Temporal profile of M1 and M2 responses in the hippocampus following early 24 h of neurotrauma

Ansari, Mubeen A.

doi:10.1016/j.jns.2015.06.062

Cited by 34 publications

(30 citation statements)

References 94 publications

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“…The study explained the importance of the combination of M1 and M2 responses, instead of M1 inhibitory action and centralized in M2 promotion in most therapeutic strategies. Indeed, rapid M1 response may assist in macrophage polarization, including M2 phenotype up-regulation to neutralize the pro-inflammatory effect of M1 macrophages soon after injury, and M2 polarization was suggested to be initiated earlier for recovery enhancement [43]. Similar results were obtained in the study of Kumar et al (2016), which further suggested that NADPH oxidase (NOX2) was responsible in M1 but not M2 polarization by using an NOX2-knockout mice model.…”

Section: Role Of Macrophages In Brain Injuries and Neuron Protectionmentioning

confidence: 60%

Chemopreventive Effects of Phytochemicals and Medicines on M1/M2 Polarized Macrophage Role in Inflammation-Related Diseases

Koh

Yang

Lai

et al. 2018

IJMS

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Macrophages can polarize into two different states (M1 and M2), which play contrasting roles during pathogenesis or tissue damage. M1 polarized macrophages produce pro-inflammatory cytokines and mediators resulting in inflammation, while M2 macrophages have an anti-inflammatory effect. Secretion of appropriate cytokines and chemokines from macrophages can lead to the modification of the microenvironment for bridging innate and adaptive immune responses. Increasing evidence suggests that polarized macrophages are pivotal for disease progression, and the regulation of macrophage polarization may provide a new approach in therapeutic treatment of inflammation-related diseases, including cancer, obesity and metabolic diseases, fibrosis in organs, brain damage and neuron injuries, and colorectal disease. Polarized macrophages affect the microenvironment by secreting cytokines and chemokines while cytokines or mediators that are produced by resident cells or tissues may also influence macrophages behavior. The interplay of macrophages and other cells can affect disease progression, and therefore, understanding the activation of macrophages and the interaction between polarized macrophages and disease progression is imperative prior to taking therapeutic or preventive actions. Manipulation of macrophages can be an entry point for disease improvement, but the mechanism and potential must be understood. In this review, some advanced studies regarding the role of macrophages in different diseases, potential mechanisms involved, and intervention of drugs or phytochemicals, which are effective on macrophage polarization, will be discussed.

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Section: Role Of Macrophages In Brain Injuries and Neuron Protectionmentioning

confidence: 60%

Chemopreventive Effects of Phytochemicals and Medicines on M1/M2 Polarized Macrophage Role in Inflammation-Related Diseases

Koh

Yang

Lai

et al. 2018

IJMS

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“…Analysis of the time course of M2-associated genes in the frontal cortex demonstrates that expression of Fizz1 and Arg1 are higher 16 hours after IL-4 infusion and begin to decline by 48 hours. Further, in response to TBI hippocampal expression of the M2 genes Arg1, Fizz1, Ym1, and CD206 were elevated within twenty-four hours of injury (Ansari, 2015). Collectively these data may indicate that normal aging leads to an exaggerated M2 response, but that the duration of this response is likely blunted in the aged as research demonstrates increased expression early on and decreased expression at later time points.…”

Section: Discussionmentioning

confidence: 99%

Differential response to intrahippocampal interleukin-4/interleukin-13 in aged and exercise mice

Littlefield

Kohman

2017

Neuroscience

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Normal aging is associated with low-grade neuroinflammation that results from age-related priming of microglial cells. Further, aging alters the response to several anti-inflammatory factors, including interleukin (IL)-4 and IL-13. One intervention that has been shown to modulate microglia activation in the aged brain, both basally and following an immune challenge, is exercise. However, whether engaging in exercise can improve responsiveness to anti-inflammatory cytokines is presently unknown. The current study evaluated whether prior exercise training increases sensitivity to anti-inflammatory cytokines that promote the M2 (alternative) microglia phenotype in adult (5-month-old) and aged (23-month-old) C57BL/6J mice. After 8 weeks of exercise or control housing, mice received bilateral hippocampal injections of an IL-4/IL-13 cocktail or vehicle. Twenty-four hours later hippocampal samples were collected and analyzed for expression of genes associated with the M1 (inflammatory) and M2 microglia phenotypes. Results show that IL-4/IL-13 administration increased expression of the M2-associated genes Fizz1, Ym1, Arginase-1 (Arg1), SOCS1, IL-1ra, and CD206. In response to IL-4/IL-13 administration, aged mice showed increased hippocampal expression of the M2-related genes Arg1, SOCS1, Ym1, and CD206 relative to adult mice. Aged mice also showed increased expression of IL-1β relative to adults, which was unaffected by wheel running or IL-4/IL-13. Wheel running was found to have modest effects on expression of Ym1 and Fizz1 in aged and adult mice. Collectively, our findings indicate that aged mice show a differential response to anti-inflammatory cytokines relative to adult mice and that exercise has limited effects on modulating this response.

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“…Increasing evidence has shown that the changed microenvironment in cerebral tissue plays an important role in cerebral injury after ischemia, particularly the inflammatory response [3]. Microglial activation and promotion of M1 microglial/macrophage polarization play central roles in neuroinflammation after brain injury [4,5]. Microglia/macrophages are known to have different phenotypes with distinct functions during the course of ischemic brain injury [5].…”

Section: Introductionmentioning

confidence: 99%

“…Microglial activation and promotion of M1 microglial/macrophage polarization play central roles in neuroinflammation after brain injury [4,5]. Microglia/macrophages are known to have different phenotypes with distinct functions during the course of ischemic brain injury [5]. M2 microglia protect neighboring cells by removing cell debris and releasing trophic factors for brain repair, based on their ability to produce interleukin 4 (IL-4) and IL-10 [6].…”

Section: Introductionmentioning

confidence: 99%

Exosomes from MiR-30d-5p-ADSCs Reverse Acute Ischemic Stroke-Induced, Autophagy-Mediated Brain Injury by Promoting M2 Microglial/Macrophage Polarization

Jiang

Wang

Jin

et al. 2018

Cell Physiol Biochem

241

191

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Background/Aims: Recent studies have indicated that exosomes secreted from adipose-derived stem cells (ADSCs) have important effects in the treatment of ischemic injury. However, the treatment mechanism is unclear. This study aimed to investigate whether ADSC-derived exosomes enriched with microRNA (miR)-30d-5p have a protective effect on acute ischemic stroke (AIS). Methods: In the current study, inflammatory factors and miR-30d-5p expression were assessed in 70 subjects with AIS and 35 healthy controls. Exosomes were characterized by transmission electron microscopy and further examined using nanoparticle tracking analyses. A rat model of AIS and an in vitro model of oxygen- and glucose-deprived (OGD) primary microglia were established to study the protective mechanism of exosomes from miR-30d-5p-overexpressing ADSCs in ischemia-induced nerve injury. Results: The results showed that following AIS, the expression of inflammatory cytokines increased, while the anti-inflammatory cytokines IL-4, IL-10, and miR-30d-5p decreased both in patients and in animal models. Moreover, in vitro studies demonstrated that suppression of autophagy significantly reduced the OGD-induced inflammatory response. In addition, exosome treatment was more effective in suppressing the inflammatory response by reversing OGD-induced and autophagy-mediated microglial polarization to M1. Furthermore, in vivo studies showed that exosomes derived from ADSCs significantly decreased the cerebral injury area of infarction by suppressing autophagy and promoting M2 microglia/macrophage polarization. Conclusions: Our results suggest that miR-30d-5p-enhanced ADSC-derived exosomes prevent cerebral injury by inhibiting autophagy-mediated microglial polarization to M1.

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Temporal profile of M1 and M2 responses in the hippocampus following early 24 h of neurotrauma

Cited by 34 publications

References 94 publications

Chemopreventive Effects of Phytochemicals and Medicines on M1/M2 Polarized Macrophage Role in Inflammation-Related Diseases

Chemopreventive Effects of Phytochemicals and Medicines on M1/M2 Polarized Macrophage Role in Inflammation-Related Diseases

Differential response to intrahippocampal interleukin-4/interleukin-13 in aged and exercise mice

Exosomes from MiR-30d-5p-ADSCs Reverse Acute Ischemic Stroke-Induced, Autophagy-Mediated Brain Injury by Promoting M2 Microglial/Macrophage Polarization

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