Inflammation and cell signaling最新文献_第2页

Potential Contribution of Microbiome In Neurodegenerative Diseases: Alzheimer's Disease 微生物组在神经退行性疾病中的潜在贡献:阿尔茨海默病

Inflammation and cell signaling Pub Date : 2017-10-17 DOI: 10.14800/ICS.1595

R. Kumari, Nirmal Verma, J. Paul

{"title":"Potential Contribution of Microbiome In Neurodegenerative Diseases: Alzheimer's Disease","authors":"R. Kumari, Nirmal Verma, J. Paul","doi":"10.14800/ICS.1595","DOIUrl":"https://doi.org/10.14800/ICS.1595","url":null,"abstract":"Alzheimer’s Disease (AD) is characterized by a slowly progressive decline of cognition and memory and is the most frequent cause of dementia. HM contribute to the regulation of multiple neuro-chemical and neuro-metabolic pathways. The pathological features of AD include amyloid beta peptide (Aβ) deposition, neuronal tangle formation and granulovacuolar degeneration. Aβ protein is a normal part of the innate immune system, the body's first-line defense against infection. However recent report shows that Ab expression protects against fungal and bacterial infections in mouse, nematode, and cell culture models of AD. However, recent research has shown that these proteins are also expressed on bacterial and fungal cell surfaces and might contribute to immune response. In addition to commensal microbes there are other pathogens like Chlamydophila pneumoniae, Toxoplasma gondii, HIV- associated neurocognitive disorders (HAND, Viroids, Hepatitis, Cytomegalovirus have been suspected to be involved in AD. Microbes are proposed to be involved in pathophysiology of neurodegenerative disease through their ability to produce relevant neurotransmitter level, immune modulation due to excess inflammation and translocation to brain from the site of infection trough blood or lymphatic system. Here we elaborated on the emerging ideas showing the contribution of the gut microbiome to human neurological diseases with special emphasis on AD. The evidences outlined in this review may prove useful in designing further studies for taxonomic and functional profiling of microbiota in patients with AD leading to new advanced therapeutic inventions.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85583161","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: 3

RNA N6-adenosine methylation (m6A) steers epitranscriptomic control of herpesvirus replication RNA n6 -腺苷甲基化(m6A)引导疱疹病毒复制的表转录组控制

Inflammation and cell signaling Pub Date : 2017-10-17 DOI: 10.14800/ICS.1604

Fengchun Ye

引用次数: 15

Studies on the mechanisms of bile acid initiated hepatic inflammation in cholestatic liver injury 胆汁淤积性肝损伤中胆汁酸引发肝脏炎症机制的研究

Inflammation and cell signaling Pub Date : 2017-06-19 DOI: 10.14800/ICS.1561

Shi-Ying Cai, J. Boyer

引用次数: 11

Development of a novel cytoplasmic hydroxyl radical-targeting antioxidant (TA293) that suppresses cellular senescence, inflammation, and apoptosis 一种新的胞质羟基自由基靶向抗氧化剂(TA293)的发展，抑制细胞衰老，炎症和凋亡

Inflammation and cell signaling Pub Date : 2017-05-24 DOI: 10.14800/ICS.1539

T. Sakai, J. Imai, Tomohiro Ito, H. Takagaki, M. Ui, S. Hatta

{"title":"Development of a novel cytoplasmic hydroxyl radical-targeting antioxidant (TA293) that suppresses cellular senescence, inflammation, and apoptosis","authors":"T. Sakai, J. Imai, Tomohiro Ito, H. Takagaki, M. Ui, S. Hatta","doi":"10.14800/ICS.1539","DOIUrl":"https://doi.org/10.14800/ICS.1539","url":null,"abstract":"Hydroxyl radicals ( • OH) exhibit the strongest oxidation potential of any reactive oxygen species (ROS) and react non-specifically with cellular components, such as nucleic acids, lipids and proteins. While mitochondrial • OH incites oxidative damage resulting in mitochondrial dysfunction, the actions of cytoplasmic • OH remain unknown as no cytoplasmic • OH-specific scavenger has been identified to date. To solve this problem, we developed the cytoplasm- and mitochondrion-specific • OH-targeted scavengers TA293 and mitoTA293, respectively. As expected, TA293 and mitoTA293 scavenged • OH, but not O 2 – or H 2 O 2 . Notably, TA293 scavenged pyocyanin-induced cytoplasmic • OH, but not mitochondrial radicals induced by antimycin A. Conversely, mitoTA293 scavenged • OH only in the mitochondria in vivo and in vitro . Interestingly, we found that cytoplasmic • OH plays a central role in cytoplasm ROS-induced oxidative stress, which potentiates cellular senescence, inflammation, and apoptosis in the kidney and lung. Based on these findings, we believe that TA293 could be a novel tool to study the effects of • OH damage within the cytoplasm.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89661912","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

Aberrant function of neutrophils in asthma 中性粒细胞在哮喘中的异常功能

Inflammation and cell signaling Pub Date : 2017-04-17 DOI: 10.14800/ICS.1535

Meijia Wang, Jianping Zhao, Jungang Xie

引用次数: 0

S100A8/A9, a potent biomarker and clinical candidate for the treatment of uveitis S100A8/A9，一种治疗葡萄膜炎的有效生物标志物和临床候选物

Inflammation and cell signaling Pub Date : 2017-03-06 DOI: 10.14800/ICS.1512

Zai-Long Chi, Xiaodan Dai

{"title":"S100A8/A9, a potent biomarker and clinical candidate for the treatment of uveitis","authors":"Zai-Long Chi, Xiaodan Dai","doi":"10.14800/ICS.1512","DOIUrl":"https://doi.org/10.14800/ICS.1512","url":null,"abstract":"Uveitis, the pathological condition of inflammation of the uvea, commonly causes severe visual impairment and blindness. Possible causes of uveitis include infection, injury, or an autoimmune or inflammatory disease. However, the pathogenesis of uveitis is not fully understood. Glucocorticoids are widely used for the treatment of uveitis, but long-term steroid use carries a risk of potential complications. Early diagnosis and proper treatment are important to prevent the complications of uveitis. Thus far, researchers have not identified an effective biological marker for auxiliary diagnosis or an appropriate method for monitoring the inflammatory activity of uveitis. S100A8/A9, also known as calprotectin, belongs to the Ca 2+ -binding S100 protein family; is mainly expressed in myeloid leukocytes; and plays a prominent role in a variety of pathological process, such as inflammation, infection and autoimmune diseases. Extracellular S100A8/A9 released from granulocytes and monocytes has recently gained a great deal of attention as a critical alarmin for the modulation of the inflammatory response. This review will summarize recent insights into the biological function of S100A8/A9 in uveitis and provide an outlook on diagnostic, inflammation monitoring and therapeutic applications targeting S100A8/A9 for the treatment of uveitis.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77890184","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: 1

Emerging role of zinc homeostasis by zinc transporter ZIP7 in intestinal homeostatic self-renewal 锌转运蛋白ZIP7在肠道内稳态自我更新中的新作用

Inflammation and cell signaling Pub Date : 2017-02-20 DOI: 10.14800/ics.1509

W. Ohashi, K. Hase, T. Fukada

引用次数: 0

Vitellogenin in inflammation and immunity in social insects 群居昆虫炎症和免疫中的卵黄原蛋白

Inflammation and cell signaling Pub Date : 2017-02-14 DOI: 10.14800/ICS.1506

Heli Salmela, L. Sundström

{"title":"Vitellogenin in inflammation and immunity in social insects","authors":"Heli Salmela, L. Sundström","doi":"10.14800/ICS.1506","DOIUrl":"https://doi.org/10.14800/ICS.1506","url":null,"abstract":"Social insects, such as the honey bee and ants, form vast colonies that are only rivalled by human settlements. Living in dense, often stationary groups is prone to increase disease transmission. Yet, social insect queens and certain worker types can lead lengthy lives compared to the life span of most solitary insects. Social insects appear to have modified insulin/insulin like signaling pathway that regulates insect life history. This modification results in extremely elevated levels of the multifunctional lipoprotein vitellogenin in the individuals with longer life span. Vitellogenin is an egg-yolk precursor, but it also regulates caste-related behaviors in social insects, has shielding effects in inflammation and infection, and it is a mediator of transgenerational immunity. Here, we compile what is known about the life span and immune actions of vitellogenin and the evolution of this protein in the honey bee and ants. Recently we identified proteins homologous to vitellogenin in several Hymenopteran species, and showed that at least one of these vitellogenin-like proteins can have a protective role similar to vitellogenin in the honey bee. The newly identified vitellogenin homologs hint that the regulation of social insect life span can be more complex than thought before.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87325568","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: 27

RNA N⁶-adenosine methylation (m⁶A) steers epitranscriptomic control of herpesvirus replication. RNA n6 -腺苷甲基化(m6A)引导疱疹病毒复制的表转录组控制。

Inflammation and cell signaling Pub Date : 2017-01-01 Epub Date: 2017-10-17

Fengchun Ye

引用次数: 0

Studies on the mechanisms of bile acid initiated hepatic inflammation in cholestatic liver injury. 胆汁淤积性肝损伤中胆汁酸引发肝脏炎症机制的研究。

Inflammation and cell signaling Pub Date : 2017-01-01 Epub Date: 2017-06-19

Shi-Ying Cai, James L Boyer

引用次数: 0