Granulocyte colony-stimulating factor improves alternative activation of microglia under microenvironment of spinal cord injury

Guo, Yongfeng; Zhang, Huanshui; Yang, Jie; Liu, S.; Lu-jun, Bing; Gao, Jiangang; Hao, Aijun

doi:10.1016/j.neuroscience.2013.01.047

Cited by 58 publications

(38 citation statements)

References 38 publications

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“…These cytokine changes were associated with increased Arg1 + staining, consistent with an M2 response, and associated with downregulation of inflammation, locomotor recovery and reduced scar formation [85]. This has been shown in several other cases, where M2 cell induction appeared to alleviate spinal cord injury pathology [86-89]. This beneficial result is not limited to spinal cord injury.…”

Section: M2 Microglial Activation During Acute Neuroinflammationmentioning

confidence: 81%

Neuroinflammation and M2 microglia: the good, the bad, and the inflamed

Cherry

Olschowka

O’Banion

2014

J Neuroinflammation

1,410

1,187

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The concept of multiple macrophage activation states is not new. However, extending this idea to resident tissue macrophages, like microglia, has gained increased interest in recent years. Unfortunately, the research on peripheral macrophage polarization does not necessarily translate accurately to their central nervous system (CNS) counterparts. Even though pro- and anti-inflammatory cytokines can polarize microglia to distinct activation states, the specific functions of these states is still an area of intense debate. This review examines the multiple possible activation states microglia can be polarized to. This is followed by a detailed description of microglial polarization and the functional relevance of this process in both acute and chronic CNS disease models described in the literature. Particular attention is given to utilizing M2 microglial polarization as a potential therapeutic option in treating diseases.

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Section: M2 Microglial Activation During Acute Neuroinflammationmentioning

confidence: 81%

Neuroinflammation and M2 microglia: the good, the bad, and the inflamed

Cherry

Olschowka

O’Banion

2014

J Neuroinflammation

1,410

1,187

View full text Add to dashboard Cite

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“…Besides acting on neural cells, G-CSF also modulates inflammatory reaction and immune cell recruitment and activation in the injured spinal cord. Recent data showed that G-CSF induces alternative activation of microglial macrophages, thus promoting tissue repair [87]. Combined with stem cell factor administration, G-CSF increases the number of activated microglial cells and oligodendrocytes [88], whilst saving oligodendrocytes from SCI-induced cell death by reducing IL-1β and TNF-α and up-regulating the anti-apoptotic protein Bcl-xL [89].…”

Section: Granulocyte Colony-stimulating Factor: Its Implication In Exmentioning

confidence: 99%

Neutrophil contribution to spinal cord injury and repair

Neirinckx

Coste

Franzen

et al. 2014

J Neuroinflammation

123

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Spinal cord injuries remain a critical issue in experimental and clinical research nowadays, and it is now well accepted that the immune response and subsequent inflammatory reactions are of significant importance in regulating the damage/repair balance after injury. The role of macrophages in such nervous system lesions now becomes clearer and their contribution in the wound healing process has been largely described in the last few years. Conversely, the contribution of neutrophils has traditionally been considered as detrimental and unfavorable to proper tissue regeneration, even if there are very few studies available on their precise impact in spinal cord lesions. Indeed, recent data show that neutrophils are required for promoting functional recovery after spinal cord trauma. In this review, we gathered recent evidence concerning the role of neutrophils in spinal cord injuries but also in some other neurological diseases, highlighting the need for further understanding the different mechanisms involved in spinal cord injury and repair.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-014-0150-2) contains supplementary material, which is available to authorized users.

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“…This could indicate a beneficial role of early microglial activation by G-CSF, as suggested in a current study on spinal cord injury. 37 Today it is suggested that microglia and infiltrating macrophages show a dynamic response to ischemia by either polarizing toward an anti-inflammatory and angiogenesis-promoting (M2) or to a detrimental pro-inflammatory M1 phenotype. 38 The reduced CD16/32 + cells in G-CSF-treated mice compared with the C-CSF+BMC group could indicate a microglial shift towards less detrimental or even beneficial action during the acute phase.…”

Section: March 2016mentioning

confidence: 99%

Combining Growth Factor and Bone Marrow Cell Therapy Induces Bleeding and Alters Immune Response After Stroke in Mice

Strecker

Olk

Hoppen

et al. 2016

Stroke

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Background and Purpose-Bone marrow cell (BMC)-based therapies, either the transplantation of exogenous cells or stimulation of endogenous cells by growth factors like the granulocyte colony-stimulating factor (G-CSF), are considered a promising means of treating stroke. In contrast to large preclinical evidence, however, a recent clinical stroke trial on G-CSF was neutral. We, therefore, aimed to investigate possible synergistic effects of co-administration of G-CSF and BMCs after experimental stroke in mice to enhance the efficacy compared with single treatments. Methods-We used an animal model for experimental stroke as paradigm to study possible synergistic effects of co-administration of G-CSF and BMCs on the functional outcome and the pathophysiological mechanism. Results-G-CSF treatment alone led to an improved functional outcome, a reduced infarct volume, increased blood vessel stabilization, and decreased overall inflammation. Surprisingly, the combination of G-CSF and BMCs abrogated G-CSFs' beneficial effects and resulted in increased hemorrhagic infarct transformation, altered blood-brain barrier, excessive astrogliosis, and altered immune cell polarization. These increased rates of infarct bleeding were mainly mediated by elevated matrix metalloproteinase-9-mediated blood-brain barrier breakdown in G-CSF-and BMCs-treated animals combined with an increased number of dilated and thus likely more fragile vessels in the subacute phase after cerebral ischemia. Conclusions-Our results provide new insights into both BMC-based therapies and immune cell biology and help to understand potential adverse and unexpected side effects.

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Granulocyte colony-stimulating factor improves alternative activation of microglia under microenvironment of spinal cord injury

Cited by 58 publications

References 38 publications

Neuroinflammation and M2 microglia: the good, the bad, and the inflamed

Neuroinflammation and M2 microglia: the good, the bad, and the inflamed

Neutrophil contribution to spinal cord injury and repair

Combining Growth Factor and Bone Marrow Cell Therapy Induces Bleeding and Alters Immune Response After Stroke in Mice

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