant structural proteins and cellular proteins, which can lead to the production of auto-antibodies. However, controversy surrounds the detection of some of these auto-antibodies as they have often been screened against native, unmodified proteins. Autoantigens arise as a result of a conformational change in the native protein exposing hidden epitopes or by the creation of neo-epitopes through chemical or enzymatic modifications, often caused by oxidative/carbonyl stress. In this study, we screened for auto-antibodies targeting key structural proteins modified by oxidative/carbonyl stress in peripheral blood from stable COPD patients versus control subjects using ELISA. We found an auto-antibody response against unmodified, carbonyl-modified and citrinylated vimentin, with the highest response observed against carbonyl-modified vimentin. Both the IgG and IgM antibody titres against carbonyl-modified were significantly increased in COPD patients compared to healthy non-smokers. Smokers also displayed increased antibody levels against carbonyl-modified vimentin, but only for the IgG isotype. Selectivity analysis indicated that 70% and 63% of COPD patients had higher IgM and IgG titres, respectively, compared to non-smokers. In contrast only 26% and 48% of smokers had higher IgM and IgG titres, respectively, than non-smokers. ROC analysis gave AUC values of 0.78 (p < 0.01) and 0.84 (p < 0.001) for IgM and IgG, respectively, for COPD versus non-smokers, which fell to 0.70 (p < 0.01) and 0.64 (NS), respectively, when asymptomatic smokers were included. No significant increase in antibody titre against carbonyl-modified elastin or collagen was observed in COPD patients or asymptomatic smokers. We conclude that IgM autoantibody responses against carbonyl modified vimentin could serve as a simple blood-based biomarker for COPD, reflecting the disease's pathophysiology, and could help in patient stratification and diagnosis.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"7"},"PeriodicalIF":4.4,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11817093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143400929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alpha-1 antitrypsin reduces inflammation and vasculopathy in mice with oxygen-induced retinopathy.","authors":"Varaporn Suphapimol, Yu-Han Liu, Sandro Prato, Alexander Karnowski, Charles Hardy, Adriana Baz Morelli, Abhirup Jayasimhan, Devy Deliyanti, Jennifer L Wilkinson-Berka","doi":"10.1186/s12950-025-00431-3","DOIUrl":"10.1186/s12950-025-00431-3","url":null,"abstract":"<p><strong>Background: </strong>Damage to the retinal vasculature is a major cause of vision loss and is influenced by a pro-inflammatory environment within retinal tissue. Alpha-1 antitrypsin (AAT) is a potent inhibitor of serine proteases and has anti-inflammatory properties. We hypothesised that AAT could reduce inflammation and vasculopathy in neovascular retinopathies including oxygen-induced retinopathy (OIR).</p><p><strong>Methods: </strong>Litters of C57BL/6J mice were randomised to develop OIR by exposure to high oxygen between postnatal days 7 to 12 resulting in vaso-obliteration (phase I OIR), and then room air from postnatal days 12 to 18 resulting in neovascularisation (phase II OIR). Control mice were exposed to room air. Separate cohorts of mice were administered control vehicle or human AAT (120 mg/kg) by intraperitoneal injection every second day in phase I or phase II OIR.</p><p><strong>Results: </strong>In phase I OIR, plasma levels of AAT were reduced compared to room air controls, and AAT treatment reduced vaso-obliteration. In phase II OIR, AAT treatment influenced inflammation by reducing the density of ionised calcium binding adaptor protein 1 + cells (microglia/macrophages) and modulating their cell process length and reducing mRNA levels of tumour necrosis factor and monocyte chemoattractant protein-1, but not interleukin-1b and interleukin-6 in retina. Furthermore, AAT treatment reduced retinal neovascularisation, gliosis, vascular endothelial growth factor mRNA and protein expression, and vascular leakage, compared to OIR controls.</p><p><strong>Conclusions: </strong>This research demonstrates the vasculo-protective actions of AAT, and thereby the potential of AAT as a therapeutic option for neovascular retinopathies.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"6"},"PeriodicalIF":4.4,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11817893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143400907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Divergence in photoreceptor cell death and neuroinflammation in transvitreal and transscleral subretinal delivery in mice.","authors":"Daniel E Maidana, Sara Pastor Puente, Catherine Wang, Shivam Chandra, Lucia Gonzalez-Buendia, Eleftherios Paschalis Ilios, Andrius Kazlauskas, Demetrios G Vavvas","doi":"10.1186/s12950-025-00433-1","DOIUrl":"10.1186/s12950-025-00433-1","url":null,"abstract":"<p><p>Subretinal injections provide direct access to photoreceptors and RPE, which is crucial for the delivery of gene therapy and neuroprotective approaches. To access the subretinal space, transvitreal (TV) and transscleral (TS) subretinal injections have been widely used in humans and animal models. In this work, we investigated recent trends and outcomes of utilizing TV and TS subretinal models of retinal detachment (RD). A literature review revealed an increasing utilization of both models over the past two decades, with TS emerging as the predominant model since 2012. Subretinal injection in CX3CR1 + /GFP CCR2 + /RFP mice revealed early inflammatory responses, with TS injections inducing higher infiltration of CD11b + CCR2 + cells compared to TV. Further leukocyte immunophenotyping indicated divergent infiltration patterns, with the TS approach exhibiting higher proportions of neutrophils and macrophages/microglia-like cells, while the TV injections had higher CD45hi CD11b + Ly6G- Ly6C + infiltration. Notably, late-stage analysis demonstrates higher photoreceptor cell death in the TS approach, paralleled by increased subretinal infiltration of CD11b + cells. Both models showed significant reactive gliosis, suggesting comparable late-stage wound healing responses. These findings underscore the utility of these approaches for subretinal delivery, offering insights into their distinctive leukocyte infiltration and late-stage tissue responses.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"5"},"PeriodicalIF":4.4,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11806547/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143371389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The injury effect of osteopontin in sepsis-associated lung injury.","authors":"Qian Wang, Zhicai Yu, Zhixin Song, Xue Lu, Zhu Li, Dandan Pi, Jing Li, Feng Xu","doi":"10.1186/s12950-025-00430-4","DOIUrl":"10.1186/s12950-025-00430-4","url":null,"abstract":"<p><strong>Background: </strong>Sepsis is a severe condition causing organ failure due to an abnormal immune reaction to infection, characterized by ongoing excessive inflammation and immune system issues. Osteopontin (OPN) is secreted by various cells and plays a crucial role in inflammatory responses and immune regulation. Nonetheless, the precise function of OPN in sepsis remains to be elucidated.</p><p><strong>Methods: </strong>In the present study, we evaluated the levels of OPN in paediatric patients with sepsis and healthy individuals. We examined the impact of OPN on survival rates, systemic inflammation, and lung injury within an experimental sepsis model using cecal ligation and puncture (CLP). Furthermore, the pro-inflammatory effects and potential mechanisms of OPN in sepsis were investigated through Mouse Hemophagocytic Synuclein (MH-S) cells.</p><p><strong>Results: </strong>The OPN level was found to be elevated in patients with sepsis (368.5 ± 249.4 ng/ml) compared to children with infections (73.78 ± 40.46 ng/ml) (p < 0.0001) and healthy individuals (44.03 ± 20.76 ng/ml) (p < 0.0001). The serum concentration of OPN was elevated in pediatric patients with septic shock compared to those with sepsis (504 ± 266.3 ng/ml vs. 238.6 ± 143.8 ng/ml, p < 0.001). Intravenous administration of OPN inhibitor into the tail vein decreased the mortality rate (HR = 0.2695, p = 0.0015), suppressed systemic inflammatory responses and mitigated lung tissue damage. The concentration of tumour necrosis factor (TNF)-α, IL-6 and IL-1β in serum of CLP mice treated with OPN inhibitor decreased compared with CLP mice. Within the sepsis mouse model, there was a marked increase in OPN expression in the lung's tissues compared to the sham group mice. This surge was accompanied by a significant accumulation of alveolar macrophages and an upregulation of inflammasome expression. Mechanistic investigations in MH-s cells revealed that OPN-siRNA suppressed the LPS-induced macrophage inflammatory response by inhibiting caspase1-dependent classical pyroptosis signaling pathway. However, recombinant OPN was supplemented after OPN silencing, the protective effects in MH-s cells treated with LPS were reversed.</p><p><strong>Conclusion: </strong>This study reveals that OPN has an adverse impact on the host's immune response to sepsis. Suppressing OPN expression holds potential therapeutic value for the treatment of sepsis.</p><p><strong>Trial registration: </strong>Study on the diagnostic value of osteopontin in children with sepsis. MR5024001771. Registered 22 January 2024. https//www.medicalresearch.org.cn.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"4"},"PeriodicalIF":4.4,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143043524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRPV4 modulates inflammatory responses and apoptosis in enteric glial cells triggered by Clostridioides difficile toxins A and B.","authors":"Dvison de Melo Pacífico, Deiziane Viana da Silva Costa, Maria Lucianny Lima Barbosa, Conceição Silva Martins Rebouças, Simone de Goes Simonato, Cirle Alcantara Warren, Maria Luana Gaudencio Dos Santos Morais, Renata Ferreira de Carvalho Leitao, Gerly Anne de Castro Brito","doi":"10.1186/s12950-024-00425-7","DOIUrl":"10.1186/s12950-024-00425-7","url":null,"abstract":"<p><p>Clostridioides difficile, a spore-forming anaerobic bacterium, is the primary cause of hospital antibiotic-associated diarrhea. Key virulence factors, toxins A (TcdA) and B (TcdB), significantly contribute to C. difficile infection (CDI). Yet, the specific impact of these toxins, particularly on enteric glial cells (EGCs), still needs to be fully understood. This study examines the role of the transient receptor potential vanilloid 4 (TRPV4), a calcium-permeable channel, in the inflammatory response and apoptosis of EGCs induced by TcdA and TcdB and evaluates TRPV4 expression in the cecum and colon of infected mice. EGCs were treated with TcdA (50ng/mL) or TcdB (1ng/mL) for 18 h, with or without the TRPV4 antagonist RN-1734 (100 µM), to assess TRPV4 gene and protein levels, inflammatory markers, and cell death. C. difficile infected mice were euthanized on day 3 post-infection for TRPV4 expression in the cecum and colon. Findings reveal that EGCs naturally express TRPV4, increasing its expression by TcdA and TcdB exposure. CDI significantly upregulates TRPV4 in the cecum and colon's submucosal and myenteric plexus regions. TRPV4 mediates TNF-α release in EGCs and is partially involved in the increase in IL-6 gene expression triggered by these toxins. Our results highlight TRPV4's role in triggering EGC apoptosis via caspase 3 activation and inhibiting the reduction of Bcl-2, an anti-apoptotic protein in EGCs caused by C. difficile toxins. These results highlight TRPV4's significant role in CDI pathogenesis and its potential as a therapeutic target to counteract the detrimental effects of C. difficile toxins on enteric glia.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"3"},"PeriodicalIF":4.4,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11731189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Progress of CCL20-CCR6 in the airways: a promising new therapeutic target.","authors":"Ya -Jing Li, Wan-Li Geng, Chen-Chen Li, Jia-Hao Wu, Fei Gao, Yong Wang","doi":"10.1186/s12950-025-00428-y","DOIUrl":"10.1186/s12950-025-00428-y","url":null,"abstract":"","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"2"},"PeriodicalIF":4.4,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11727789/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142980686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Downregulation of miR-223 promotes HMGB2 expression and induces oxidative stress to activate JNK and promote autophagy in an in vitro model of acute lung injury.","authors":"Hao-Yu Tan, Bei Qing, Xian-Mei Luo, Heng-Xing Liang","doi":"10.1186/s12950-024-00424-8","DOIUrl":"https://doi.org/10.1186/s12950-024-00424-8","url":null,"abstract":"","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"1"},"PeriodicalIF":4.4,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11702141/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142959334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}