scholarly journals For Better or for Worse: A Look Into Neutrophils in Traumatic Spinal Cord Injury

2021 ◽  
Vol 15 ◽  
Author(s):  
Sandra Zivkovic ◽  
Maryam Ayazi ◽  
Grace Hammel ◽  
Yi Ren

Neutrophils are short-lived cells of the innate immune system and the first line of defense at the site of an infection and tissue injury. Pattern recognition receptors on neutrophils recognize pathogen-associated molecular patterns or danger-associated molecular patterns, which recruit them to the destined site. Neutrophils are professional phagocytes with efficient granular constituents that aid in the neutralization of pathogens. In addition to phagocytosis and degranulation, neutrophils are proficient in creating neutrophil extracellular traps (NETs) that immobilize pathogens to prevent their spread. Because of the cytotoxicity of the associated granular proteins within NETs, the microbes can be directly killed once immobilized by the NETs. The role of neutrophils in infection is well studied; however, there is less emphasis placed on the role of neutrophils in tissue injury, such as traumatic spinal cord injury. Upon the initial mechanical injury, the innate immune system is activated in response to the molecules produced by the resident cells of the injured spinal cord initiating the inflammatory cascade. This review provides an overview of the essential role of neutrophils and explores the contribution of neutrophils to the pathologic changes in the injured spinal cord.

Spinal Cord ◽  
2019 ◽  
Vol 57 (11) ◽  
pp. 953-959 ◽  
Author(s):  
Laura Mordillo-Mateos ◽  
Antonio Sánchez-Ramos ◽  
Francesca Coperchini ◽  
Ines Bustos-Guadamillas ◽  
Carlos Alonso-Bonilla ◽  
...  

2006 ◽  
Vol 24 (5) ◽  
pp. 1457-1469 ◽  
Author(s):  
I. A. Scarisbrick ◽  
P. Sabharwal ◽  
H. Cruz ◽  
N. Larsen ◽  
A. G. Vandell ◽  
...  

2013 ◽  
Vol 94 (4) ◽  
pp. S125-S136 ◽  
Author(s):  
Wenqiang Tian ◽  
Ching-Hui Hsieh ◽  
Gerben DeJong ◽  
Deborah Backus ◽  
Suzanne Groah ◽  
...  

Brain ◽  
2020 ◽  
Author(s):  
Tobias Zrzavy ◽  
Carmen Schwaiger ◽  
Isabella Wimmer ◽  
Thomas Berger ◽  
Jan Bauer ◽  
...  

Abstract Traumatic spinal cord injury is a devastating insult followed by progressive cord atrophy and neurodegeneration. Dysregulated or non-resolving inflammatory processes can disturb neuronal homeostasis and drive neurodegeneration. Here, we provide an in-depth characterization of innate and adaptive inflammatory responses as well as oxidative tissue injury in human traumatic spinal cord injury lesions compared to non-traumatic control cords. In the lesion core, microglia were rapidly lost while intermediate (co-expressing pro- as well as anti-inflammatory molecules) blood-borne macrophages dominated. In contrast, in the surrounding rim, TMEM119+ microglia numbers were maintained through local proliferation and demonstrated a predominantly pro-inflammatory phenotype. Lymphocyte numbers were low and mainly consisted of CD8+ T cells. Only in a subpopulation of patients, CD138+/IgG+ plasma cells were detected, which could serve as candidate cellular sources for a developing humoral immunity. Oxidative neuronal cell body and axonal injury was visualized by intracellular accumulation of amyloid precursor protein (APP) and oxidized phospholipids (e06) and occurred early within the lesion core and declined over time. In contrast, within the surrounding rim, pronounced APP+/e06+ axon-dendritic injury of neurons was detected, which remained significantly elevated up to months/years, thus providing mechanistic evidence for ongoing neuronal damage long after initial trauma. Dynamic and sustained neurotoxicity after human spinal cord injury might be a substantial contributor to (i) an impaired response to rehabilitation; (ii) overall failure of recovery; or (iii) late loss of recovered function (neuro-worsening/degeneration).


2020 ◽  
Vol 17 (6) ◽  
pp. 676-683
Author(s):  
Chao Zhang ◽  
Anming Hu ◽  
Yingli Jing ◽  
Degang Yang ◽  
Jianjun Li

Background: The research about anti-edema effects of mannitol on acute traumatic spinal cord injury (SCI) in rats is rare. Objective: This study aimed to explore the effect of mannitol on spinal cord edema after SCI in rats. Methods: Seventy-eight adult female rats were assigned to three groups randomly: a sham control group (n = 18), a contusion and normal saline contrast group (n=30), and a contusion and mannitol treatment group (n=30). We used the open-field test to estimate the functional recovery of rats weekly. Spinal cord water content was measured to determine the spinal cord edema. The ultrastructure features of the injured dorsolateral spinal cord were determined on the 7th day after SCI by HE staining. Results: The mannitol group had greatly improved Basso-Beattie-Bresnahan (BBB) scores when compared with the saline contrast group. The spinal cord water content was increased significantly after SCI, and there was no significant difference in the water content between the NaCl and mannitol groups 1 day after SCI. The water content at 3 and 7 days after SCI was significantly lower in the mannitol group than in the NaCl group (p < 0.05). Mannitol can reduce spinal cord edema by increasing the number of red blood cells in the injured spinal cord and decrease the ratio (dorsoventral diameter/ mediolateral diameter) of spinal cord 7 days post-SCI. Conclusion: Mannitol increases recovery of motor function in rats, reduces spinal cord edema and increases the number of red blood cells in the injured spinal cord, decreasing the ratio of spinal cord to reduce pressure.


2018 ◽  
Vol 19 (9) ◽  
pp. 2550 ◽  
Author(s):  
Damien Pearse ◽  
Johana Bastidas ◽  
Sarah Izabel ◽  
Mousumi Ghosh

The transplantation of Schwann cells (SCs) has been shown to provide tissue preservation and support axon growth and remyelination as well as improve functional recovery across a diverse range of experimental spinal cord injury (SCI) paradigms. The autologous use of SCs has progressed to Phase 1 SCI clinical trials in humans where their use has been shown to be both feasible and safe. The contribution of immune modulation to the protective and reparative actions of SCs within the injured spinal cord remains largely unknown. In the current investigation, the ability of SC transplants to alter the innate immune response after contusive SCI in the rat was examined. SCs were intraspinally transplanted into the lesion site at 1 week following a thoracic (T8) contusive SCI. Multicolor flow cytometry and immunohistochemical analysis of specific phenotypic markers of pro- and anti-inflammatory microglia and macrophages as well as cytokines at 1 week after SC transplantation was employed. The introduction of SCs significantly attenuated the numbers of cluster of differentiation molecule 11B (CD11b)+, cluster of differentiation molecule 68 (CD68)+, and ionized calcium-binding adapter molecule 1 (Iba1)+ immune cells within the lesion implant site, particularly those immunoreactive for the pro-inflammatory marker, inducible nitric oxide synthase (iNOS). Whereas numbers of anti-inflammatory CD68+ Arginase-1 (Arg1+) iNOS− cells were not altered by SC transplantation, CD68+ cells of an intermediate, Arg1+ iNOS+ phenotype were increased by the introduction of SCs into the injured spinal cord. The morphology of Iba1+ immune cells was also markedly altered in the SC implant, being elongated and in alignment with SCs and in-growing axons versus their amoeboid form after SCI alone. Examination of pro-inflammatory cytokines, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and anti-inflammatory cytokines, interleukin-4 (IL-4) and interleukin-10 (IL-10), by multicolor flow cytometry analysis showed that their production in CD11b+ cells was unaltered by SC transplantation at 1 week post-transplantation. The ability of SCs to subdue the pro-inflammatory iNOS+ microglia and macrophage phenotype after intraspinal transplantation may provide an important contribution to the neuroprotective effects of SCs within the sub-acute SCI setting.


2018 ◽  
Vol 25 (4) ◽  
pp. 739-746 ◽  
Author(s):  
Daryoush Fatehi ◽  
Mohammad Ali Dayani ◽  
Ayoob Rostamzadeh

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