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Different TLR4 expression and microglia/macrophage activation induced by hemorrhage in the rat spinal cord after compressive injury

BACKGROUND: Hemorrhage is a direct consequence of traumatic injury to the central nervous system and may cause innate immune reactions including cerebral Toll-like receptor (TLR) 4 upregulation which usually leads to poor outcome in the traumatic brain injury. In spinal cord injury (SCI), however, h...

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Autores principales: Zhang, Yu-Kai, Liu, Jin-Tao, Peng, Zheng-Wu, Fan, Hong, Yao, An-Hui, Cheng, Peng, Liu, Ling, Ju, Gong, Kuang, Fang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3847110/
https://www.ncbi.nlm.nih.gov/pubmed/24015844
http://dx.doi.org/10.1186/1742-2094-10-112
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author Zhang, Yu-Kai
Liu, Jin-Tao
Peng, Zheng-Wu
Fan, Hong
Yao, An-Hui
Cheng, Peng
Liu, Ling
Ju, Gong
Kuang, Fang
author_facet Zhang, Yu-Kai
Liu, Jin-Tao
Peng, Zheng-Wu
Fan, Hong
Yao, An-Hui
Cheng, Peng
Liu, Ling
Ju, Gong
Kuang, Fang
author_sort Zhang, Yu-Kai
collection PubMed
description BACKGROUND: Hemorrhage is a direct consequence of traumatic injury to the central nervous system and may cause innate immune reactions including cerebral Toll-like receptor (TLR) 4 upregulation which usually leads to poor outcome in the traumatic brain injury. In spinal cord injury (SCI), however, how hemorrhage induces innate immune reaction in spinal parenchyma remains unknown. The present study aimed to see whether blood component and/or other factor(s) induce TLR4 and microglia/macrophages involved innate immune reactions in the rat spinal cord after traumatic injury. METHODS: Using the compressive SCI model of the rat, hemorrhage in the spinal cord was identified by hematoxylin-eosin staining. Microglia/macrophage activation, TLR4 expression, and cell apoptosis were investigated by immunohistochemistry. Nuclear factor (NF)-κB p50 level of the two segments of the cord was detected by western blotting assay. With carbon powder injection, blood origination of the hematoma was explored. The blood-spinal cord barrier (BSCB) states of the lesion site and the hematoma were compared with immunohistochemistry and tannic acid-ferric chloride staining. RESULTS: Histological observation found blood accumulated in the center of compression lesion site (epicenter) and in the hematoma approximately 1.5 cm away from the epicenter. TLR4 expression, microglia//macrophage activation, and subsequent apoptosis in the area of far-away hematoma were late and weak in comparison to that in epicenter. In addition, TLR4 positive microglia/macrophages appeared to be phagocytotic in the far-away hematoma more obviously than that in the epicenter. Injected carbon powder indicated that accumulated blood of the far-away hematoma originated from the bleeding of the lesion epicenter, and the BSCB around the hematoma was not compromised in the early phase. Accordingly, at 3 days post injury, NF-κB p50 was upregulated based on the similar levels of blood component hemoglobin, and cell apoptosis was obvious in the epicenter but not in the far-away hematoma. CONCLUSION: These data suggest that besides blood component, BSCB compromise and the extent of tissue injury contribute more to TLR4 and microglia/macrophage responses to the spinal cord hemorrhage. Therefore, the innate immune environment is a necessary consideration for the SCI therapy targeting TLR4 and microglia/macrophages.
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spelling pubmed-38471102013-12-04 Different TLR4 expression and microglia/macrophage activation induced by hemorrhage in the rat spinal cord after compressive injury Zhang, Yu-Kai Liu, Jin-Tao Peng, Zheng-Wu Fan, Hong Yao, An-Hui Cheng, Peng Liu, Ling Ju, Gong Kuang, Fang J Neuroinflammation Research BACKGROUND: Hemorrhage is a direct consequence of traumatic injury to the central nervous system and may cause innate immune reactions including cerebral Toll-like receptor (TLR) 4 upregulation which usually leads to poor outcome in the traumatic brain injury. In spinal cord injury (SCI), however, how hemorrhage induces innate immune reaction in spinal parenchyma remains unknown. The present study aimed to see whether blood component and/or other factor(s) induce TLR4 and microglia/macrophages involved innate immune reactions in the rat spinal cord after traumatic injury. METHODS: Using the compressive SCI model of the rat, hemorrhage in the spinal cord was identified by hematoxylin-eosin staining. Microglia/macrophage activation, TLR4 expression, and cell apoptosis were investigated by immunohistochemistry. Nuclear factor (NF)-κB p50 level of the two segments of the cord was detected by western blotting assay. With carbon powder injection, blood origination of the hematoma was explored. The blood-spinal cord barrier (BSCB) states of the lesion site and the hematoma were compared with immunohistochemistry and tannic acid-ferric chloride staining. RESULTS: Histological observation found blood accumulated in the center of compression lesion site (epicenter) and in the hematoma approximately 1.5 cm away from the epicenter. TLR4 expression, microglia//macrophage activation, and subsequent apoptosis in the area of far-away hematoma were late and weak in comparison to that in epicenter. In addition, TLR4 positive microglia/macrophages appeared to be phagocytotic in the far-away hematoma more obviously than that in the epicenter. Injected carbon powder indicated that accumulated blood of the far-away hematoma originated from the bleeding of the lesion epicenter, and the BSCB around the hematoma was not compromised in the early phase. Accordingly, at 3 days post injury, NF-κB p50 was upregulated based on the similar levels of blood component hemoglobin, and cell apoptosis was obvious in the epicenter but not in the far-away hematoma. CONCLUSION: These data suggest that besides blood component, BSCB compromise and the extent of tissue injury contribute more to TLR4 and microglia/macrophage responses to the spinal cord hemorrhage. Therefore, the innate immune environment is a necessary consideration for the SCI therapy targeting TLR4 and microglia/macrophages. BioMed Central 2013-09-10 /pmc/articles/PMC3847110/ /pubmed/24015844 http://dx.doi.org/10.1186/1742-2094-10-112 Text en Copyright © 2013 Zhang et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Zhang, Yu-Kai
Liu, Jin-Tao
Peng, Zheng-Wu
Fan, Hong
Yao, An-Hui
Cheng, Peng
Liu, Ling
Ju, Gong
Kuang, Fang
Different TLR4 expression and microglia/macrophage activation induced by hemorrhage in the rat spinal cord after compressive injury
title Different TLR4 expression and microglia/macrophage activation induced by hemorrhage in the rat spinal cord after compressive injury
title_full Different TLR4 expression and microglia/macrophage activation induced by hemorrhage in the rat spinal cord after compressive injury
title_fullStr Different TLR4 expression and microglia/macrophage activation induced by hemorrhage in the rat spinal cord after compressive injury
title_full_unstemmed Different TLR4 expression and microglia/macrophage activation induced by hemorrhage in the rat spinal cord after compressive injury
title_short Different TLR4 expression and microglia/macrophage activation induced by hemorrhage in the rat spinal cord after compressive injury
title_sort different tlr4 expression and microglia/macrophage activation induced by hemorrhage in the rat spinal cord after compressive injury
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3847110/
https://www.ncbi.nlm.nih.gov/pubmed/24015844
http://dx.doi.org/10.1186/1742-2094-10-112
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