User:Geh17/sandbox

Neuroinflammation: Creating a new section titled "Spinal Cord Injury" below the section called "Traumatic Brain Injury", making it the new section 5
1) summarizes your article and says why it is important that it be accurate and updated

The article titled "Neuroinflammation" encompasses topics ranging from what causes inflammation in the CNS and PNS, to various diseases that result from neruoinflammation. The main reasoning behind me wanting to update this article is due to the large amount of novel information being published in the past 3 to 5 years about inflammation in spinal cord injuries and how it causes chronic symptoms. There is also a lot of new research being done on the immune cells causing the inflammatory response after spinal cord injury and what can be done to prevent chronic inflammation after injury. This along with the fact that a page providing information about neuroinflammation did not have any facts about inflammation in the spinal cord, the complex that makes up half of the central nervous system, showed me the importance in updating the page with information about inflammation following spinal cord injury. Knowing that the information I plan on adding does make the amount of overall page space unbalanced in favor of SCI, I hope to continue contributing to this page to further develop the other sections and sub-sections in order to have a more balanced but also a more thoroughly comprehensive and developed page overall.

2) name specifically which parts, sections, or paragraphs assigned to you.

Creating a new section titled "Spinal Cord Injury" below the section called "Traumatic Brain Injury", making it the new section 5.

3) summarize your plan or suggestions for improvement (i.e. discuss what to improve, not yet making the specific edits - just your plan for the instructor to review and give feedback.

- I wanted to develop a section explaining what SCI is, what signals and cells contribute to the inflammation caused by SCI, and an explanation as to why the inflammation is chronic in SCI. I also plan on adding Spinal Cord Injury to the bulleted list under the "Causes" section.

DRAFT 1:

Spinal cord injury (SCI) is caused by damage to the spinal chord and can lead to potentially permanent loss of function below the site of injury. SCI induces an inflammatory response   which releases several pro-inflammatory cytokines  including interleukin 1β (IL-1β) and tumor necrosis factor α (TNFα). This inflammatory response will not only activate local microglia cells, but also will attract various immune cells such as naive bone-marrow derived macrophages. These activated microglia and macrophages play a role in the parthenogenesis of SCI and contribute to secondary injury. Once a macrophages infiltrates into the epicenter of the site of injury they will change their phenotype from an M2 phenotype to and M1-like phenotype. M2 macrophage phenotype is associated with anti-inflammatory factors and contribute to wound healing and tissue repair, while the M1-like phenotype is associated with pro-inflammatory cytokines and reactive oxygen species that contribute to increased damage and inflammation. This phenotype switching is induced my myelin debris formed by the injury at the damage site.

FINAL DRAFT:

During the SCI induced inflammatory response, several pro-inflammatory cytokines including interleukin 1β (IL-1β), inducible Nitric Oxide Synthase (iNOS), Interferon-γ (IFN-γ), IL-6, IL-23, and tumor necrosis factor α (TNFα) are produced, which activate local microglia and attracts various immune cells such as naive bone-marrow derived macrophages to the injury site. These activated microglia and macrophages play a role in the pathogenesis of SCI.

Upon infiltration of the injury site’s epicenter, macrophages will undergo phenotype switching from an M2 phenotype to an M1-like phenotype. The M2 phenotype is associated with anti-inflammatory factors such as IL-10, IL-4, and IL-13 and contributes to wound healing and tissue repair. However, the M1-like phenotype is associated with pro-inflammatory cytokines and reactive oxygen species that contribute to increased damage and inflammation. Factors such as myelin debris, which is formed by the injury at the damage site, has been shown to induce the phenotype shift from M2 to M1. A decreased population of M2 macrophages and an increased population of M1 macrophages is associated with chronic inflammation. Short term inflammation is important in clearing cell debris from the site of injury, but it is this chronic, long-term inflammation that will lead to further cell death and damage radiating from the site of injury.

Paragraph 1 of Draft 2 was a collaboration between Sara J. and I.

4) Create a section in your Sandbox titled "Bibliography" and compile a list of relevant, reliable books, journal articles, or other sources that you will use to support your work. Post that bibliography to the talk page of the article you'll be working on, and in your sandbox. Make sure to check in on the Talk page to see if anyone has advice on your bibliography.

Bibliography: