Mediators of Inflammation最新文献

{"title":"TLR2 Derangements Likely Play a Significant Role in the Inflammatory Response and Thrombosis in Patients with <i>Ph</i>(-) Classical Myeloproliferative Neoplasm.","authors":"Jen Chin Wang, Guanfang Shi, Chi Chen, Ching Wong, Vladimir Gotlieb, Gardith Joseph, Kiron V Nair, Lakshmi Boyapati, Enayati Ladan, James T Symanowski, Lishi Sun","doi":"10.1155/2024/1827127","DOIUrl":"10.1155/2024/1827127","url":null,"abstract":"<p><p>We investigated the role of toll-like receptors (TLRs) in inflammatory pathways in Philadelphia chromosome-negative myeloproliferative neoplasms (<i>Ph</i>(-)MPNs). TLR2 expression was increased in ET, PV, and MPN (grouped as (PV + (ET) + MF)), whereas TLR4 was elevated only in MPN. TLR3, 7, and 9 were not elevated. Cultured monocyte-derived dendritic cells and plasma assays in TLR2-elevated patients were found to secrete more cytokines than those from TLR2-normal patients. These facts suggest that TLR2 is the major inflammatory pathways in MPN. We also measured S100A9 and reactive oxygen species (ROS), revealing increased S100A9 in PV, MF, and MPN, while ROS were only increased in MF. These data suggests that MPNs initially involve TLR2, with minor contributions from TLR4, and with S100A9, leading to ROS formation, JAK2 mutation, and progression to MF or leukemia. Furthermore, patients with JAK2 mutations or leukocytosis exhibited higher TLR2 expression. In leukocyte-platelet interactions, cells from MPN patients displayed a stronger response to a TLR2 agonist than TLR4 agonist. A TLR2 inhibitor (but not a TLR4 inhibitor) attenuated this response. Thrombosis incidence was higher in TLR2-elevated patients (29%) than in TLR2-normal patients (19%). These findings suggest that TLR2 likely contributes to thrombosis in MPN.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"1827127"},"PeriodicalIF":4.4,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11329310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000383","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 Function of Necroptosis and Its Treatment Target in IBD.","authors":"Francis Atim Akanyibah, Yi Zhu, Tao Jin, Dickson Kofi Wiredu Ocansey, Fei Mao, Wei Qiu","doi":"10.1155/2024/7275309","DOIUrl":"10.1155/2024/7275309","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD), which encompasses Crohn's disease (CD) and ulcerative colitis (UC), is a complicated illness whose exact cause is yet unknown. Necroptosis is associated with IBD pathogenesis, leading to intestinal barrier abnormalities and uncontrolled inflammation. Molecules involved in necroptosis, however, exhibit different expression levels in IBD and its associated colorectal cancer. Multiple studies have shown that inhibiting these molecules alleviates necroptosis-induced IBD. Moreover, due to the severe scarcity of clinical medications for treating IBD caused by necroptosis, we review the various functions of crucial necroptosis molecules in IBD, the stimuli regulating necroptosis, and the current emerging therapeutic strategies for treating IBD-associated necroptosis. Eventually, understanding the pathogenesis of necroptosis in IBD will enable the development of additional therapeutic approaches for the illness.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"7275309"},"PeriodicalIF":4.4,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11306684/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141908843","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":"Anti-Inflammatory and Antioxidant Properties of a New Mixture of Vitamin C, Collagen Peptides, Resveratrol, and Astaxanthin in Tenocytes: Molecular Basis for Future Applications in Tendinopathies.","authors":"Monica Marzagalli, Stefania Battaglia, Michela Raimondi, Fabrizio Fontana, Marco Cozzi, Francesca R Ranieri, Roberto Sacchi, Valeria Curti, Patrizia Limonta","doi":"10.1155/2024/5273198","DOIUrl":"10.1155/2024/5273198","url":null,"abstract":"<p><p>Tendinopathy is one of the most frequent musculoskeletal disorders characterized by sustained tissue inflammation and oxidative stress, accompanied by extracellular matrix remodeling. Patients suffering from this pathology frequently experience pain, swelling, stiffness, and muscle weakness. Current pharmacological interventions are based on nonsteroidal anti-inflammatory drugs; however, the effectiveness of these strategies remains ambiguous. Accumulating evidence supports that oral supplementation of natural compounds can provide preventive, and possibly curative, effects. Vitamin C (Vit C), collagen peptides (Coll), resveratrol (Res), and astaxanthin (Asx) were reported to be endowed with potential beneficial effects based on their anti-inflammatory and antioxidant activities. Here, we analyzed the efficacy of a novel combination of these compounds (Mix) in counteracting proinflammatory (IL-1<i>β</i>) and prooxidant (H₂O₂) stimuli in human tenocytes. We demonstrated that Mix significantly impairs IL-6-induced IL-1<i>β</i> secretion, NF-<i>κ</i>B nuclear translocation, and MMP-2 production; notably, a synergistic effect of Mix over the single compounds could be observed. Moreover, Mix was able to significantly counteract H₂O₂-triggered ROS production. Together, these results point out that Mix, a novel combination of Vit C, Coll, Resv, and Asx, significantly impairs proinflammatory and prooxidant stimuli in tenocytes, mechanisms that contribute to the onset of tendinopathies.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"5273198"},"PeriodicalIF":4.4,"publicationDate":"2024-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303056/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141897772","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":"mTOR Deletion Alleviates CD4+ T-Cell Dysfunction in Sepsis through Reducing CTLA4 Accumulation Mediated by Rescuing Autophagy.","authors":"Xianli Lei, Guoyu Zhao, Yawen Xie, Na Cui","doi":"10.1155/2024/4233439","DOIUrl":"10.1155/2024/4233439","url":null,"abstract":"<p><p>Sepsis has been the leading cause of death in ICU patients. CD4+ T cells are the mainstay of the body's immune system, and the depletion of CD4+ T cells in sepsis is of great concern. Cytotoxic T lymphocyte-associated protein 4 (CTLA4) is a negative immunomodulator for T cell activation and degradation through the autophagy-lysosome pathway. Mammalian target of rapamycin (mTOR) is the most classical upstream regulator of autophagy. With a mouse model of sepsis through cecal ligation and puncture (CLP), T cell specific-mTOR/tuberous sclerosis complex 1 (TSC1)-knockout mice, and bafilomycin A1, a specific autophagosome-lysosome (A-L) fusion inhibitor, we primarily proved that mTOR could modulate the expression and accumulation of CTLA4 by regulating the onset process of autophagy such as A-L fusion. Given such a regulatory relationship, targeting mTOR could provide new light to improve immune function in sepsis, and the prospect of using rapamycin in the clinic would be worth exploring further.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"4233439"},"PeriodicalIF":4.4,"publicationDate":"2024-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141893801","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":"ALBI Grade Is Associated with Clinical Outcomes of Critically Ill Patients with AKI: A Cohort Study with Cox Regression and Propensity Score Matching.","authors":"Chao Yang, Zhikang Yu, Bo Peng, Changkun Mao, Junting Li, Yongsheng Cao","doi":"10.1155/2024/1412709","DOIUrl":"10.1155/2024/1412709","url":null,"abstract":"<p><strong>Background: </strong>The albumin-bilirubin (ALBI) grade has surfaced as a viable substitute for assessing liver functional reserve in individuals afflicted with hepatocellular carcinoma (HCC). ALBI grade also demonstrates the capacity to stratify distinct patient subcohorts bearing disparate prognostic implications in not only HCC but also other inflammatory diseases like acute pancreatitis. However, the association between ALBI grade and clinical outcomes of acute kidney injury (AKI) remains mysterious.</p><p><strong>Methods: </strong>The dataset was sourced from the Multiparameter Intelligent Monitoring in Intensive Care Database IV (MIMIC-IV) version 2.0. ALBI grade was calculated in a nomogram utilizing albumin and bilirubin. In order to ascertain the connection between ALBI grades and clinical outcomes of patients with AKI, Cox proportional hazards regression analysis was employed with in-hospital, 30- and 90-day mortality as end points, respectively. The Kaplan-Meier (K-M) curve was employed to gauge the cumulative incidence of mortality based on various ALBI grades. To explore potential nonlinear relationships, the Restricted Cubic Spline (RCS) approach was adopted. Furthermore, a subgroup analysis was conducted to validate the durability of the correlation between ALBI grade and in-hospital mortality. Furthermore, equilibrium of confounding variables was also achieved through the application of propensity score matching (PSM).</p><p><strong>Results: </strong>The study encompassed a total of 12,518 patients (ALBI grade 1 : 2878, grade 2 : 6708, and grade 3 : 2932). Patients with heightened ALBI grades displayed a significant correlation with increased mortality in both univariate and various multivariate Cox regression models. RCS depicted a predominantly linear relationship. The robustness of the correlation was also affirmed across multifarious subpopulations through subgroup analysis. The association still remains after PSM.</p><p><strong>Conclusion: </strong>Elevated ALBI grade was associated with worse clinical outcomes of critically ill patients with AKI.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"1412709"},"PeriodicalIF":4.4,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11272401/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141759621","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":"5-Methoxytryptophan Alleviates Dextran Sulfate Sodium-Induced Colitis by Inhibiting the Intestinal Epithelial Damage and Inflammatory Response.","authors":"Yanling Wang,Jun Li,Qinyuan Yang,Zhenhang Zhu,Fang Cheng,Xiangyan Ai,Yang Liu,Dongbao Zhao,Futao Zhao,Peng Cheng","doi":"10.1155/2024/1484806","DOIUrl":"https://doi.org/10.1155/2024/1484806","url":null,"abstract":"BackgroundColitis is a refractory intestinal inflammatory disease significantly affecting the quality of a patient's life and increasing the risk of exacerbation. The primary factors leading to colitis encompass infections, insufficient blood flow, and the buildup of collagen as well as white blood cells. Among various available therapeutics, 5-methoxytryptophan (5-MTP) has emerged as one of the protectants by inhibiting inflammatory damage. Nonetheless, there is no report on the role of 5-MTP in the treatment of colitis.Materials and MethodsTo verify the anti-inflammatory effect of 5-MTP in vivo, we first constructed mouse model with dextran sulfate sodium-induced colitis. Furthermore, the macrophage infiltration and release of inflammatory factors through western blot (WB) and hematoxylin-eosin staining analyses were examined. Intestinal epithelial cell tight junction damage and apoptosis were investigated by WB analysis, immunofluorescence, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Finally, we examined the generation of cellular inflammation and analyzed the influence of 5-MTP on M1 polarization at the cellular level.ResultsThis study initially confirmed that 5-MTP possessed an excellent therapeutic effect on colitis. 5-MTP inhibits macrophage infiltration and the generation of inflammatory factors. In addition to its effects on immune cells, 5-MTP significantly inhibits intestinal epithelial cell tight junction damage and apoptosis in vivo. Moreover, it inhibits inflammation and M1 polarization response in vitro.Conclusion5-MTP counteracts excessive inflammation, thereby preventing intestinal epithelial tight junction damage. In addition, inhibition of apoptosis suggests that 5-MTP may be a potential therapeutic agent for colitis.","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"46 1","pages":"1484806"},"PeriodicalIF":4.6,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142208505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of <i>Kynu</i>, <i>Defb2</i>, <i>Camp</i>, and <i>Penk</i> Expression Levels as Psoriasis Marker in the Imiquimod-Induced Psoriasis Model.","authors":"Zahra Emami, Saeideh Sadat Shobeiri, Razia Khorrami, Navideh Haghnavaz, Mohammad Ali Rezaee, Malihe Moghadam, Safoora Pordel, Mojtaba Sankian","doi":"10.1155/2024/5821996","DOIUrl":"10.1155/2024/5821996","url":null,"abstract":"<p><strong>Background: </strong>Psoriasis is a noncontagious auto-inflammatory chronic skin disease. So far, some of the inflammatory genes were upregulated in mouse model of psoriasis. This study examined changes in skin mRNA expression of L-kynureninase (<i>Kynu</i>), cathelicidin antimicrobial peptide (<i>Camp</i>), beta-defensin 2 (<i>Defb2</i>), and proenkephalin (<i>Penk</i>) in a mouse model of imiquimod-induced psoriasis.</p><p><strong>Materials and methods: </strong>Tree groups of C57BL/6 female mice were allocated. The imiquimod (IMQ) cream was administered to the mice dorsal skin of the two groups to induce psoriatic inflammation. In the treatment group, IMQ was administered 10 min after hydrogel-containing M7 anti-IL-17A aptamer treatment. Vaseline (Vas) was administered to the negative control group. The psoriatic skin lesions were evaluated based on the psoriasis area severity index (PASI) score, histopathology, and mRNA expression levels of <i>Kynu</i>, <i>Camp</i>, <i>Defb2</i>, and <i>Penk</i> using real-time PCR. In order to assess the systemic response, the spleen and lymph node indexes were also evaluated.</p><p><strong>Results: </strong>The PASI and epidermal thickness scores were 6.01 and 1.96, respectively, in the IMQ group, and they significantly decreased after aptamer administration to 1.15 and 0.90, respectively (<i>P</i> < 0.05). Spleen and lymph node indexes showed an increase in the IMQ group, followed by a slight decrease after aptamer treatment (<i>P</i> > 0.05). Additionally, the mRNA expression levels of <i>Kynu</i>, <i>Defb2</i>, <i>Camp</i>, and <i>Penk</i> genes in the IMQ-treated region showed a significant 2.70, 4.56, 3.29, and 2.61-fold increase relative to the Vas mice, respectively (<i>P</i> < 0.05). The aptamer-treated region exhibited a significant decrease in these gene expression levels (<i>P</i> < 0.05). A positive correlation was found between <i>Kynu</i>, <i>Penk</i>, and <i>Camp</i> expression levels and erythema, as well as <i>Camp</i> expression with PASI, scaling, and thickness (<i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>According to our results, it seems that <i>Kynu</i>, <i>Camp</i>, and <i>Penk</i> can be considered appropriate markers for the evaluation of psoriasis in IMQ-induced psoriasis. Also, the anti-IL-17 aptamer downregulated these important genes in this mouse model.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"5821996"},"PeriodicalIF":4.4,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11265934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141752097","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":"Psoralen Isolated from the Roots of <i>Dorstenia psilurus</i> Welw. Modulate Th1/Th2 Cytokines and Inflammatory Enzymes in LPS-Stimulated RAW 264.7 Macrophages.","authors":"Adamu Imam Isa, Hugues Fouotsa, Osama A Mohammed, Mushabab Alghamdi, Bappa Adamu, Jaber Alfaifi, Abubakar Mohammed Jibo, Mohannad Mohammed Saleh Alamri, Sameer Khan, Masoud Ishag Elkhalifa Adam, Abdullah Ali Alqarni, Mohamed O'haj Mohamed, Joël Eddy Terence Ateba, Jean Paul Dzoyem","doi":"10.1155/2024/8233689","DOIUrl":"10.1155/2024/8233689","url":null,"abstract":"<p><p><i>Dorstenia psilurus</i> is a widely used plant spice in traditional African medicine to treat pain-related conditions. However, the anti-inflammatory mechanisms underlying this activity and the main active ingredients of <i>D. psilurus</i> have not yet been fully characterized. This study aimed to isolate and identify the main active anti-inflammatory constituents of the <i>D. psilurus</i> extract and to investigate the underlying anti-inflammatory mechanisms in murine macrophages. Chromatographic techniques and spectroscopic data were used for compound isolation and structure elucidation. The Griess reagent method and the ferrous oxidation-xylenol orange assay were used to evaluate the inhibition of NO production and 15-lipoxygenase activity, respectively. Cyclooxygenase activity was assessed using the fluorometric COX activity assay kit, and Th1/Th2 cytokine measurement was performed using a flow cytometer. The results indicated that the extract and fractions of <i>D. psilurus</i> inhibit NO production and proliferation of RAW 264.7 macrophage cells. Bioguided fractionation led to the identification of psoralen, a furocoumarin, as the main bioactive anti-inflammatory compound. Psoralen inhibited NO production and 15-lipoxygenase activity and reduced pro-inflammatory Th1 cytokines (IFN-<i>γ</i>, TNF-<i>α</i>, and IL-2) while increasing the secretion of anti-inflammatory cytokines (IL-4, IL-6, and IL-10) in activated RAW 264.7 macrophage cells. The encouraging results obtained in this study suggest that psoralen-based multiple modulation strategies could be a useful approach to address the treatment of inflammatory diseases.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"8233689"},"PeriodicalIF":4.4,"publicationDate":"2024-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11257762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141723867","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":"Dietary Fiber-Derived Microbial Butyrate Suppresses ILC2-Dependent Airway Inflammation in COPD.","authors":"Min Jiang, Jing Wang, Zheng Li, Dan Xu, Jing Jing, Fengsen Li, Jianbing Ding, Qifeng Li","doi":"10.1155/2024/6263447","DOIUrl":"10.1155/2024/6263447","url":null,"abstract":"<p><p>Group 2 innate lymphoid cells (ILC2) strongly modulate COPD pathogenesis. However, the significance of microbiota in ILC2s remains unelucidated. Herein, we investigated the immunomodulatory role of short-chain fatty acids (SCFAs) in regulating ILC2-associated airway inflammation and explores its associated mechanism in COPD. In particular, we assessed the SCFA-mediated regulation of survival, proliferation, and cytokine production in lung sorted ILC2s. To elucidate butyrate action in ILC2-driven inflammatory response in COPD models, we administered butyrate to BALB/c mice via drinking water. We revealed that SCFAs, especially butyrate, derived from dietary fiber fermentation by gut microbiota inhibited pulmonary ILC2 functions and suppressed both IL-13 and IL-5 synthesis by murine ILC2s. Using <i>in vivo</i> and <i>in vitro</i> experimentation, we validated that butyrate significantly ameliorated ILC2-induced inflammation. We further demonstrated that butyrate suppressed ILC2 proliferation and GATA3 expression. Additionally, butyrate potentially utilized histone deacetylase (HDAC) inhibition to enhance NFIL3 promoter acetylation, thereby augmenting its expression, which eventually inhibited cytokine production in ILC2s. Taken together, the aforementioned evidences demonstrated a previously unrecognized role of microbial-derived SCFAs on pulmonary ILC2s in COPD. Moreover, our evidences suggest that metabolomics and gut microbiota modulation may prevent lung inflammation of COPD.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"6263447"},"PeriodicalIF":4.4,"publicationDate":"2024-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11251798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141627049","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":"Neutrophil-Lymphocytes Ratio as Potential Early Marker for Alzheimer's Disease.","authors":"Carlo Cervellati, Dario Pedrini, Pietro Pirro, Paola Guindani, Carlo Renzini, Gloria Brombo, Giovanni Zuliani","doi":"10.1155/2024/6640130","DOIUrl":"10.1155/2024/6640130","url":null,"abstract":"<p><strong>Background: </strong>Neutrophil-lymphocyte ratio (NLR) is a noninvasive, inexpensive, and easily applicable marker of inflammation. Since immune dysregulation leading to inflammation is regarded as a hallmark of dementia, in particular Alzheimer's disease (AD), we decided to investigate the potentials of NLR as a diagnostic and predictive biomarker in this clinical setting.</p><p><strong>Materials and methods: </strong>NLR was measured in the blood of patients with AD (<i>n</i> = 103), amnestic type mild cognitive impairment (aMCI, <i>n</i> = 212), vascular dementia (VAD, <i>n</i> = 34), and cognitively healthy Controls (<i>n</i> = 61). One hundred twelve MCI patients underwent a regular clinical follow-up. Over a 36-months median follow-up, 80 remained stable, while 32 progressed to overt dementia.</p><p><strong>Results: </strong>NLR was higher in patients with aMCI or dementia compared to Controls; however, the difference was statistically significant only for aMCI (+13%, <i>p</i>=0.04) and AD (+20%, <i>p</i>=0.03). These results were confirmed by multivariate logistic analysis, which showed that high NLR was associated with an increase in the likelihood of receiving a diagnosis of aMCI (odd ratio (OR): 2.58, 95% confidence interval (CI): 1.36-4.89) or AD (OR: 3.13, 95%CI: 1.47-6.70), but not of VAD. NLR did not differ when comparing stable vs. progressing aMCI.</p><p><strong>Conclusions: </strong>This is the first report showing that NLR is significantly increased in MCI and AD but not in VAD. We also found that NLR was unable to predict the conversion from aMCI to AD. Further research on larger cohorts is warranted to definitely ascertain the application of NLR as a possible marker for aMCI and AD.</p>","PeriodicalId":18371,"journal":{"name":"Mediators of Inflammation","volume":"2024 ","pages":"6640130"},"PeriodicalIF":4.4,"publicationDate":"2024-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11227945/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141555214","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}