Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Apr 22:15:648076.
doi: 10.3389/fncel.2021.648076. eCollection 2021.

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

Affiliations
Review

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

Sandra Zivkovic et al. Front Cell Neurosci. .

Abstract

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.

Keywords: cytokines; inflammation; myelin debris; neutrophils; secondary injury; spinal cord injury.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Immunohistochemical analysis showing neutrophils (red) in the injury site at 24 h after SCI in CX3CR1GFP/+ mice where CX3CR1 is a marker for microglia, and Gr-1 is a marker for neutrophils. The injury lesion is circled with dotted lines. Although neutrophils can be detected as early as 3 h postinjury and peak 12 h postinjury, they remain elevated up to 24 h postinjury and decrease in concentration 3 days post-SCI. Adapted from Wang et al. (2015).

Similar articles

Cited by

References

    1. Ahuja C. S., Wilson J. R., Nori S., Kotter M. R. N., Druschel C., Curt A., et al. (2017). Traumatic spinal cord injury. Nat. Rev. Dis. Primers 3:17018. 10.1038/nrdp.2017.18 - DOI - PubMed
    1. Albrecht U., Yang X., Asselta R., Keitel V., Tenchini M. L., Ludwig S., et al. (2007). Activation of NF-kappaB by IL-1beta blocks IL-6-induced sustained STAT3 activation and STAT3-dependent gene expression of the human gamma-fibrinogen gene. Cell Signal 19 1866–1878. 10.1016/j.cellsig.2007.04.007 - DOI - PubMed
    1. Alizadeh A., Dyck S. M., Karimi-Abdolrezaee S. (2019). Traumatic spinal cord injury: an overview of pathophysiology, models and acute injury mechanisms. Front. Neurol. 10:282. 10.3389/fneur.2019.00282 - DOI - PMC - PubMed
    1. Amarante-Mendes G. P., Adjemian S., Branco L. M., Zanetti L. C., Weinlich R., Bortoluci K. R. (2018). Pattern recognition receptors and the host cell death molecular machinery. Front. Immunol. 9:2379. 10.3389/fimmu.2018.02379 - DOI - PMC - PubMed
    1. Anwar M. A., Al Shehabi T. S., Eid A. H. (2016). Inflammogenesis of secondary spinal cord injury. Front. Cell Neurosci. 10:98. 10.3389/fncel.2016.00098 - DOI - PMC - PubMed