Journal of clinical & experimental immunology最新文献

Corrected Version: Protection of Mice from Controlled Cortical Impact Injury by Food Additive Glyceryl Tribenzoate. 修正版：食品添加剂三苯甲酸甘油对小鼠控制性皮质撞击损伤的保护作用。

Journal of clinical & experimental immunology Pub Date : 2026-04-28 DOI: 10.33140/jcei.11.02.01

Suresh B Rangasamy, Jit Poddar, Kalipada Pahan

{"title":"Corrected Version: Protection of Mice from Controlled Cortical Impact Injury by Food Additive Glyceryl Tribenzoate.","authors":"Suresh B Rangasamy, Jit Poddar, Kalipada Pahan","doi":"10.33140/jcei.11.02.01","DOIUrl":"10.33140/jcei.11.02.01","url":null,"abstract":"Despite intense investigations, no effective therapy is available to halt the pathogenesis of traumatic brain injury (TBI), a major health concern, which sometimes leads to long-term neurological disability, especially in war veterans and young adults. This study highlights the use of glyceryl tribenzoate (GTB), a flavoring ingredient, in ameliorating the disease process of controlled cortical impact (CCI)-induced TBI in mice. Oral administration of GTB decreased the activation of microglia and astrocytes to inhibit the expression of inducible nitric oxide synthase (iNOS) in hippocampus and cortex of TBI mice. Accordingly, GTB treatment protected and/or restored synaptic maturation in the hippocampus of TBI mice as revealed by the status of PSD-95, NR-2A, and GluR1. Furthermore, oral GTB also reduced the size of lesion cavity in the brain of TBI mice. Finally, GTB treatment improved locomotor functions and protected spatial learning and memory in TBI mice. These results outline a novel neuroprotective property of GTB in which it may be beneficial for TBI.","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"11 2","pages":"1-15"},"PeriodicalIF":0.0,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13245557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148213731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Benzoate Drugs for Traumatic Brain Injury. 创伤性脑损伤的苯甲酸酯类药物。

Journal of clinical & experimental immunology Pub Date : 2026-01-01 Epub Date: 2026-03-14 DOI: 10.33140/jcei.11.01.02

Swarupa Pahan, Kalipada Pahan

引用次数: 0

Corrected Version: IL-12 p40 Monomer is Different from Other IL-12 Family Members to Selectively Inhibit IL-12Rβ1 Internalization and Suppress EAE. 修正版：il - 12p40单体与其他IL-12家族成员不同，选择性抑制IL-12Rβ1内化，抑制EAE。

Journal of clinical & experimental immunology Pub Date : 2026-01-01 Epub Date: 2026-07-13 DOI: 10.33140/jcei.11.03.02

Susanta Mondal, Madhuchhanda Kundu, Malabendu Jana, Suresh B Rangasamy, Khushbu K Modi, Roumen Balabanov, Kalipada Pahan

{"title":"Corrected Version: IL-12 p40 Monomer is Different from Other IL-12 Family Members to Selectively Inhibit IL-12Rβ1 Internalization and Suppress EAE.","authors":"Susanta Mondal, Madhuchhanda Kundu, Malabendu Jana, Suresh B Rangasamy, Khushbu K Modi, Roumen Balabanov, Kalipada Pahan","doi":"10.33140/jcei.11.03.02","DOIUrl":"10.33140/jcei.11.03.02","url":null,"abstract":"Multiple sclerosis (MS) is the most common human demyelinating disease of the CNS. The IL-12 family of cytokines has four members which are IL-12 (p40:p35), IL-23 (p40:p19), the p40 monomer (p40), and the p40 homodimer (p402). Since all four members contain p40 in different forms, it is important to use specific monoclonal antibody (mAb) to characterize these molecules. Here, by using such mAb, we describe selective loss of p40 in serum of MS patients as compared to healthy controls. Similarly, we also observed decrease in p40 and increase in IL-12, IL-23 and p402 in serum of mice with experimental autoimmune encephalomyelitis (EAE), an animal model of MS, as compared to control mice. Interestingly, weekly supplementation of mouse and human recombinant p40 ameliorated clinical symptoms and disease progression of EAE. On the other hand, IL-12, IL-23 and p402 did not exhibit such inhibitory effect. In addition to EAE, p40 also suppressed collagen-induced arthritis in mice. Using IL-12Rβ1-/-, IL-12Rβ2-/- and IL-12Rβ1+/-/IL-12Rβ2-/- mice, we observed that p40 required IL-12Rβ1, but not IL-12Rβ2, to suppress EAE. Interestingly, p40 arrested IL-12-, IL-23- or p402-mediated internalization of IL-12Rβ1, but neither IL-12Rβ2 nor IL-23R, protected regulatory T cells, and suppressed Th1 and Th17 biasness. These studies identify p40 as a new anti-autoimmune cytokine with biological role different from IL-12, IL-23 and p402 in which it attenuates autoimmune signaling via suppression of IL-12Rβ1 internalization, which may be beneficial in patients with MS and other autoimmune disorders.","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"11 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13576398/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148979002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Prospect of Muscle-Building Supplement HMB in Alzheimer's Disease. 增肌补剂HMB治疗阿尔茨海默病的前景。

Journal of clinical & experimental immunology Pub Date : 2026-01-01 Epub Date: 2026-07-13 DOI: 10.33140/jcei.11.03.01

Abhiram Uppalapati, Ahiri Vishnubhotla, Kalipada Pahan

{"title":"Prospect of Muscle-Building Supplement HMB in Alzheimer's Disease.","authors":"Abhiram Uppalapati, Ahiri Vishnubhotla, Kalipada Pahan","doi":"10.33140/jcei.11.03.01","DOIUrl":"10.33140/jcei.11.03.01","url":null,"abstract":"Alzheimer's disease (AD) is the most common progressive and irreversible neurodegenerative disorder in humans that affects memory, thinking and behavior. Impairment in synaptic plasticity is one of the hallmarks in AD, with most of the impairment occurring in the hippocampal region, a key part of the brain for memory and learning. Therefore, the upregulation of hippocampal plasticity is critical to remediate the progression of AD and preserve memory formation and cognitive functions. Recent studies have described β-hydroxy-β-methylbutyrate (HMB), a body building supplement commonly used by athletes, as a candidate molecule for improving hippocampal plasticity. Clinically, AD is characterized by the abnormal accumulation of beta amyloid (Aβ) plaques, coupled with intracellular aggregates of hyperphosphorylated tau protein. In addition to enhancing hippocampal plasticity, HMB has been also demonstrated to lower amyloid plaques in a mouse model of AD. Although liver is rich in peroxisome proliferator-activated receptor alpha (PPARα), recent findings have established the presence of PPARα in hippocampus and other parts of the brain. Interestingly, HMB has been shown to utilize PPARα for lowering plaques and increasing hippocampal plasticity. Here, we discuss these newly described features of HMB with possible implications for the use of HMB supplement in patients with dementia and AD.","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"11 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13441409/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148681312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrected Version: Neutralization of RANTES and Eotaxin Prevents the Loss of Dopaminergic Neurons in a Mouse Model of Parkinson's Disease. 纠正版本：RANTES和Eotaxin的中和可防止帕金森病小鼠模型中多巴胺能神经元的损失。

Journal of clinical & experimental immunology Pub Date : 2026-01-01 Epub Date: 2026-08-03 DOI: 10.33140/JCEI.11.03.04

Goutam Chandra, Suresh B Rangasamy, Kalipada Pahan

{"title":"Corrected Version: Neutralization of RANTES and Eotaxin Prevents the Loss of Dopaminergic Neurons in a Mouse Model of Parkinson's Disease.","authors":"Goutam Chandra, Suresh B Rangasamy, Kalipada Pahan","doi":"10.33140/JCEI.11.03.04","DOIUrl":"10.33140/JCEI.11.03.04","url":null,"abstract":"Parkinson's disease (PD) is second only to Alzheimer's disease as the most common human neurodegenerative disorder. Despite intense investigation, no interdictive therapy is available for PD. Recent studies indicate that both innate and adaptive immune processes are active in PD. Accordingly, we found rapid increase in RANTES (regulated on activation, normal T cell expressed and secreted) and eotaxin, chemokines that are involved in T cell trafficking, in vivo in the substantia nigra pars compacta (SNpc) and the serum of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated mice. RANTES and eotaxin were also upregulated in the SNpc of postmortem PD brains as compared to age-matched controls. Therefore, we investigated whether neutralization of RANTES and eotaxin could protect against nigrostriatal degeneration in MPTP-intoxicated mice. Interestingly, after peripheral administration, functional blocking antibodies against RANTES and eotaxin reduced the infiltration of CD4+ and CD8+ T cells into the nigra, attenuated nigral expression of proinflammatory molecules, and suppressed nigral activation of glial cells. These findings paralleled dopaminergic neuronal protection, normalized striatal neurotransmitters, and improved motor functions in MPTP-intoxicated mice. Therefore, we conclude that attenuation of chemokine-dependent adaptive immune response may be of therapeutic benefit for PD patients.","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"11 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13456536/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148708843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrected Version: Sodium Benzoate, A Metabolite of Cinnamon and A Food Additive, Improves Cognitive Functions in Mice After Controlled Cortical Impact Injury. 修正版本：苯甲酸钠，肉桂和食品添加剂的代谢物，改善小鼠在控制皮质撞击损伤后的认知功能。

Journal of clinical & experimental immunology Pub Date : 2026-01-01 Epub Date: 2026-03-30 DOI: 10.33140/jcei.11.01.03

Suresh B Rangasamy, Sumita Raha, Sridevi Dasarathi, Kalipada Pahan

{"title":"Corrected Version: Sodium Benzoate, A Metabolite of Cinnamon and A Food Additive, Improves Cognitive Functions in Mice After Controlled Cortical Impact Injury.","authors":"Suresh B Rangasamy, Sumita Raha, Sridevi Dasarathi, Kalipada Pahan","doi":"10.33140/jcei.11.01.03","DOIUrl":"10.33140/jcei.11.01.03","url":null,"abstract":"Traumatic brain injury (TBI) is a major health concern, sometimes leading to long-term neurological disability, especially in children, young adults, and war veterans. Although the research investigators and clinicians have applied different treatment strategies or neurosurgical procedures to solve this health issue, we are still in need of effective therapy to halt the pathogenesis of brain injury. Earlier we have reported that sodium benzoate (NaB), a metabolite of cinnamon and a Food and Drug Administration-approved drug against urea cycle disorders and glycine encephalopathy, protects neurons in animal models of Parkinson's disease and Alzheimer's disease. This study was undertaken to examine the therapeutic efficacy of NaB in controlled cortical impact (CCI)-induced preclinical mouse model of TBI. Oral treatment with NaB, but not sodium formate (NaFO), was found to decrease the activation of microglia and astrocytes and inhibits the expression of inducible nitric oxide synthase (iNOS) in hippocampus and cortex of CCI-insulted mice. Further, administration of NaB also reduced the vascular damage and decreased the size of lesion cavity in the brain of CCI-induced mice. Importantly, NaB-treated mice showed significant improvements in memory and locomotor functions as well as displayed substantial reduction in depression like behaviors. These results delineate a novel neuroprotective property of NaB, highlighting its possible therapeutic importance in TBI.","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"11 1","pages":"11-26"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13218369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148140037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nutritional Management of Celiac Disease 乳糜泻的营养管理

Journal of clinical & experimental immunology Pub Date : 2023-04-01 DOI: 10.33140/jcei.08.02.03

Daris I. González Hernández, Xiomara Herrera Argüelles

{"title":"Nutritional Management of Celiac Disease","authors":"Daris I. González Hernández, Xiomara Herrera Argüelles","doi":"10.33140/jcei.08.02.03","DOIUrl":"https://doi.org/10.33140/jcei.08.02.03","url":null,"abstract":"Celiac disease (CD) is a chronic disease causing inflammation of the proximal small intestine that occurs in genetically predisposed individuals when they eat gluten which is a binding protein common in grains wheat, barley, and rye. The disease injury usually resolves when gluten is excluded from the diet. Although the injury will heal, the reaction to gluten is permanent and will recur with the reintroduction of gluten. The condition is surprisingly common, affecting as many as 1% of white populations. The consequences of the disease are predominantly those of malnutrition due to maldigestion and malabsorption, such as diarrhea, weight loss, and anemia. Symptoms caused by inflammation of the small intestine are also common. CD, although it is common and its pathology is well understood, frequently goes undiagnosed, probably because of the nonspecific or vague nature of many of the symptoms that occur. The cornerstone of treatment for CD is elimination of gluten from the diet. In most patients diagnosed with CD, a strict gluten‐free diet (GFD) alone should result in complete symptomatic and histologic resolution of the disease and reduce risk of complications. Noncompliance with diet is the leading cause of failure to respond in patients with CD. For these reasons, thorough assessment and counseling and management at the time of diagnosis and ongoing care are crucial. This article addresses the overview and diagnosis of CD and addresses its nutritional management in detail.","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"19 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136185946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Other Sea Star Igkappa Gene Cloning Assay in E.Coli with New Parameters 其他海星Igkappa基因在大肠杆菌中的克隆试验

Journal of clinical & experimental immunology Pub Date : 2023-04-01 DOI: 10.33140/jcei.08.02.02

引用次数: 0

Australian COVID-19 pandemic: A Bradford Hill Analysis of Iatrogenic Excess Mortality 澳大利亚COVID-19大流行:医源性超额死亡率的Bradford Hill分析

Journal of clinical & experimental immunology Pub Date : 2023-04-01 DOI: 10.33140/jcei.08.02.01

引用次数: 0

Cinnamein Inhibits the Induction of Nitric Oxide and Proinflammatory Cytokines in Macrophages, Microglia and Astrocytes. 肉桂素抑制巨噬细胞、小胶质细胞和星形胶质细胞中一氧化氮和促炎细胞因子的诱导。

Journal of clinical & experimental immunology Pub Date : 2023-01-01 DOI: 10.33140/jcei.08.01.01

Swarupa Pahan, Sumita Raha, Sridevi Dasarathi, Kalipada Pahan

{"title":"Cinnamein Inhibits the Induction of Nitric Oxide and Proinflammatory Cytokines in Macrophages, Microglia and Astrocytes.","authors":"Swarupa Pahan, Sumita Raha, Sridevi Dasarathi, Kalipada Pahan","doi":"10.33140/jcei.08.01.01","DOIUrl":"https://doi.org/10.33140/jcei.08.01.01","url":null,"abstract":"Chronic inflammation driven by proinflammatory cytokines (TNFα, IL-1β, IL-6, etc.), and nitric oxide (NO) plays an important role in the pathogenesis of several autoimmune, inflammatory as well as neurodegenerative disorders like rheumatoid arthritis, multiple sclerosis, Alzheimer's disease, Parkinson's disease, Huntington's disease, etc. Therefore, identification of nontoxic anti-inflammatory drugs may be beneficial for these autoimmune, inflammatory and neurodegenerative disorders. Cinnamein, an ester derivative of cinnamic acid and benzyl alcohol, is used as a flavoring agent and for its antifungal and antibacterial properties. This study underlines the importance of cinnamein in inhibiting the induction of proinflammatory molecules in RAW 264.7 macrophages and primary mouse microglia and astrocytes. Stimulation of RAW 264.7 macrophages with lipopolysaccharide (LPS) and interferon γ (IFNγ) led to marked production of NO. However, cinnamein pretreatment significantly inhibited LPS- and IFNγ-induced production of NO in RAW 264.7 macrophages. Cinnamein also reduced the mRNA expression of inducible nitric oxide synthase (iNOS) and TNFα in RAW cells. Accordingly, LPS and viral double-stranded RNA mimic polyinosinic: polycytidylic acid (polyIC) stimulated the production of TNFα, IL-1β and IL-6 in primary mouse microglia, which was inhibited by cinnamein pretreatment. Similarly, cinnamein also inhibited polyIC-induced production of TNFα and IL-6 in primary mouse astrocytes. These results suggest that cinnamein may be used to control inflammation in different autoimmune, inflammatory and neurodegenerative disorders.","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"8 1","pages":"520-529"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9949320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9423908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1