scholarly journals Bioactive polypeptide improves neuroinflammation by regulating microglia polarization

2021 ◽  
Author(s):  
Liping Zhai ◽  
Heping Shen ◽  
Yongjia Sheng ◽  
weiqun Guo ◽  
Qiaobing Guan ◽  
...  
Keyword(s):  
Microglia Polarization

Retinal microglia polarization in diabetic retinopathy

2021 ◽  
Vol 38 ◽  
Author(s):  
Xin Li ◽  
Zi-Wei Yu ◽  
Hui-Yao Li ◽  
Yue Yuan ◽  
Xin-Yuan Gao ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Diabetic Retinopathy ◽  
Cytokine Production ◽  
Immune Cell ◽  
Microvascular Disease ◽  
Retinal Diseases ◽  
Microglia Polarization ◽  
Retinal Microglia ◽  
The Central Nervous System ◽  
Retinal Neurodegeneration

Abstract Microglia, the main immune cell of the central nervous system (CNS), categorized into M1-like phenotype and M2-like phenotype, play important roles in phagocytosis, cell migration, antigen presentation, and cytokine production. As a part of CNS, retinal microglial cells (RMC) play an important role in retinal diseases. Diabetic retinopathy (DR) is one of the most common complications of diabetes. Recent studies have demonstrated that DR is not only a microvascular disease but also retinal neurodegeneration. RMC was regarded as a central role in neurodegeneration and neuroinflammation. Therefore, in this review, we will discuss RMC polarization and its possible regulatory factors in early DR, which will provide new targets and insights for early intervention of DR.

scholarly journals Short-chain fatty acids contribute to neuropathic pain via regulating microglia activation and polarization

2021 ◽  
Vol 17 ◽  
pp. 174480692199652
Author(s):  
Feng Zhou ◽  
Xian Wang ◽  
Baoyu Han ◽  
Xiaohui Tang ◽  
Ru Liu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Thermal Hyperalgesia ◽  
Short Chain Fatty Acids ◽  
Antibiotic Administration ◽  
Tnf Α ◽  
Microglia Polarization ◽  
Inflammatory Phenotype ◽  
Phenotype Markers ◽  
Anti Inflammatory

Microglia activation and subsequent pro-inflammatory responses play a key role in the development of neuropathic pain. The process of microglia polarization towards pro-inflammatory phenotype often occurs during neuroinflammation. Recent studies have demonstrated an active role for the gut microbiota in promoting microglial full maturation and inflammatory capabilities via the production of Short-Chain Fatty Acids (SCFAs). However, it remains unclear whether SCFAs is involved in pro-inflammatory/anti-inflammatory phenotypes microglia polarization in the neuropathic pain. In the present study, chronic constriction injury (CCI) was used to induce neuropathic pain in mice, the mechanical withdrawal threshold, thermal hyperalgesia were accomplished. The levels of microglia markers including ionized calcium-binding adaptor molecule 1 (Iba1), cluster of differentiation 11b (CD11b), pro-inflammatory phenotype markers including CD68, interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and anti-inflammatory phenotype markers including CD206, IL-4 in the hippocampus and spinal cord were determined on day 21 after CCI. The results showed that CCI produced mechanical allodynia and thermal hyperalgesia, and also increased the expressions of microglia markers (Iba1, CD11b) and pro-inflammatory phenotype markers (CD68, IL-1β, and TNF-α), but not anti-inflammatory phenotype marker (CD206, IL-4) in the hippocampus and spinal cord, accompanied by increased SCFAs in the gut. Notably, antibiotic administration reversed these abnormalities, and its effects was also bloked by SCFAs administration. In conclusion, data from our study suggest that CCI can lead to mechanical and thermal hyperalgesia, while SCFAs play a key role in the pathogenesis of neuropathic pain by regulating microglial activation and subsequent pro-inflammatory phenotype polarization. Antibiotic administration may be a new treatment for neuropathic pain by reducing the production of SCFAs and further inhibiting the process of microglia polarization.

scholarly journals MSX3 Switches Microglia Polarization and Protects from Inflammation-Induced Demyelination

2015 ◽  
Vol 35 (16) ◽  
pp. 6350-6365 ◽  
Author(s):  
Z. Yu ◽  
D. Sun ◽  
J. Feng ◽  
W. Tan ◽  
X. Fang ◽  
...  
Keyword(s):  
Microglia Polarization

Treatment targets for M2 microglia polarization in ischemic stroke

2018 ◽  
Vol 105 ◽  
pp. 518-525 ◽  
Author(s):  
Ji wang ◽  
Hongyi xing ◽  
Lin wan ◽  
Xingjun jiang ◽  
Chen wang ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Treatment Targets ◽  
M2 Microglia ◽  
Microglia Polarization

scholarly journals Inhibiting HMGB1-RAGE axis prevents pro-inflammatory macrophages/microglia polarization and affords neuroprotection after spinal cord injury

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Hong Fan ◽  
Hai-Bin Tang ◽  
Zhe Chen ◽  
Hu-Qing Wang ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Western Blot ◽  
Functional Recovery ◽  
Sterile Inflammation ◽  
Qrt Pcr ◽  
Cord Injury ◽  
Microglia Polarization ◽  
Anti Inflammatory ◽  
Inflammatory Macrophages

Abstract Background Spinal cord injury (SCI) favors a persistent pro-inflammatory macrophages/microglia-mediated response with only a transient appearance of anti-inflammatory phenotype of immune cells. However, the mechanisms controlling this special sterile inflammation after SCI are still not fully elucidated. It is known that damage-associated molecular patterns (DAMPs) released from necrotic cells after injury can trigger severe inflammation. High mobility group box 1(HMGB1), a ubiquitously expressed DNA binding protein, is an identified DAMP, and our previous study demonstrated that reactive astrocytes could undergo necroptosis and release HMGB1 after SCI in mice. The present study aimed to explore the effects and the possible mechanism of HMGB1on macrophages/microglia polarization, as well as the neuroprotective effects by HMGB1 inhibition after SCI. Methods In this study, the expression and the concentration of HMGB1 was determined by qRT-PCR, ELISA, and immunohistochemistry. Glycyrrhizin was applied to inhibit HMGB1, while FPS-ZM1 to suppress receptor for advanced glycation end products (RAGE). The polarization of macrophages/microglia in vitro and in vivo was detected by qRT-PCR, immunostaining, and western blot. The lesion area was detected by GFAP staining, while neuronal survival was examined by Nissl staining. Luxol fast blue (LFB) staining, DAB staining, and western blot were adopted to evaluate the myelin loss. Basso-Beattie-Bresnahan (BBB) scoring and rump-height Index (RHI) assay was applied to evaluate locomotor functional recovery. Results Our data showed that HMGB1 can be elevated and released from necroptotic astrocytes and HMGB1 could induce pro-inflammatory microglia through the RAGE-nuclear factor-kappa B (NF-κB) pathway. We further demonstrated that inhibiting HMGB1 or RAGE effectively decreased the numbers of detrimental pro-inflammatory macrophages/microglia while increased anti-inflammatory cells after SCI. Furthermore, our data showed that inhibiting HMGB1 or RAGE significantly decreased neuronal loss and demyelination, and improved functional recovery after SCI. Conclusions The data implicated that HMGB1-RAGE axis contributed to the dominant pro-inflammatory macrophages/microglia-mediated pro-inflammatory response, and inhibiting this pathway afforded neuroprotection for SCI. Thus, therapies designed to modulate immune microenvironment based on this cascade might be a prospective treatment for SCI.

scholarly journals Hyperbaric oxygen preconditioning attenuates brain injury after intracerebral hemorrhage by regulating microglia polarization in rats

2019 ◽  
Vol 25 (10) ◽  
pp. 1126-1133 ◽  
Author(s):  
Ming Wang ◽  
Lin Cheng ◽  
Zhong‐Liang Chen ◽  
Rajneesh Mungur ◽  
Shan‐Hu Xu ◽  
...  
Keyword(s):  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Hyperbaric Oxygen ◽  
Microglia Polarization ◽  
Hyperbaric Oxygen Preconditioning
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