Immunity, Inflammation and Disease最新文献

{"title":"The Joint Effect of Renal Function Status and Coagulation Biomarkers on In-Hospital Outcomes in Acute Ischemic Stroke Patients With Intravenous Thrombolysis","authors":"Manli Lu,&nbsp;Junwen Xue,&nbsp;Yi Wang,&nbsp;Dongqin Chen,&nbsp;Yongjun Cao,&nbsp;Chongke Zhong,&nbsp;Xia Zhang","doi":"10.1002/iid3.70099","DOIUrl":"10.1002/iid3.70099","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To demonstrate whether combining renal function status [estimating glomerular filtration rate (eGFR)] with coagulation biomarkers [fibrinogen (Fg) and <span>d</span>-dimer] is more beneficial in predicting in-hospital outcomes following intravenous thrombolysis (IVT) in acute ischemic stroke (AIS) patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We studied 417 AIS patients with IVT. According to the cut-offs of coagulation biomarkers (Fg and <span>d</span>-dimer) and eGFR determined by receiver operating characteristic (ROC) curves, the patients were divided into four groups: LFLG (low Fg and low eGFR), LFHG (low Fg and high eGFR), HFLG (high Fg and low eGFR), and HFHG (high Fg and high eGFR); or LDLG (low <span>d</span>-dimer and low eGFR), LDHG (low <span>d</span>-dimer and high eGFR), HDLG (high <span>d</span>-dimer and low eGFR), and HDHG (high <span>d</span>-dimer and high eGFR). Logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for poor outcomes at discharge and post-stroke pneumonia across the four groups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The patients in the HFLG and HDLG groups had the poorest prognosis at discharge and the highest risk of in-hospital pneumonia. They experienced 3.00 or 4.59 times higher risk of in-hospital pneumonia than those in the LFHG and LDHG groups (95%CI: 1.07–8.44, <i>p</i> &lt; 0.05; 95%CI: 1.58–13.32, <i>p</i> = 0.005). Similarly, the risk of adverse outcome at discharge was 3.02 and 1.52 times higher in HFLG and HDLG groups (95%CI: 1.63–9.91, <i>p</i> &lt; 0.005; 95%CI: 1.11–5.74, <i>p</i> &lt; 0.05) compared to that in LFHG and LDHG groups. Adding eGFR and Fg or <span>d</span>-dimer to the risk model improved the risk reclassification for in-hospital pneumonia and functional outcomes at discharge.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Combining renal function status and coagulation biomarkers within 4.5 h after onset could better predict in-hospital outcomes of AIS patients with IVT.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"12 12","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11633047/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-17A Mediates Depressive-Like Symptoms by Inducing Microglia Activation in Psoriasiform Dermatitis Mice","authors":"Yue Dou,&nbsp;Jingjing You,&nbsp;Jing Wang,&nbsp;Xinxin Li,&nbsp;Yawen Lin,&nbsp;Bin Liu,&nbsp;Lei Ma","doi":"10.1002/iid3.70092","DOIUrl":"10.1002/iid3.70092","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Psoriasis is recognized as a systemic disease for its accompanying comorbidities, among which psychological disorders present a high incidence rate and affect patients’ life quality. Interleukin (IL)-17A is the central pathological factor in the pathogenesis and development of psoriasis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To clarify if psoriasis-induced systemic IL-17A increase can mediate the neuronal inflammation and result in depressive-like symptoms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Psoriasiform dermatitis model was established by imiquimod (IMQ) application on male BALB/c mice and IL-17A intervention was performed by lateral ventricular catheterization. Skin structural, histopathological characteristics, and behavioral tests were assessed. Serum IL-17A levels were detected by Enzyme-linked immunosorbent assay. mRNA expression of pro-inflammatory factors IL-1β, IL-6, and tumor necrosis factor-α (TNF-α) as well as anti-inflammatory factors IL-4 and IL-10 in the hippocampus and cortex were measured by RT-qPCR. The number of microglia and hippocampal neurons was quantified by immunofluorescent assay.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>IMQ treatment resulted in significant skin structural and histopathological characters of psoriasiform dermatitis with elevated serum IL-17A levels, obvious depressive-like behaviors, microglia activation with increased IL-1β, IL-6, and TNF-α expression levels in the hippocampus and cortex, and notable inhibition of hippocampal neurogenesis. While, IL-17A neutralization by intracerebroventricular injection of anti-IL-17A antibody can remarkably inhibit microglia activation and decrease the abnormally increased expression levels of IL-1β, IL-6, and TNF-α in the hippocampus and cortex of psoriasiform dermatitis mice, promote hippocampal neurogenesis, thus alleviate the depressive-like behaviors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In the pathological condition of psoriasis, systemic IL-17A elevation can trigger microglia activation, provoke pro-inflammation mediators to release, evoke neuroinflammation, subsequently inhibit hippocampal neurogenesis, and result in depression. IL-17A, as an important pathogenic factor in psoriasis, contributes to its critical role in mediating systemic inflammation and depression comorbidity.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"12 12","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142805592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Monocyte-Derived Macrophages Induce Alveolar Macrophages Death via TNF-α in Acute Lung Injury","authors":"Junjie Xiao,&nbsp;Fei Hou,&nbsp;Huan Wang,&nbsp;Ruixuan Wang,&nbsp;Ying Liu,&nbsp;Xiayan Wu,&nbsp;Lixin Xie","doi":"10.1002/iid3.70081","DOIUrl":"10.1002/iid3.70081","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Acute lung injury (ALI) and its subsequent progression to acute respiratory distress syndrome (ARDS) are severe respiratory conditions. They are marked by rapid lung function deterioration and extensive pulmonary inflammation, often resulting in critical patient outcomes. Alveolar macrophages (AMs) and monocyte-derived macrophages (MDMs) are two distinct subsets of lung macrophages present in the alveoli during ALI. Both are critical mediators of pulmonary inflammation. Our study examined the interplay between AMs and MDMs in the inflammatory environment of ALI/ARDS.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Mice were treated with lipopolysaccharide (LPS) to establish ALI models. The lung tissues of mice were subjected to hematoxylin-eosin staining to observe the degree of tissue damage. In vivo, CCR2-deficient mice or depleting peripheral blood mononuclear cells by clodronate liposomes were used to reduce MDMs recruitment. The bronchoalveolar lavage fluid (BALF) supernatants were used for cytokine and total protein analyses. AMs and MDMs in the BALF were analyzed by flow cytometry. The levels of AMs death were determined through propidium iodide staining and measured by flow cytometry. In vitro, primary AMs were exposed to MDM-conditioned medium or TNF-α, and their death levels were assessed under a fluorescence microscope with propidium iodide staining.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>AMs significantly decrease in number and undergo extensive cell death during ALI. The reduced MDMs recruitment can increase the number of AMs, reduce AMs death, and alleviate lung injury. In vitro, MDM-conditioned medium can induce AMs death and TNF-α is one of the major secretions. It indicates that TNF-α stimulation in vitro promotes AMs death. In vivo, MDMs are identified as the primary cells secreting TNF-α. Additionally, the treatment with TNF-α antagonists can reduce AMs death and the severity of lung injury.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our study demonstrates that MDMs contribute to AMs death during ALI through TNF-α. Targeting TNF-α may offer a therapeutic strategy to mitigate AMs death and lung injury in ALI/ARDS.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"12 12","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632899/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"N6-Methyladenosine Modification on the Function of Female Reproductive Development and Related Diseases","authors":"Xiangrong Cui,&nbsp;Huihui Li,&nbsp;Xia Huang,&nbsp;Tingting Xue,&nbsp;Shu Wang,&nbsp;Xinyu Zhu,&nbsp;Xuan Jing","doi":"10.1002/iid3.70089","DOIUrl":"10.1002/iid3.70089","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>N6-methyladenosine (m6A) modification is a widespread and reversible epigenetic alteration in eukaryotic mRNA, playing a pivotal role in various biological functions. Its significance in female reproductive development and associated diseases has recently become a focal point of research.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This review aims to consolidate current knowledge of the role of m6A modification in female reproductive tissues, emphasizing its regulatory dynamics, functional significance, and implications in reproductive health and disease.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A comprehensive analysis of recent studies focusing on m6A modification in ovarian development, oocyte maturation, embryo development, and the pathogenesis of reproductive diseases.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>m6A modification exhibits dynamic regulation in female reproductive tissues, influencing key developmental stages and processes. It plays critical roles in ovarian development, oocyte maturation, and embryo development, underpinning essential aspects of reproductive health. m6A modification is intricately involved in the pathogenesis of several reproductive diseases, including polycystic ovary syndrome (PCOS), premature ovarian failure (POF), and endometriosis, offering insights into potential molecular mechanisms and therapeutic targets.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The review highlights the crucial role of m6A modification in female reproductive development and related diseases. It underscores the need for further research to explore innovative diagnostic and therapeutic strategies for reproductive disorders, leveraging the insights gained from understanding m6A modification's impact on reproductive health.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"12 12","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632877/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Post-COVID immunity in patients with solid tumor or hematological malignancies treated with SARS-CoV-2 monoclonal antibodies","authors":"Gilberto Sabino-Santos,&nbsp;Cathryn E. Leggio,&nbsp;Sean M. Litwin,&nbsp;Najia Waheed,&nbsp;Shuangyi Bai,&nbsp;Sinem Ulusan,&nbsp;Anoli Karunathilake,&nbsp;Debra H. Elliott,&nbsp;Ashley R. Smira,&nbsp;Sruti Chandra,&nbsp;Lin Li,&nbsp;Bo Ning,&nbsp;Tony Hu,&nbsp;John S. Schieffelin,&nbsp;Bronwyn M. Gunn,&nbsp;James E. Robinson,&nbsp;Jyotsna Fuloria,&nbsp;Elizabeth B. Norton","doi":"10.1002/iid3.70039","DOIUrl":"10.1002/iid3.70039","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Purpose&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;SARS-CoV-2 monoclonal antibody (mAB) therapy has effectively treated severe COVID-19, although how this contributes to protective antiviral immunity in settings of malignancy is poorly defined.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Patients and Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;We evaluated the development of post-infection immunity in five patients with malignancies who received mAB therapy targeting spike protein for their PCR-confirmed SARS-CoV-2 infection in 2021, compared with non-mAB controls. Patients were identified from a larger study on oncology with a history or documented current infection with SARS-CoV-2. Subjects include two patients with lymphoma and CD20-depletion therapy, one with myeloma and two with solid tumor (stage IIA rectal adenocarcinoma and metastatic breast cancer). Cancer therapies and COVID vaccination history varied by patient. Blood samples (1–4 per patient) were collected 71–635 days post-mAB therapy. We employed clinical histories with comprehensive immunoprofiling analysis, including systems serology antibody isotyping and effector function, T-cell immunophenotyping for subset and memory cells, and sensitive blood viral RNA detection up to 2 years post-mAB therapy.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;B-cell deficiency was confirmed in 3/5 patients. All patients had detectable anti-spike and nucleoprotein antibody isotypes, effector functions, and neutralizing antibodies (which increased over time by subject) at similar levels to the control group. Virus-specific T-cell activation and phenotypes varied by time and patient. Spike-specific effector and memory CD8 + T-cells were significantly elevated in mAB subjects compared to the control group. SARS-CoV-2 viral RNA detection was also higher in mAB-treated patients. One patient on bortezomib therapy had unique alterations in these populations.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusion&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;All mAB-treated patients with malignancies developed polyfunctional immunity humoral and T-cell immunity to SARS-CoV-2 even in the setting of B-cell deficiency. The evolution of this immunity, including new variant-specific antibodies, without secondary illnesses suggests that patients were protected from symptomatic re-infection, and mAB therapy did not blunt the development of host immunity. Future studies are warranted to better characterize immunologic memory over time with exposures to new viral variants, evaluate prolonged viral shedding and the continued use of appropriate mAB for infection in high-risk patients.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 ","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"12 12","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632117/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum Level of RIPK1/3 Correlated With the Prognosis in ICU Patients With Acute Ischemic Stroke","authors":"Jianhong Dong,&nbsp;Xinli Xiong","doi":"10.1002/iid3.70085","DOIUrl":"10.1002/iid3.70085","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Acute ischemic stroke (AIS) is a common cerebrovascular disease with high mortality. AIS patients in the intensive care unit (ICU) often have severe conditions that require close monitoring and timely treatment. Receptor-interacting protein kinase 1 (RIPK1) and RIPK3 play important roles in cell apoptosis and inflammation. However, the relevance of serum RIPK1/3 to AIS patients in the ICU has not been clarified.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To explore the correlation of serum RIPK1 and RIPK3 with the prognosis of AIS patients in the ICU.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>One hundred and twenty AIS patients were selected as the research subjects for the retrospective analysis. The subjects were grouped based on the volume of cerebral infarction and the score of the National Institute of Health Stroke Scale (NIHSS) and mRS. The correlation was explored using Pearson analysis. The predictive value was valued using the ROC curve.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The content of serum RIPK1 and RIPK3 was gradually elevated with increased cerebral infarction volume and the severity of the disease (<i>p</i> &lt; 0.05). Patients with poor prognosis had a higher content of serum RIPK1 and RIPK3 than those with good prognosis (<i>p</i> &lt; 0.05). Serum RIPK1 and RIPK3 levels were positively correlated with infarct volume, NHISS, and mRS scores (<i>p</i> &lt; 0.001). The area under the curve (AUC) of RIPK1 and RIPK3 for predicting the severity of AIS was 0.703, 0.883, and 0.912, respectively. The AUC for predicting poor prognosis of AIS was 0.797, 0.721, and 0.893, respectively. The cooperative detection of RIPK1 and RIPK3 had higher clinical value.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>AIS patients in the ICU had abnormally elevated content of serum RIPK1 and RIPK3, which was closely related to the volume of cerebral infarction, severity, and prognosis. Combined detection of RIPK1 and RIPK3 might help to early identify the severity and evaluate the prognosis, providing a reference basis for clinical doctors to develop treatment strategies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"12 12","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11631146/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blocking of Tim-3 Ameliorates Spinal Cord Ischemia-Reperfusion Injury Through Inhibiting Neuroinflammation and Promoting M1-to-M2 Phenotypic Polarization of Microglia","authors":"Zhenxing Li,&nbsp;Binbin Zhou,&nbsp;Guanghui Chen,&nbsp;Xiangyu Yang,&nbsp;Han Su,&nbsp;Bolin Li","doi":"10.1002/iid3.70084","DOIUrl":"10.1002/iid3.70084","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Blocking of Tim-3 exerts therapeutic effects in a series of ischemia-reperfusion injury (IRI).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this work, a cross-clamped aortic arch was conducted to establish SCIRI rat model. Besides, rat spinal microglia was subjected to OGD/R to mimic I/R-like conditions in vitro. The in vivo and in vitro therapeutic effects of Tim-3 antibody in SCIRI were investigated from these aspects: neuronal apoptosis, neuroinflammation, microglia activation, and polarization.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>It was verified that Tim-3 was highly expressed in spinal cord tissues of SCIRI rats and blocking of Tim-3 attenuated SCIRI-induced pathological injury, neuronal apoptosis, neuroinflammation, and microglia activation (M1 polarization). In addition, it was verified that Tim-3 was highly expressed in OGD/R-treated rat spinal microglia and blocking of Tim-3 attenuated OGD/R-induced inflammation and spinal microglia activation (M1 polarization).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Tim-3 antibody can exert therapeutic effects in SCIRI through inhibiting neuroinflammation and promoting microglia polarization from M1 to M2 phenotype.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"12 12","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11621861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Diagnosis and Prognosis Value of Circulating Exosomal lncRNA MALAT1 and LNC_000226 in Patients With Acute Myocardial Infarction: An Observational Study","authors":"Xiaodong Gu,&nbsp;Jingyuan Hou,&nbsp;Ruiqiang Weng,&nbsp;Jiawei Rao,&nbsp;Sudong Liu","doi":"10.1002/iid3.70088","DOIUrl":"10.1002/iid3.70088","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Acute myocardial infarction (AMI) stands as a leading cause of global morbidity and mortality. This study aims to explore the potential roles of circulating exosomal lncRNA MALAT1 and LNC_000226 in AMI diagnosis and prognosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This retrospective observational study included 90 patients with AMI and 88 patients with normal coronary artery (NCA). Plasma exosomes were isolated via ultracentrifugation, and the levels of exosomal lncRNA MALAT1 and LNC_000226 were examined using qRT-PCR. Major adverse cardiovascular events (MACEs) that occurred during 1-year follow-up post-stent implantation were collected. The diagnostic value of exosomal MALAT1 and LNC_000226 was determined by receiver operating characteristic (ROC) analysis. The association between exosomal LNC_000226 and MACEs was assessed by Kaplan–Meier and Cox regression analysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Both lncRNA MALAT1 and LNC_000226 levels in plasma exosomes were elevated in AMI patients compared to NCA controls. Moreover, LNC_000226 (AUC: 0.889, sensitivity: 82%, specificity: 72%) exhibited superior diagnostic performance compared to MALAT1 (AUC: 0.707, sensitivity: 71%, specificity: 57%). During 1-year follow-up period, the incidence of MACEs was significantly higher among patients with high exosomal LNC_000226 levels compared to those with low exosomal LNC_000226 levels [64% (29/45) vs. 40% (18/45), <i>p</i> &lt; 0.05]. Multivariable Cox regression analysis revealed a positive association between exosomal LNC_000226 level and the risk of MACEs in AMI patients (HR: 1.959, 95% CI: 1.040–3.689).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Circulating exosomal lncRNA MALAT1 and LNC_000226 are promising biomarkers for diagnosing AMI, with LNC_000226 potentially indicating a prognosis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"12 12","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11621859/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of the Inflammatory Burden Index With Increased Mortality Among Cancer Patients: Insights From the NHANES Study","authors":"Xiuxiu Qiu,&nbsp;Yiyi Zhang,&nbsp;Yingjie Zhu,&nbsp;Ming Yang,&nbsp;Li Tao","doi":"10.1002/iid3.70067","DOIUrl":"10.1002/iid3.70067","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The systemic inflammatory response significantly influences the progression and prognosis of various cancers. The novel Inflammatory Burden Index (IBI) was recently introduced as a biomarker to gauge systemic inflammation and evaluate cancer patient prognosis. However, studies investigating the relationship between IBI and mortality rates in cancer patients remain limited.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This study analyzed data from 2748 cancer patients enrolled in the National Health and Nutrition Examination Surveys between 1999 and 2018. We used weighted Cox regression analysis and restricted cubic spline models to examine the relationship between the IBI and mortality due to all causes, cardiovascular disease (CVD), and cancer. Furthermore, we employed Kaplan-Meier survival curves, subgroup analyses, and receiver operating characteristic curves to elaborate on these associations.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Over a median follow-up period of 112 months, the cohort experienced 1067 deaths, including 320 from cancer, 239 attributable to heart disease, and 508 from various other causes. The Kaplan-Meier curve indicated that individuals in the higher quartiles of the IBI faced significantly increased mortality risks compared to those in lower quartiles. Analyses using weighted Cox proportional hazards models demonstrated that subjects in the top IBI quartile were at a substantially higher risk for all-cause mortality (Hazard Ratio [HR] 2.09, 95% Confidence Interval [CI] 1.67–2.62, <i>p</i> &lt; 0.001), CVD mortality (HR = 1.95, 95% CI= 1.18–3.23, <i>p</i> = 0.010), and cancer mortality (HR = 2.06, 95% CI = 1.31–3.26, <i>p</i> = 0.002). Furthermore, stratification and interaction analyses affirmed the uniformity of these initial findings. The areas under the curve for the 3-, 5-, and 10-year survival predictions for all-cause mortality were 0.62, 0.62, and 0.67, respectively; for cardiovascular mortality, they were 0.64, 0.64, and 0.70; and for cancer mortality, they were 0.62, 0.77, and 0.70.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In cancer patients, higher IBI levels significantly correlate with increased mortality from all causes, CVD, and cancer-specific deaths. This index could possess considerable diagnostic and prognostic importance, possibly acting as a new biomarker for evaluating outcomes in cancer patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"12 12","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11621858/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142784938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serotype 3 Streptococcus pneumoniae Escapes the Immune Responses Induced by PCV13 in Mice With High Susceptibility to Infection","authors":"Giuliana S. Oliveira,&nbsp;Johanna Rivera,&nbsp;Tasson C. Rodrigues,&nbsp;Giovanna B. Carneiro,&nbsp;Orlando G. Ribeiro,&nbsp;Eliane N. Miyaji,&nbsp;Liise-anne Pirofski,&nbsp;Maria Leonor S. Oliveira","doi":"10.1002/iid3.70062","DOIUrl":"10.1002/iid3.70062","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p><i>Streptococcus pneumoniae</i> (pneumococcus) is a common cause of respiratory and invasive infections in humans. PCV13, a pneumococcal conjugate vaccine used globally, is highly effective against diseases caused by pneumococcal serotypes included in its formulation. However, one of them, the serotype 3 (ST3) is still being relatively commonly isolated from patients, suggesting an escape from vaccine-induced immunity. The thick capsule produced by ST3 facilitates bacterial evasion from the immune system. Additionally, host immune responses may influence the outcome of ST3 infection. Here we evaluated the influence of inflammation in the adaptive immune responses and protection induced by PCV13 against ST3, using two outbred mice lines that were phenotypically selected for high (AIRmax) and low (AIRmin) inflammatory responses.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>AIRmin and AIRmax mice were immunized with PCV13. Inbred BALB/c mice were used as reference for vaccine efficacy. Induction of IgG against polysaccharides (PS) from pneumococcal serotype 1 (ST1) and ST3 were evaluated by ELISA. Protection was tested against invasive infections with ST1 and ST3 pneumococcal strains. Sera were compared by IgG binding to pneumococcal surface, induction of pneumococcal agglutination and opsonophagocytosis. The phagocytic capacity of mice-derived neutrophils was also evaluated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Immunization of AIRmin, AIRmax and BALB/c mice with PCV13 induced IgG against PS from ST1 and ST3 pneumococci. Despite vaccination, AIRmin mice were not protected against fatal infection with ST3. Sera from AIRmin mice immunized with PCV13 presented lower levels of anti-PS3 IgG, with reduced capacity to bind to pneumococcal surface. Reduced capacity to induce opsonophagocytosis of ST3 pneumococci in vitro was also observed. Conversely, PCV13 protected AIRmin mice against fatal infection with ST1 and this correlated with the capacity of the sera to induce ST1 opsonophagocytosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our results show that both host and bacterial features can influence the outcome of protection induced by PCV13 against ST3 pneumococcal infection.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"12 12","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11621863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}