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Microbial Resistance to Photodynamic Therapy 微生物对光动力疗法的耐药性
Pub Date : 2022-09-12 DOI: 10.33696/immunology.4.139
A. Mackay
Microbial resistance to antibiotics has become a major area of research having caused over a million human deaths in 2019. At present, lower respiratory infection is the most burdensome disease. Antimicrobial Photodynamic Therapy (PDT) is regularly reported not to cause resistance in any pathogen, and to eradicate both microbes that are susceptible to antibiotics and those that are resistant. However, evidence now suggests that resistance to photosensitiser drugs at low concentrations is possible, and that tolerance to the reactive oxygen species (ROS) created during subsequent light exposure will occur eventually. Additionally, an increased optical fluence and the addition of medication have been necessary to destroy antibiotic resistant strains of Staphylococcus Aureus . Research has mostly focussed on bacteria, though the importance of fungi is highlighted here given the ubiquity of clinical manifestations like mycosis and urinary tract infection. Proposed next steps are the definition of terminology and methodology for experiments on microbial resistance/tolerance to PDT, varying the photosensitiser used for repeat PDT while controlling oxygen and salt levels, and alternative treatments including the interception of neuroimmunological signalling. Similar to the ESKAPE ranking of antibiotic resistant pathogens, a list summarising the degree of microbial resistance to PDT may have a place.
微生物对抗生素的耐药性已成为一个主要研究领域,2019年已导致100多万人死亡。目前,下呼吸道感染是最严重的疾病。抗菌光动力疗法(PDT)经常被报道不会对任何病原体产生耐药性,并且可以根除对抗生素敏感的微生物和耐药的微生物。然而,现在的证据表明,在低浓度下对光敏剂药物的耐药性是可能的,并且最终会对随后的光照中产生的活性氧产生耐受性。此外,增加光学通量和添加药物对于摧毁金黄色葡萄球菌的抗生素耐药性菌株是必要的。研究主要集中在细菌上,尽管考虑到真菌病和尿路感染等临床表现的普遍性,真菌的重要性在这里得到了强调。建议的下一步是定义微生物对PDT的耐药性/耐受性实验的术语和方法,在控制氧气和盐水平的同时改变用于重复PDT的光敏剂,以及包括阻断神经免疫信号在内的替代治疗。类似于抗生素耐药性病原体的ESKAPE排名,总结微生物对PDT的耐药性程度的列表可能有一席之地。
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引用次数: 2
BIOMODULINA T® Modulates Lymphocyte Compartments in Institutionalized Cuban Geriatric Patients BIOMODULINA T®调节古巴住院老年患者的淋巴细胞区室
Pub Date : 2022-07-30 DOI: 10.33696/immunology.4.135
Imilla Casado Hernández, V. M. Suárez, Elizabeth Hernández Ramos, Yenisey Triana Marrero, Gabriela Díaz Domínguez, Yaneisy Duarte Pérez, Mary Carmen Reyes Zamora, Sahily Estradé Fernandez, Consuelo Milagros Macías Abraham, Luis Felipe Heredia Guerra
Modulates Compartments in Abstract BIOMODULINA T® is a biological immunomodulator of natural origin, not blood derived, which promises to be a strategy for immune restoration in the elderly, in the midst of the worldwide epidemiological crisis due to the SARS-CoV-2 virus. This research aimed to determine the changes induced by BT in the distribution of lymphocyte compartments of institutionalized Cuban geriatric patients. The significant expansion of the naïve CD4 + and CD8 + , CD19 + , NK T cells and of the CD3 + HLA-DR + and CD3 + CD25 + activation populations was observed; while the rest of the populations of T, B compartments, the T population that co-express CD4 and CD8, and the CD4-CD8-TCRαβ + T cells did not show significant changes. BT had an effect on the immune restoration of T and B lymphocyte populations of Cuban older adults. It modulates the immune response and inflammation, restores immunity, and can contribute to a strategy to prevent and treat COVID-19 in elderly.
摘要中的调节室BIOMULINA T®是一种天然来源的生物免疫调节剂,而不是血液来源的,在严重急性呼吸系统综合征冠状病毒2型导致的全球流行病学危机中,它有望成为老年人免疫恢复的一种策略。本研究旨在确定BT诱导的古巴老年住院患者淋巴细胞区室分布的变化。观察到幼稚的CD4+和CD8+、CD19+、NK T细胞以及CD3+HLA-DR+和CD3+CD25+活化群体的显著扩增;而其余的T、B区群、共表达CD4和CD8的T群以及CD4-CD8-TCRαβ+T细胞没有显示出显著的变化。BT对古巴老年人T和B淋巴细胞群的免疫恢复有影响。它调节免疫反应和炎症,恢复免疫力,并有助于预防和治疗老年人新冠肺炎的策略。
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引用次数: 0
A Nonagenarian’s View of Dietary Impacts on Cellular Immunology 饮食对细胞免疫的影响
Pub Date : 2022-06-30 DOI: 10.33696/immunology.4.136
B. Lands
Descriptions of immune functions and diets often use oversimplified terms that lead to misunderstandings plus expectations that conflict with reality. “ Unexpected events are a clear marker for the frontier of knowledge and a new opportunity to learn” [1]. Terms like lipid, fluidity, unsaturated, essential, lipoprotein, receptor, immune and inflammatory have many unmentioned components and attributes that may be either causal mediators or associated epiphenomena in heath disorders. Including neglected details can help investigators design dietary interventions with observed consequences that fit their expectations. Over the years, new evidence and explicit terminology allow expected outcomes for interventions to fit reality. A recent review, “ Lipid nutrition: ‘In silico’ studies and undeveloped experiments ” [1], describes some aspects of fatty acid chemistry and nutrition with important consequences on chronic immune-inflammatory processes. The review points to long-known details of lipid-protein interactions which younger colleagues can consider as they develop new experiments to gather evidence on how food choices might prevent healthy physiology from drifting into pathophysiology.
对免疫功能和饮食的描述经常使用过于简单的术语,导致误解和与现实相冲突的期望。“意外事件是知识前沿的清晰标志,也是学习的新机会”[1]。脂质、流动性、不饱和、必需、脂蛋白、受体、免疫和炎症等术语有许多未提及的成分和属性,这些成分和属性可能是健康障碍的因果介质或相关副现象。包括被忽视的细节可以帮助研究人员设计饮食干预措施,观察到的结果符合他们的预期。多年来,新的证据和明确的术语使干预措施的预期结果符合现实。最近的一篇综述“脂质营养:‘计算机’研究和未开发的实验”[1]描述了脂肪酸化学和营养的一些方面,这些方面对慢性免疫炎症过程具有重要影响。这篇综述指出了脂蛋白相互作用的长期已知细节,年轻的同事可以在开发新的实验时考虑这些细节,以收集食物选择如何阻止健康生理学转变为病理生理学的证据。
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引用次数: 0
FLIP-expressing myeloid cells as driver of systemic immune disorders 表达FLIP的骨髓细胞作为系统免疫疾病的驱动因素
Pub Date : 2022-06-30 DOI: 10.33696/immunology.4.138
Alberto Atanasio, D. Rizzini, S. Ugel
The role of FLIP as a moonlighting protein is becoming progressively evident since this protein is often involved in various processes correlated to aberrant immunological responses independently from its function as master anti-apoptotic regulator. It has been uncovered that FLIP drives the acquisition of immunosuppression and inflammation-associated pathways in myeloid cells. The clinical picture raised during SARS-CoV-2 pandemic has given the possibility to deeply investigate FLIP involvement in releasing a systemic cytokine storm, also linked to a chronic inflammatory syndrome associated with immune suppression and cancer progression. Indeed, a FLIP/STAT3 axis orchestrates an aberrant inflammatory program in myeloid cells of COVID-19 patients and SARS-CoV-2 infected hACE2 transgenic mice. Moreover, the same activated FLIP/STAT3 axis was confirmed in a chimeric vFLIP mouse model, where vFLIP overexpression was restricted exclusively in myeloid cells by using a tissue-specific CRE-driver (e.g., LysMCre mice), validating this model as a feasible platform to study the late phase of COVID-19 disease. The STAT3 pro-inflammatory pathway triggered by the aberrant expression of FLIP in myeloid cells well correlates to the outcome of the cytokine release syndrome (CRS) that is the latest and most severe phase in COVID-19 disease confirming FLIP-mediated myeloid reprogramming as a cornerstone of systemic immune disorders.
FLIP作为一种兼职蛋白的作用越来越明显,因为该蛋白通常独立于其作为主要抗凋亡调节因子的功能,参与与异常免疫反应相关的各种过程。已经发现FLIP驱动骨髓细胞中免疫抑制和炎症相关途径的获得。在SARS-CoV-2大流行期间提出的临床情况为深入研究FLIP参与释放系统性细胞因子风暴提供了可能性,该风暴也与免疫抑制和癌症进展相关的慢性炎症综合征有关。事实上,FLIP/STAT3轴在新冠肺炎患者和SARS-CoV-2感染的hACE2转基因小鼠的髓细胞中协调异常炎症程序。此外,在嵌合vFLIP小鼠模型中证实了相同的激活的FLIP/STAT3轴,其中通过使用组织特异性CRE-driver(例如LysMCre小鼠)仅限制vFLIP在髓系细胞中的过度表达,验证了该模型作为研究新冠肺炎疾病晚期的可行平台。髓系细胞中FLIP异常表达触发的STAT3促炎途径与细胞因子释放综合征(CRS)的结果密切相关,该综合征是新冠肺炎疾病的最新和最严重阶段,证实FLIP介导的髓系重编程是全身免疫疾病的基石。
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引用次数: 0
LncZFAS1 Inhibit MPP+-Induced Neuroinflammation Through TXNIP/MIB1 E3 Ubiquitin Ligase/NLRP3 Axis LncZFAS1通过TXNIP/MIB1 E3泛素连接酶/NLRP3轴抑制MPP+诱导的神经炎症
Pub Date : 2022-04-30 DOI: 10.33696/immunology.4.134
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引用次数: 0
Sticky Interactions in Lupus Nephritis 狼疮性肾炎中的粘性相互作用
Pub Date : 2022-03-31 DOI: 10.33696/immunology.4.126
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引用次数: 0
Towards a Better Understanding of Staphylococcus aureus Skin Infections-The Interactions with Dendritic Cells 更好地了解金黄色葡萄球菌皮肤感染——与树突状细胞的相互作用
Pub Date : 2022-03-31 DOI: 10.33696/immunology.4.127
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引用次数: 0
Glucose Metabolism is a Better Marker for Predicting Clinical Alzheimer’s Disease than Amyloid or Tau 葡萄糖代谢是预测临床阿尔茨海默病的更好标志物,而不是淀粉样蛋白或Tau
Pub Date : 2022-03-18 DOI: 10.33696/immunology.4.128
Tyler C. Hammond, Ai-Ling Lin
Alzheimer’s disease (AD) research has long been dominated with communications regarding the amyloid hypothesis and targeting amyloid clearance through pharmacological therapies from the brain [1]. Unfortunately, this research strategy has yielded only one new FDA-accelerated approved therapeutic for early AD, and its clinical benefit still needs to be verified [2]. It may be time to employ a new strategy in AD therapeutics research. Hammond et al. reported that diminished uptake of glucose in the brain is a better marker for classifying AD than beta-amyloid (A β ) or phosphorylated tau deposition [3]. The National Institute on Aging and the Alzheimer’s Association published revised guidelines for the diagnosis of AD to include the measurement of amyloid (A), tau (T), and neurodegeneration (N), when diagnosing and treating AD [4]. It is highly relevant to AD therapeutic research whether amyloid, tau, and neurodegeneration contribute equally to the progression of AD at all phases of the disease or in a matter dependent on disease phase. To be able to successfully treat or prevent AD, there is a pressing need to identify precision biomarkers that are sensitive to disease progression and able to predict onset of cognitive impairment [5]. Hammond et al. used an advanced statistical learning machine learning method, random forest, on data provided by the Alzheimer’s Disease Neuroimaging Initiative (ADNI) to measure the ability of beta-amyloid measured by positron emission tomography (A β -PET), phosphorylated tau measured in the cerebral spinal fluid (CSF-pTau), fluorodeoxyglucose measured by positron emission tomography (FDG-PET) and structural imaging measured by magnetic resonance imaging (MRI) to classify AD diagnosis. Their results demonstrated that amyloid, tau, and neurodegeneration have a phase-dependent impact on the development of AD. A β and pTau are better predictors of the early dementia status that is often defined as mild cognitive impairment (MCI), and neurodegeneration, especially low glucose uptake, is a better predictor of later dementia status, or clinical AD. A
长期以来,阿尔茨海默病(AD)的研究一直以淀粉样蛋白假说和通过脑卒中药物治疗清除淀粉样蛋白为主导。不幸的是,这一研究策略只产生了一种新的fda加速批准的早期AD治疗药物,其临床效益仍有待验证。也许是时候在阿尔茨海默病治疗研究中采用一种新的策略了。Hammond等人报道,大脑中葡萄糖摄取减少是一种比β -淀粉样蛋白(a β)或磷酸化tau沉积[3]更好的AD分类标记。国家衰老研究所和阿尔茨海默氏症协会发布了AD诊断的修订指南,包括在诊断和治疗AD时测量淀粉样蛋白(A), tau (T)和神经变性(N)。淀粉样蛋白、tau蛋白和神经退行性变是否在疾病的所有阶段或依赖于疾病阶段的物质中对AD的进展贡献相同,这与AD治疗研究高度相关。为了能够成功地治疗或预防AD,迫切需要确定对疾病进展敏感并能够预测认知障碍发病的精确生物标志物。Hammond等人利用一种先进的统计学习机器学习方法——随机森林,根据阿尔茨海默病神经影像学倡议(ADNI)提供的数据,测量了正电子发射断层扫描(A β -PET)测量的β -淀粉样蛋白、脑脊液中测量的磷酸化tau蛋白(CSF-pTau)、正电子发射断层扫描(FDG-PET)测量的氟脱氧葡萄糖和磁共振成像(MRI)测量的结构成像对AD诊断分类的能力。他们的研究结果表明,淀粉样蛋白、tau蛋白和神经变性对阿尔茨海默病的发展具有阶段性影响。A β和pTau是早期痴呆状态的较好预测因子,通常被定义为轻度认知障碍(MCI),而神经退行性变,特别是低糖摄取,是晚期痴呆状态或临床AD的较好预测因子。一个
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引用次数: 9
Glucose Metabolism is a Better Marker for Predicting Clinical Alzheimer's Disease than Amyloid or Tau. 糖代谢比淀粉样蛋白或Tau蛋白更能预测临床阿尔茨海默病
Pub Date : 2022-01-01
Tyler C Hammond, Ai-Ling Lin
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引用次数: 0
PD-L1 as a Novel Mediator of Lung Fibroblast to Myofibroblast Transition. PD-L1作为肺成纤维细胞向肌成纤维细胞过渡的新介质。
Pub Date : 2022-01-01 DOI: 10.33696/immunology.4.142
Xia Guo, Guoqing Qian
of levels of high PD-L1
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引用次数: 0
期刊
Journal of cellular immunology
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