A polarizing view on posttraumatic brain injury inflammatory response

Traumatic brain injury (TBI) activates the simultaneous proliferation of various pro- and anti-inflammatory molecules. Considering the amount of factors participating, this response is naturally complex. However, there is an increasing trend in neurotrauma research to delineate the injury-induced in...
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Autor*in:	Susanna Rosi [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	Categorization inflammatory response M1/M2 phenotype expression traumatic brain injury

Übergeordnetes Werk:	In: Brain Circulation - Wolters Kluwer Medknow Publications, 2017, 2(2016), 3, Seite 126-128
Übergeordnetes Werk:	volume:2 ; year:2016 ; number:3 ; pages:126-128

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.4103/2394-8108.192517

Katalog-ID:	DOAJ003862089

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520			\|a Traumatic brain injury (TBI) activates the simultaneous proliferation of various pro- and anti-inflammatory molecules. Considering the amount of factors participating, this response is naturally complex. However, there is an increasing trend in neurotrauma research to delineate the injury-induced inflammatory responses within the constraints of in vitro defined macrophage polarization phenotypes “M1” and “M2”. Here, we evaluate research examining the complexity of the inflammatory response that cannot be so easily characterized using this binary nomenclature. TBI is demonstrated to induce a broad spectrum of simultaneous expression responses involving both pro- and anti-inflammatory reactions. Specifically, the research revealed a very heterogeneous parenchymal landscape associated with TBI. The concurrent expression of both “M1” and “M2” phenotypic markers on the microglia/macrophages involved suggests that the polarization phenotypes cannot be neatly defined in this M1/M2 paradigm. Recent studies displaying neurotrauma also report similar conflict with the constraints of this binary categorization of “M1/M2”, demonstrating that microglia/macrophages cannot effectively cross-over to strictly polarized “M1-only” or “M2-only” phenotype. Therefore, the complex signaling events surrounding this response indicate that a binary M1/M2 characterization is not adequate to define inflammatory profile. This paper is a review article. Referred literature in this paper has been listed in the references part. The datasets supporting the conclusions of this article are available online by searching the PubMed. Some original points in this article come from the laboratory practice in our research centers and the authors' experiences.
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author	Susanna Rosi
spellingShingle	Susanna Rosi misc R855-855.5 misc RC666-701 misc Categorization misc inflammatory response misc M1/M2 misc phenotype expression misc traumatic brain injury misc Medical technology misc Diseases of the circulatory (Cardiovascular) system A polarizing view on posttraumatic brain injury inflammatory response
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topic_title	R855-855.5 RC666-701 A polarizing view on posttraumatic brain injury inflammatory response Categorization inflammatory response M1/M2 phenotype expression traumatic brain injury
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title	A polarizing view on posttraumatic brain injury inflammatory response
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title_full	A polarizing view on posttraumatic brain injury inflammatory response
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title_sort	polarizing view on posttraumatic brain injury inflammatory response
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title_auth	A polarizing view on posttraumatic brain injury inflammatory response
abstract	Traumatic brain injury (TBI) activates the simultaneous proliferation of various pro- and anti-inflammatory molecules. Considering the amount of factors participating, this response is naturally complex. However, there is an increasing trend in neurotrauma research to delineate the injury-induced inflammatory responses within the constraints of in vitro defined macrophage polarization phenotypes “M1” and “M2”. Here, we evaluate research examining the complexity of the inflammatory response that cannot be so easily characterized using this binary nomenclature. TBI is demonstrated to induce a broad spectrum of simultaneous expression responses involving both pro- and anti-inflammatory reactions. Specifically, the research revealed a very heterogeneous parenchymal landscape associated with TBI. The concurrent expression of both “M1” and “M2” phenotypic markers on the microglia/macrophages involved suggests that the polarization phenotypes cannot be neatly defined in this M1/M2 paradigm. Recent studies displaying neurotrauma also report similar conflict with the constraints of this binary categorization of “M1/M2”, demonstrating that microglia/macrophages cannot effectively cross-over to strictly polarized “M1-only” or “M2-only” phenotype. Therefore, the complex signaling events surrounding this response indicate that a binary M1/M2 characterization is not adequate to define inflammatory profile. This paper is a review article. Referred literature in this paper has been listed in the references part. The datasets supporting the conclusions of this article are available online by searching the PubMed. Some original points in this article come from the laboratory practice in our research centers and the authors' experiences.
abstractGer	Traumatic brain injury (TBI) activates the simultaneous proliferation of various pro- and anti-inflammatory molecules. Considering the amount of factors participating, this response is naturally complex. However, there is an increasing trend in neurotrauma research to delineate the injury-induced inflammatory responses within the constraints of in vitro defined macrophage polarization phenotypes “M1” and “M2”. Here, we evaluate research examining the complexity of the inflammatory response that cannot be so easily characterized using this binary nomenclature. TBI is demonstrated to induce a broad spectrum of simultaneous expression responses involving both pro- and anti-inflammatory reactions. Specifically, the research revealed a very heterogeneous parenchymal landscape associated with TBI. The concurrent expression of both “M1” and “M2” phenotypic markers on the microglia/macrophages involved suggests that the polarization phenotypes cannot be neatly defined in this M1/M2 paradigm. Recent studies displaying neurotrauma also report similar conflict with the constraints of this binary categorization of “M1/M2”, demonstrating that microglia/macrophages cannot effectively cross-over to strictly polarized “M1-only” or “M2-only” phenotype. Therefore, the complex signaling events surrounding this response indicate that a binary M1/M2 characterization is not adequate to define inflammatory profile. This paper is a review article. Referred literature in this paper has been listed in the references part. The datasets supporting the conclusions of this article are available online by searching the PubMed. Some original points in this article come from the laboratory practice in our research centers and the authors' experiences.
abstract_unstemmed	Traumatic brain injury (TBI) activates the simultaneous proliferation of various pro- and anti-inflammatory molecules. Considering the amount of factors participating, this response is naturally complex. However, there is an increasing trend in neurotrauma research to delineate the injury-induced inflammatory responses within the constraints of in vitro defined macrophage polarization phenotypes “M1” and “M2”. Here, we evaluate research examining the complexity of the inflammatory response that cannot be so easily characterized using this binary nomenclature. TBI is demonstrated to induce a broad spectrum of simultaneous expression responses involving both pro- and anti-inflammatory reactions. Specifically, the research revealed a very heterogeneous parenchymal landscape associated with TBI. The concurrent expression of both “M1” and “M2” phenotypic markers on the microglia/macrophages involved suggests that the polarization phenotypes cannot be neatly defined in this M1/M2 paradigm. Recent studies displaying neurotrauma also report similar conflict with the constraints of this binary categorization of “M1/M2”, demonstrating that microglia/macrophages cannot effectively cross-over to strictly polarized “M1-only” or “M2-only” phenotype. Therefore, the complex signaling events surrounding this response indicate that a binary M1/M2 characterization is not adequate to define inflammatory profile. This paper is a review article. Referred literature in this paper has been listed in the references part. The datasets supporting the conclusions of this article are available online by searching the PubMed. Some original points in this article come from the laboratory practice in our research centers and the authors' experiences.
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title_short	A polarizing view on posttraumatic brain injury inflammatory response
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A polarizing view on posttraumatic brain injury inflammatory response

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