Mediators of Inflammation最新文献

{"title":"Sublingual Immunotherapy Decreased the Serum Levels of Interleukin-36<i>γ</i> in Allergic Rhinitis.","authors":"Xiaowei Qin, Chunrui Wang, Jueqi Li, Xiaopeng Zhang, Tianhong Zhang","doi":"10.1155/2024/9692031","DOIUrl":"10.1155/2024/9692031","url":null,"abstract":"<p><p><b>Background:</b> Allergy immunotherapy (AIT), a treatment approach for allergic rhinitis (AR), is recognized for its potential to modify the disease course beyond mere symptom relief. Interleukin-36<i>γ</i> (IL-36<i>γ</i>), a key player in immune responses, has been implicated in promoting eosinophilic inflammation in AR by activating eosinophils. We aimed to investigate the effect of IL-36<i>γ</i> on group II lymphoid cell (ILC2) in AR patients who underwent sublingual immunotherapy (SLIT). <b>Methods:</b> Twenty-four AR patients were enrolled and administered with SLIT. Serum proteins of IL-36<i>γ</i>, interleukin-5 (IL-5), and interleukin-13 (IL-13) during SLIT were quantitatively assessed using enzyme-linked immunosorbent assay (ELISA). The proportion of ILC2 was determined by flow cytometry. Sorted ILC2s were stimulated by IL-36<i>γ</i> and ILC2 cell differentiation, and type II cytokines expression were examined. <b>Results:</b> SLIT treatment decreased the serum protein levels of IL-36<i>γ</i>, IL-5, IL-13, and the proportion of ILC2 significantly. IL-36<i>γ</i> suppressed the proliferation of ILC2 by inhibiting the levels of ILC2 transcription factor. IL-36<i>γ</i> also inhibited IL-5 and IL-13 expression from ILC2. <b>Conclusion:</b> The changes of IL-36<i>γ</i> during SLIT were related to the inhibited function of ILC2, implying that IL-36<i>γ</i> may be used as a new biomarker for monitoring the efficacy of SLIT in AR.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"9692031"},"PeriodicalIF":4.4,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11561173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142623693","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 Role of Ca²⁺/PI3K/Akt/eNOS/NO Pathway in Astragaloside IV-Induced Inhibition of Endothelial Inflammation Triggered by Angiotensin II.","authors":"Shiyu Zhang, Shijie Li, Shiyang Xie, Lin Cui, Yuan Gao, Youping Wang","doi":"10.1155/2024/3193950","DOIUrl":"https://doi.org/10.1155/2024/3193950","url":null,"abstract":"<p><p>Inflammation induced by angiotensin II (Ang II) is a key event in the progression of numerous cardiovascular diseases. Astragaloside IV (AS-IV), a glycoside extracted from <i>Astragalus membranaceus Bunge</i>, has been shown to inhibit Ang II-induced inflammatory responses in vivo. However, the mechanisms underlying the beneficial effects are still unclear. This study investigated whether AS-IV attenuates endothelial inflammation induced by Ang II via the activation of endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) pathway. Human umbilical vein endothelial cells (HUVECs) were cultured in the presence of AS-IV with or without the specific inhibitor of NOS or Ca²⁺- and phosphatidylinositol 3-kinase (PI3K)/Akt-dependent cascade prior to Ang II exposure. Incubation of HUVECs with AS-IV enhanced NO production and eNOS^ser1177 phosphorylation. These responses were abrogated by the inhibition of NOS or Ca²⁺- and PI3K/Akt-dependent pathway. In addition, preincubation of HUVECs with AS-IV inhibited Ang II-induced cytokine and chemokine production, adhesion molecule expression, monocyte adhesion, and nuclear factor kappa B (NF-κB) activation as evidenced by the attenuation of inhibitor of kappa B alpha phosphorylation and subsequent NF-κB DNA binding. These effects of AS-IV were abolished by the suppression of NOS or Ca²⁺- and PI3K/Akt-dependent cascade. Our findings indicate that AS-IV attenuates inflammatory responses triggered by Ang II possibly via the activation of Ca²⁺/PI3K/Akt/eNOS/NO pathway in endothelial cells.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"3193950"},"PeriodicalIF":4.4,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142605269","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":"ITGA1 Promotes Glioma Cell Proliferation and Affects Immune Cell Infiltration in Low-Grade Glioma.","authors":"Yanhong Ren, Jianchang Xu, Zhengkui Zhang, Rutong Yu","doi":"10.1155/2024/6147483","DOIUrl":"10.1155/2024/6147483","url":null,"abstract":"<p><p><b>Background:</b> Low-grade glioma (LGG) is a commonly occurring type of central nervous system cancer. Integrin α1 (ITGA1), a family member of integrins, is implied in the malignant development of cancers, but the fundamental role of ITGA1 has not been illustrated yet in glioma. This study aimed to evaluate the prognostic value of ITGA1. <b>Methods:</b> Correlations between ITGA1 and relevant clinical features were analyzed in the LGG datasets based on Chinese Glioma Genome Atlas (CGGA) and Tumor Genome Atlas (TCGA). Glioma clinical samples and glioma cell lines were identified at the level of mRNA and protein level by Western blot. Cox regression were developed to assess the involvement of ITGA1 expression in predicting survival in LGG patients. Application of GSEA enrichment analysis to reveal ITGA1-mediated biological functions in LGG. Using TIMER 2.0 to analyze correlations between immune cell infiltration. In addition, ITGA1 high expression was analyzed for correlation with immune checkpoint-related genes and cumulative survival time. <b>Results:</b> ITGA1 was significantly more expressed in LGG than in normal samples. Cox regression indicated that ITGA1 was a risk factor independently for prognosis in LGG patients. GSEA enrichment analysis indicated that ITGA1 was engaged in several immunomodulatory processes. ITGA1 expression was shown to be highly correlated with the immune score, stromal score, and estimate score in LGG. ITGA1 was significantly related to the immune checkpoint-associated gene expression. In vivo experiments showed that overexpression of ITGA1 promoted glioma cell invasion. <b>Conclusion:</b> High ITGA1 expression is correlated with immune infiltration of the low-grade tumor, leading to poor prognoses in LGG patients.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"6147483"},"PeriodicalIF":4.4,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11537738/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142583371","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 AMPK-mTOR Pathway Is Inhibited by Chaihu Shugan Powder, Which Relieves Nonalcoholic Steatohepatitis by Suppressing Autophagic Ferroptosis.","authors":"Zheng Liang, Dajin Pi, Jianwei Zhen, Haizhen Yan, Chuiyang Zheng, July Liang Chen, Wen Fan, Qingliang Song, Jinyue Pan, Dongdong Liu, Maoxing Pan, Qinhe Yang, Yupei Zhang","doi":"10.1155/2024/4777789","DOIUrl":"10.1155/2024/4777789","url":null,"abstract":"<p><p>Nonalcoholic steatohepatitis (NASH) is the advanced stage of nonalcoholic fatty liver disease (NAFLD), which is distinguished by the accumulation of fat in the liver, damage to liver cells, and inflammation. Chaihu Shugan powder (CSP), a renowned traditional Chinese medicine (TCM) blend extensively utilized in China to address liver disease, has demonstrated its efficacy in reducing lipid buildup and effectively combating inflammation. Hence, the primary objective of this research is to examine the impacts and possible mechanisms of CSP on NASH through assessments of liver histopathology, lipidomic analysis, and gene expression. To induce a mouse model of NASH, we employed a diet which deficient in methionine and choline, known as methionine-choline deficient (MCD) diet. Initially, we examined the impact of administering CSP to NASH mice by assessing the levels of serum and liver indicators. We found that CSP was able to reduce lipid buildup and inflammation in mice. In addition, a total of 1009 genes exhibited enrichment in both the autophagy and ferroptosis pathways. The liver protein levels of Adenosine monophosphate-activated protein kinase-mammalian target of rapamycin (AMPK-mTOR)-mediated autophagy and ferroptosis markers, such as p-AMPK<i>α</i>/AMPK<i>α</i>, p-mTOR/mTOR, Beclin-1, microtubule associated protein 1 light chain 3 gamma (LC3), p62 (sequestosome 1 [SQSTM1/p62]), Kelch-like ECH-associated protein 1 (KEAP1), nuclear factor erythroid 2-related factor 2 (Nrf-2), ferritin heavy chain 1 (FTH1), and glutathione peroxidase 4 (GPX4), were restored by CSP. Furthermore, our findings indicated that the suppression of autophagy had a repressive impact on the occurrence of ferroptosis in the mouse model, indicating that autophagy activation likely plays a role in mediating ferroptosis in NASH.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"4777789"},"PeriodicalIF":4.4,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11535263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142583377","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":"Functional Involvement of TANK-Binding Kinase 1 in the MyD88-Dependent NF-<i>κ</i>B Pathway Through Syk.","authors":"Han Gyung Kim, Ji Hye Kim, Tao Yu, Jae Youl Cho","doi":"10.1155/2024/8634515","DOIUrl":"10.1155/2024/8634515","url":null,"abstract":"<p><p>Inflammation is a vital immune defense mechanism regulated by Toll-like receptors (TLRs) and the nuclear factor-kappa B (NF-<i>κ</i>B) pathway. TANK-binding kinase 1 (TBK1) is central to immunity and inflammation and influences antiviral responses and cellular processes. However, the precise role of TBK1 in modulating the NF-<i>κ</i>B pathway through interactions with other proteins, such as spleen tyrosine kinase (Syk), remains poorly understood. As dysregulation of TBK1 and NF-<i>κ</i>B can lead to a variety of diseases, they are important therapeutic targets. In this work, inflammatory processes involving the TBK1-Syk-NF-<i>κ</i>B pathway were elucidated using lipopolysaccharide (LPS)-induced macrophages; human embryonic kidney 293 (HEK293) cells overexpressing MyD88, TBK1, and Syk proteins and their mutants; and real-time polymerase chain reaction (PCR), immunoblotting analyses, and kinase assays. TBK1 was activated in LPS-, poly I:C-, and Pam3CSK-stimulated macrophages. Transcript levels of <i>TNF</i>, <i>NOS2</i>, and <i>IL1B</i> were increased in cells overexpressing TBK1 but not in cells overexpressing TBK1 K38A. The transcription of <i>TNF</i>, <i>NOS2</i>, and <i>IL1B</i> and NF-<i>κ</i>B luciferase activity were inhibited by silencing TBK1 in LPS-stimulated RAW264.7 cells and MyD88-transfected HEK293 cells. Syk was the key mediator of the TBK1-dependent NF-<i>κ</i>B pathway and bound directly to the coiled coil domain of TBK1, which was necessary to activate Syk and the Syk-p85 pathway. This research advances the understanding of the role of TBK1 in NF-<i>κ</i>B signaling, emphasizing Syk as a key mediator. The interaction between TBK1 and Syk has potential for precise immune modulation that can be applied to treat immune-related disorders.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"8634515"},"PeriodicalIF":4.4,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11531359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142569121","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":"Autophagy Improves Inflammatory Response in Sepsis Accompanied by Changes in Gut Microbiota.","authors":"La Wang, WenJia Wang, GuiTong Jiang, ZunLi Ke, RuiXi Luo, WeiYi Tian","doi":"10.1155/2024/9550301","DOIUrl":"10.1155/2024/9550301","url":null,"abstract":"<p><p><b>Background:</b> Sepsis is defined as a life-threatening disease. Autophagy and the microbiome are increasingly connected with sepsis. The aim of this study was to investigate the protective effect of autophagy and the possible mechanisms. <b>Methods:</b> The septic rat model was established by cecal ligation perforation (CLP). Rapamycin (Rap), 3-methyladenine (3-MA), and chloroquine (CQ) were administered to interfere autophagy. Western blot (WB) was used to detect the expression of key proteins in autophagy. Hematoxylin and eosin (H&E) staining and enzyme-linked immunosorbent assays (ELISAs) were used to identify the effect of autophagy on various organs. 16S ribosomal RNA gene sequencing was used to analyze the changes of the gut microbiota. <b>Results:</b> Rap significantly upregulated the expression of key autophagy proteins, and 3-MA reduced the relative expression compared to the CLP group. The autophagic flux showed a corresponding trend. Interestingly, the autophagy inducer significantly decreased the mortality and the lipopolysaccharide (LPS) level in serum compared with the CLP group. Autophagy activation significantly improves the inflammatory response in sepsis. Histopathological sections showed that CLP destroyed the tight junctions between ileal epithelial cells, while autophagy induction reversed the damage. The sequencing results showed that autophagy activation increased the alpha diversity and alterted the composition and structure of gut microbiota. The abundance of Proteobacteria was markedly decreased in the Rap group, whereas Bacteroidetes was notably increased compared with the CLP group. Additionally, the protective effect of autophagy further changed the biomarkers in the microbial community. The top 35 functions in each sample were analyzed to obtain 18 genes including RNA synthesis, ATP binding and transport, chromosome assignment, osmotic polysaccharide transport, transcytosis, and methylation. <b>Conclusion:</b> Autophagy is able to improve inflammation and may directly or indirectly regulate the microbiota of septic rats. Autophagy may be an important target for future clinical interventions in the treatment of sepsis.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"9550301"},"PeriodicalIF":4.4,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11511597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142503545","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 Role of CXCR3 in Nervous System-Related Diseases.","authors":"Fangyuan Wang, Bing Guo, Ziyang Jia, Zhou Jing, Qingyi Wang, Minghe Li, Bingqi Lu, Wulong Liang, Weihua Hu, Xudong Fu","doi":"10.1155/2024/8347647","DOIUrl":"10.1155/2024/8347647","url":null,"abstract":"<p><p>Inflammatory chemokines are a group of G-protein receptor ligands characterized by conserved cysteine residues, which can be divided into four main subfamilies: CC, CXC, XC, and CX3C. The C-X-C chemokine receptor (CXCR) 3 and its ligands, C-X-C chemokine ligands (CXCLs), are widely expressed in both the peripheral nervous system (PNS) and central nervous system (CNS). This comprehensive literature review aims to examine the functions and pathways of CXCR3 and its ligands in nervous system-related diseases. In summary, while the related pathways and the expression levels of CXCR3 and its ligands are varied among different cells in PNS and CNS, the MPAK pathway is the core via which CXCR3 exerts physiological functions. It is not only the core pathway of CXCR3 after activation but also participates in the expression of CXCR3 ligands in the nervous system. In addition, despite CXCR3 being a common inflammatory chemokine receptor, there is no consensus on its precise roles in various diseases. This uncertainty may be attributable to distinct inflammatory characteristics, that inflammation simultaneously possesses the dual properties of damage induction and repair facilitation.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"8347647"},"PeriodicalIF":4.4,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11488998/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469521","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":"Protective Effects of Baicalein on Lipopolysaccharide-Induced AR42J PACs through Attenuation of Both Inflammation and Pyroptosis via Downregulation of miR-224-5p/PARP1.","authors":"Ming-Wei Liu, Chun-Hai Zhang, Shou-Hong Ma, De-Qiong Zhang, Li-Qiong Jiang, Yang Tan","doi":"10.1155/2024/6618927","DOIUrl":"https://doi.org/10.1155/2024/6618927","url":null,"abstract":"<p><strong>Background: </strong>Baicalein has been used to treat inflammation-related diseases; nevertheless, its specific mechanism of action is unclear. Therefore, we examined the protective effects of baicalein on lipopolysaccharide-induced damage to AR42J pancreatic acinar cells (PACs) and determined its mechanism of action for protection.</p><p><strong>Methods: </strong>An <i>in vitro</i> cell model of acute pancreatitis (AP) was established using lipopolysaccharide (LPS) (1 mg/L)-induced PACs (AR42J), and the relative survival rate was determined using the 3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-di-phenytetrazoliumromide (MTT) technique. Flow cytometry was applied to evaluate the apoptotic rates of AR42J PACs. The RNA and protein expression of miR-224-5p, poly ADP-ribose polymerase-1 (PARP1), nuclear transcription factor-<i>κ</i>B65 (NF-<i>κ</i>B65), phospho-kappa B alpha(p-I<i>κ</i>B-<i>α</i>), interleukin(IL)-18R, NOD-like receptor thermal protein domain-associated protein 3 (NLRP3), gasdermin D (GSDMD), apoptosis-associated speck-like protein containing a CARD (ASC), and caspase-1 was detected based on the WB and RT-PCR assays. IL-1<i>β</i>, IL-6, IL-18, and TNF-<i>α</i> expression levels in AR42J cells were measured via ELISA method. The cell morphology was examined using the AO/EB method.</p><p><strong>Results: </strong>The experiment confirmed a significant increase in the activity of AR42J cells treated with various doses of baicalein. Moreover, IL-1<i>β</i>, IL-6, TNF-<i>α</i>, and IL-18 expression levels in AR42J cells were dramatically reduced (<i>P</i>  < 0.05), while miR-224-5p level was obviously enhanced. The protein and gene expression of PARP1, NF-<i>κ</i>B65, p-I<i>κ</i>B-<i>α</i>, IL-18R, GSDMD, ASC, NLRP3, and caspase-1 was obviously decreased (<i>P</i> < 0.05). Apoptosis in AR42J cells was significantly reduced with significant improvement in cell morphology.</p><p><strong>Conclusion: </strong>Baicalein may significantly alleviate LPS-induced AR42J PAC damage by inhibiting the inflammatory response and pyroptosis. Its mode of action might be linked to higher miR-224-5p expression, which inhibits the PARP1/NF-<i>κ</i>B and NLPR3/ASC/caspase-1/GSDMD pathways.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"6618927"},"PeriodicalIF":4.4,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11486537/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469520","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":"Lipocalin-2 Serum Levels in Rheumatoid Arthritis Patients Treated with Adalimumab and Its Correlation with Proinflammatory Factors.","authors":"Javier Conde-Aranda, Morena Scotece, María Varela-García, Carlos Torrijos-Pulpón, Laura Arosa, Miguel Camba-Gómez, Jesús Pino, Oreste Gualillo","doi":"10.1155/2024/7264704","DOIUrl":"https://doi.org/10.1155/2024/7264704","url":null,"abstract":"<p><strong>Background: </strong>Obesity is associated with an increased risk for different chronic diseases such as osteoarthritis (OA) or rheumatoid arthritis (RA). In fact, adipose tissue is now recognized as an endocrine organ able to secrete a wide variety of factors called adipokines, which have been demonstrated to participate in the pathophysiology of RA by regulating inflammation and immunity. LCN2 is one of these adipose tissue-derived factors. However, scarce information is available about the levels of this adipokine in different rheumatic diseases. Therefore, we aimed to analyze LCN2 serum levels in healthy, OA, and RA patients under different treatments.</p><p><strong>Methods: </strong>Serum levels of LCN2, among other proinflammatory and chemotactic factors, have been measured by ELISA or Multiplex in the following four groups of individuals: healthy, OA, and RA patients treated with conventional treatment or adalimumab.</p><p><strong>Results: </strong>We found increased serum levels of LCN2 in OA and RA patients. Interestingly, LCN2 serum levels show a similar pattern to that observed for different proinflammatory and chemotactic factors, being increased in RA conventional treated patients in comparison to RA patients treated with adalimumab. Also, RA patients under conventional treatment revealed a positive and significant correlation between LCN2 and CCL2, CCL3, IL-8, IL-1<i>β</i>, IL-6, and CRP. In patients with RA treated with adalimumab, only IL-6 and CRP correlated significantly with LCN2.</p><p><strong>Conclusions: </strong>Our results clearly suggest that LCN2 is modulated and associated with inflammation in rheumatic diseases. Therefore, the serum levels of this adipokine might be used as an additional biomarker of the inflammatory/disease activity.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"7264704"},"PeriodicalIF":4.4,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11473169/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469519","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":"Glutathione: A Key Regulator of Extracellular Matrix and Cell Death in Intervertebral Disc Degeneration.","authors":"Fudong Li, Shaofei Li, Yangyang Shi, Feng Lin, Lining Rui, Jiangang Shi, Kaiqiang Sun","doi":"10.1155/2024/4482642","DOIUrl":"https://doi.org/10.1155/2024/4482642","url":null,"abstract":"<p><p>Intervertebral disc degeneration (IVDD) is a degenerative disease accompanied by the loss of nucleus pulposus cells and the degradation of extracellular matrix (ECM), which tends to be associated with lower back pain. The ECM and various types of cell death in IVDD are regulated by multiple factors, such as inflammatory responses and oxidative stress. The glutathione (GSH) redox system is the most important antioxidant defense system in cells. GSH is one of the most abundant thiol antioxidants in mammalian cells, which functions directly and indirectly by scavenging peroxides through the GSH redox system. In these reactions, GSH is oxidized by electrophilic substances, such as reactive oxygen species and free radicals, to form glutathione disulfide to exert antioxidative effects. It has been reported that GSH can protect cells against the damage of oxidative stress and various pathophysiological stimulus that can lead to different types of cell death. In addition, it was reported that the level of GSH widely participates in apoptosis, autophagy, ferroptosis, and oxidative stress in many diseases including osteoarthritis and IVDD. Therefore, we summarized the effects of GSH on ECM metabolism and cells' functions during IVDD. In addition, we summarized the regulatory effects of small molecule compounds on GSH to explore potential ways to regulate the level of GSH. Better understanding the underlying role of GSH in regulating IVDD will facilitate the goal of preventing and retarding the progress of IVDD in the future.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"4482642"},"PeriodicalIF":4.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11473174/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142469518","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}