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Mechanism of inflammatory response and therapeutic effects of stem cells in ischemic stroke:current evidence and future perspectives

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Neural Regeneration research 2025年第1期20卷 67-81页

作者： Yubo Wang Tingli Yuan Tianjie Lyu Ling Zhang Meng Wang Zhiying He Yongjun Wang Zixiao Li Vascular Neurology Department of NeurologyBeijing Tiantan HospitalCapital Medical UniversityBeijingChina China National Clinical research Center for Neurological diseases Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Shanghai Engineering research Center of Stem Cells Translational Medicine ShanghaiChina National Center for Healthcare Quality Management in Neurological diseases Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Institute for Regenerative Medicine Shanghai East HospitalSchool of Life Sciences and TechnologyTongji UniversityShanghaiChina Chinese Institute for Brain research BeijingChina research unit of Artificial Intelligence in Cerebrovascular Disease Chinese Academy of Medical SciencesBeijingChina Beijing Engineering research Center of Digital Healthcare for Neurological diseases BeijingChina

Ischemic stroke is a leading cause of death and disability worldwide,with an increasing trend and tendency for onset at a younger ***,in particular,bears a high burden of stroke *** recent years,the inflammatory response after stroke has become a research hotspot:understanding the role of inflammatory response in tissue damage and repair following ischemic stroke is an important direction for its *** review summarizes several major cells involved in the inflammatory response following ischemic stroke,including microglia,neutrophils,monocytes,lymphocytes,and ***,we have also highlighted the recent progress in various treatments for ischemic stroke,particularly in the field of stem cell ***,understanding the complex interactions between inflammation and ischemic stroke can provide valuable insights for developing treatment strategies and improving patient *** cell therapy may potentially become an important component of ischemic stroke treatment.

关键词： cell therapy immune cell inflammatory ischemic stroke stem cell

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Vascular endothelial growth factor:a double-edged sword in the development of white matter lesions

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Neural Regeneration research 2025年第1期20卷 191-192页

作者： Narek Manukjan Daniel Fulton Zubair Ahmed WMatthijs Blankesteijn Sébastien Foulquier Department of Pharmacology and Toxicology Maastricht UniversityMaastrichtThe Netherlands CARIM-School for Cardiovascular diseases Maastricht UniversityMaastrichtThe Netherlands Neuroscience and Ophthalmology Institute of Inflammation and AgeingUniversity of BirminghamEdgbastonBirminghamUK Centre for Trauma Sciences research University of BirminghamEdgbastonBirminghamUK MHeNs-School for Mental Health and Neuroscience Maastricht UniversityMaastrichtThe Netherlands Department of Neurology Maastricht University Medical CenterMaastrichtThe Netherlands

As the population ages,the burden of age-related diseases becomes ***,over 55 million people suffer from dementia worldwide,with Alzheimer’s disease being the most common ***,it is becoming clearer that underlying vascular pathology such as cerebral small vessel disease(cSVD)may be a more detrimental cause for dementia(Cuadrado-Godia et al.,2018).It is estimated that 10%-30%of the elderly population and 35%-90%of all dementia patients exhibit signs of *** term cSVD refers to pathology affecting the small vessels of the brain,which can lead to lacunar cerebral infarcts,enlarged perivascular spaces,and cortical hemorrhages(Cuadrado-Godia et al.,2018).CSVD is often associated with cognitive decline,gait problems,and dementia(Cuadrado-Godia et al.,2018).

关键词： pathology becoming white

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Epigenetic regulation of the inflammatory response in stroke

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Neural Regeneration research 2025年第11期20卷 3045-3062页

作者： Jingyi Liang Fei Yang Zixiao Li Qian Li School of Basic Medical Sciences Capital Medical UniversityBeijingChina Department of Neurobiology School of Basic Medical SciencesCapital Medical UniversityBeijingChina Laboratory for Clinical Medicine Beijing Key Laboratory of Neural Regeneration and RepairCapital Medical UniversityBeijingChina Department of Neurology Beijing Tiantan HospitalCapital Medical UniversityBeijingChina China National Clinical research Center for Neurological diseases Beijing Tiantan HospitalCapital Medical UniversityBeijingChina National Center for Healthcare Quality Management in Neurological diseases Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Chinese Institute for Brain research BeijingChina research unit of Artificial Intelligence in Cerebrovascular Disease Chinese Academy of Medical SciencesBeijingChina Beijing Engineering research Center of Digital Healthcare for Neurological diseases BeijingChina Department of Biochemistry and Molecular Biology School of Basic Medical SciencesCapital Medical UniversityBeijingChina Beijing Key Laboratory of Cancer Invasion and Metastasis research Capital Medical UniversityBeijingChina

Stroke is classified as ischemic or hemorrhagic,and there are few effective treatments for either *** mechanisms play a critical role in secondary brain injury following a stroke,which manifests as cytokine release,blood–brain barrier disruption,neuronal cell death,and ultimately behavioral *** the inflammatory response has been shown to mitigate this cascade of events in experimental stroke ***,in clinical trials of anti-inflammatory agents,longterm immunosuppression has not demonstrated significant clinical benefits for *** may be attributable to the dichotomous roles of inflammation in both tissue injury and repair,as well as the complex pathophysiologic inflammatory processes in *** acute harmful inflammatory responses or inducing a phenotypic shift from a pro-inflammatory to an anti-inflammatory state at specific time points after a stroke are alternative and promising therapeutic *** agents that can modulate inflammation requires a detailed understanding of the inflammatory processes of ***,epigenetic reprogramming plays a crucial role in modulating post-stroke inflammation and can potentially be exploited for stroke *** this review,we summarize current findings on the epigenetic regulation of the inflammatory response in stroke,focusing on key signaling pathways including nuclear factor-kappa B,Janus kinase/signal transducer and activator of transcription,and mitogen-activated protein kinase as well as inflammasome *** also discuss promising molecular targets for stroke *** evidence to date indicates that therapeutic targeting of the epigenetic regulation of inflammation can shift the balance from inflammation-induced tissue injury to repair following stroke,leading to improved post-stroke outcomes.

关键词： DNA methylation histone modification intracerebral hemorrhage ischemic stroke neuroinflammation neuroprotection non-coding RNA RNA methylation subarachnoid hemorrhage treatment

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Which form of collagen is suitable for nerve cell culture?

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Neural Regeneration research 2013年第23期8卷 2165-2170页

作者： Mohsen Fathi Najafi Saber Zahri Fatemeh Vahedi Leila Esmaililian Toosi Nazila Ariaee Razi Vaccine and Serum research Institute Departamnt of Biology University of Mohaghegh Ardebili inflammation and Inflammatory diseases research Center Mashhad University of Medical Science

In this study, we investigated the effects of hydrolyzed and non-hydrolyzed collagen and two-di- mensional and three-dimensional collagen matrices on cell survival, attachment and neurite out- growth of primary cultured nerve cells using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide （MTT） colorimetric assay and inverted microscopy. Hydrolyzed collagen facilitated nerve cell survival and neurite outgrowth, but it had no obvious influences on cell attachment. In contrast, non-hydrolyzed two-dimensional collagen matrix had no obvious effects on neurite outgrowth. These findings suggest that hydrolyzed collagen is an ideal nerve cell culture media.

关键词： neural regeneration nerve cells collagen primary culture survival cell attachment growth matrix grants-supported paper neuroregeneration

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Clash of the Cytokine Titans： counter-regulation of interleukin-1 and type I interferon-mediated inflammatory responses

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Cellular & Molecular Immunology 2017年第1期14卷 22-35页

作者： Katrin D Mayer-Barber Bo Yan inflammation and Innate Immunity unit Laboratory of Clinical Infectious Diseases National Institute of Allergy and Infectious Diseases National Institutes of Health. Bethesda. MD 20892. USA

Over the past decades the notion of ＇inflammation＇ has been extended beyond the original hallmarks of rubor （redness）, calor （heat）, tumor （swelling） and dolor （pain） described by Celsus. We have gained a more detailed understanding of the cellular players and molecular mediators of inflammation which is now being applied and extended to areas of biomedical research such as cancer, obesity, heart disease, metabolism, auto-inflammatory disorders, autoimmunity and infectious diseases. Innate cytokines are often central components of inflammatory responses. Here, we discuss how the type I interferon and interleukin-1 cytokine pathways represent distinct and specialized categories of inflammatory responses and how these key mediators of inflammation counter-regulate each other.

关键词： cytokines infection inflammation interleukin-1 tuberculosis type-1 interferons

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Epigenetic regulation of SARS-Cov-2 spike protein modulates cellular viability and nascent RNA transcription in neuronal cells

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Genes & diseases 2024年第2期11卷 535-538页

作者： Xi Kong Peng Lu Jinyue Zhang Zheng Bao Chenghao Kuang Bingqing Xie Jianhua Peng Ning Ma Yong Jiang Shigang Yin Laboratory of Neurological diseases and Brain Function The Affiliated Hospital of Southwest Medical UniversityLuzhouSichuan 646000China Institute of Epigenetics and Brain Science Southwest Medical UniversityLuzhouSichuan 646000China Department of Neurosurgery The Affiliated Hospital of Southwest Medical UniversityLuzhouSichuan 646000China inflammation and allergic diseases research unit The Affiliated Hospital of Southwest Medical UniversityLuzhouSichuan 646000China

SARS-CoV-2 has been demonstrated to be highly susceptible to neuron-and glial-like cells,1 but there is no consensus regarding how the virus affects neurons following *** is therefore unknown if and how SARS-CoV-2 maintains the homeostasis of neuronal ***,we revealed that the receptor-binding domain(RBD)of the SARS-CoV-2 spike protein acted as an extracellular remodeling component to undermine epigenetic regulation,perturbnascentRNA(nsRNA)transcription,promote mitochondrial biogenesis,and increase cellular viability in SH-SY5Y cells.

关键词： invasion homeostasis maintain

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Sterile signals generate weaker and delayed macrophage NLRP3 inflammasome responses relative to microbial signals

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Cellular & Molecular Immunology 2017年第1期14卷 118-126页

作者： Jelena S Bezbradica Rebecca C Coll Kate Schroder Institute for Molecular Bioscience (IMB) IMB Centre for Inflammation and Disease Research and Australian Infectious Diseases Research Centre The University of Queensland Brisbane St Lucia Queensland 4072 Australia

inflammation is the host response to microbial infection or sterile injury that aims to eliminate the insult, repair the tissue and restore homeostasis. Macrophages and the NLRP3 inflammasome are key sentinels for both types of insult. Although it is well established that the NLRP3 inflammasome is activated by microbial products and molecules released during sterile injury, it is unclear whether the responses elicited by these different types of signals are distinct. In this study, we used lipopolysaccharide and tumor necrosis factor as prototypical microbial and sterile signal 1 stimuli, respectively, to prime the NLRP3 inflammasome. We then used the bacterial toxin nigericin and a common product released from necrotic cells, ATP, as prototypical microbial and sterile signal 2 stimuli, respectively, to trigger the assembly of the NLRP3 inflammasome complex in mouse and human macrophages. We found that NLRP3 inflammasome responses were weakest when both signal 1 and signal 2 were sterile, but responses were faster and stronger when at least one of the two signals was microbial. Ultimately, the most rapid and potent responses were elicited when both signals were microbial. Together, these data suggest that microbial versus sterile signals are distinct, both kinetically and in magnitude, in their ability to generate inflammasome-dependent responses. This hierarchy of NLRP3 responses to sterile versus microbial stimuli likely reflects the urgent need for the immune system to respond rapidly to the presence of infection to halt pathogen dissemination.

关键词： inflammasome NLRP3 sterile inflammation TNF

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Local and systemic effects of IL-17 in joint inflammation:a historical perspective from discovery to targeting

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Cellular & Molecular Immunology 2021年第4期18卷 860-865页

作者： Pierre Miossec Department of Clinical Immunology and Rheum atology and the Immunogenomics and inflammation research unit University of Lyon Hdpital Edouard Herriot LyonFrance

The role of IL-17 in many inflammatory and autoimmune diseases is now well established,with three currently registered anti-IL-17-targeted *** story has taken place over a period of 20 years and led to the demonstration that a T cell product could regulate,and often amplify,the inflammatory *** first results described the contribution of IL-17 to local features in ***,understanding was extended to its systemic effects,with a focus on cardiovascular *** review provides a historical perspective of these discoveries focused on arthritis,which started in 1995,followed 10 years later by the description of Th17 ***,IL-17 inhibitors for three chronic inflammatory diseases have been *** options are now being tested in ongoing and future clinical *** of IL-17 family members and Th17 cells ranging from antibodies to small molecules are under active *** identification of patients with IL-17-driven disease is a key target for the improved selection of patients expected to have a strongly positive response.

关键词： Interleukin-17 Th17 cells inflammation Arthritis,targeting

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Reactivation of latent tuberculosis with TNF inhibitors: critical role of the beta 2 chain of the IL-12 receptor

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Cellular & Molecular Immunology 2021年第7期18卷 1644-1651页

作者： Marie Robert Pierre Miossec Department of Clinical Immunology and Rheumatology and immunogenomics and inflammation research unitUniversity of LyonHôpital Edouard HerriotLyonFrance

Tumor necrosis factor(TNF)inhibitors have improved a lot the treatment of numerous diseases,with the well-known example of rheumatoid arthritis(RA).In the early 2000s,postmarketing data quickly revealed an alarming number of severe tuberculosis(TB)under such *** findings were consistent with previous results in mice where TNF is essential for lymph node formation and granuloma *** effects of TNF inhibition on RA synovium structure are very similar to those on granuloma,with changes in cellular interactions,cytokine,and chemokine *** addition to the role of TNF in granuloma,the interleukin(IL)-12/interferon(IFN)-γpathway is required for an efficient host defense against *** and secondary immunodeficiencies affecting this pathway lead to severe bacillus Calmette-Guérin(BCG)reaction or full *** chronic inflammation as in RA induces a systemic Th1 defect that predisposes to TB through specific downregulation of the IL-12Rß2 *** TNF inhibitors are initiated,this transiently increases this risk of TB,through effects on cellular interactions in a latent TB *** a later stage,when a better control disease activity is obtained,the risk of TB is reduced but not *** the clear benefit from TNF inhibition,latent TB infection screening at baseline is essential for an optimal safety.

关键词： tuberculosis TNF inhibition rheumatoid arthritis cytokines

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Therapeutic Effects of DNA Vaccine on Allergen-Induced allergic Airway inflammation in Mouse Model

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Cellular & Molecular Immunology 2006年第5期3卷 379-384页

作者： Guoping Li Zhigang Liu Nanshan Zhong Bin Liao Ying Xiong Inflammafion ＆ allergic diseases research unit Affiliated Hospital of Luzhou Medical College Luzhou 646000 Sichuan China College of Life Sciences Shenzhen University Shenzhen 518060 China Guangzhou Institute of Respiratory diseases Guangzhou Medical College Guangzhou 510120 China Department of Respiratory Disease Affiliated Hospital of Luzhou Medical College Luzhou 646000 China

Vaccination with DNA encoding Dermatophagoides pteronyssinus group 2 （Der p 2） allergen previously showed its effects of immunologic protection on Der p 2 allergen-induced allergic airway inflammation in mice. In present study, we investigated whether DNA vaccine encoding Der p 2 could exert therapeutic role on allergen-induced allergic airway inflammation in mouse model and explored the mechanism of DNA vaccination in asthma specific-allergen immunotherapy. After sensitized and challenged by Der p 2, the BALB/c mice were immunized with DNA vaccine. The degrees of cellular infiltration were scored. IgE levels in serum and IL-4/IL-13 levels in BALF were determined by ELISA. The lung tissues were assessed by histological examinations. Expressions of STAT6 and NF-kB in lung were determined by immunohistochemistry staining. Vaccination of mice with DNA vaccine inhibited the development of airway inflammation and the production of mucin induced by allergen, and reduced the level of Der p 2-specific IgE level. Significant reductions of eosinophil infiltration and levels of IL-4 and IL-13 in BALF were observed after vaccination. Further more, DNA vaccination inhibited STAT6 and NF-kB expression in lung tissue in Der p 2-immunized mice. These results indicated that DNA vaccine encoding Der p 2 allergen could be used for therapy of allergen-induced allergic airway inflammation in our mouse model. Cellular ＆ Molecular Immunology.

关键词： DNA vaccine Dermatophagoides pteronyssinus group 2 allergic airway inflammation

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