Interleukin, schminterleukin: Inflammatory Language No.2
|Flasks by Skycaptaintwo 2006|
There are many interleukins (35 proteins and counting) with various functions within the immune system. Starting at the beginning is interleukin-1 (IL-1). IL-1 comes in many types (alpha, beta…and so on). Among its extensive list of duties is to be a leader and recruiter of other cells to join in the fight, either actively or by releasing their own specific chemicals—the cytokine cascade is born and hard to stop. From IL-1’s leadership, a cycle of many things, including inflammation, results.
|This diagram only begins to show the complexity of the|
cytokine cascade: from Cellular-immunity.blogspot.com
|Interleukin-1-rich immune cells infiltrating the |
beta-amyloid plaques seen in Alzheimer's disease;
photograph from Shaftel SS, Kyrkanides S, and
Olschowka JA, et al from the University of Rochester; 2007
IL-1 would be ineffective if other cells didn’t have a way to respond to it. The cells that respond to IL-1 would have an IL-1 receptor. This receptor is much like a lock on a door—that opens only when a specific key is placed into it. The IL-1 receptor recognizes IL-1 and responds, allowing IL-1 access to the cell and/or its actions. One of the resulting actions is inflammation in which damage may result--depending on the location and extent of inflammation.
To stop the inflammation born by IL-1 is tricky, and not always necessary. Just stopping IL-1 is like stopping one wheel on a massive semi—not real effective in slowing its actions down. A multi-prong approach to stopping inflammation is needed. It is important to note here that IL-1 is not the only inflammatory cytokine.
Some research looking at the role of IL-1 in inflammation and cellular damage:
Interleukin-1's role in inflammation and neuronal damage as that seen in Alzheimer's disease or atherosclerosis.
Shaftel SS, Kyrkanides S, Olschowka JA, Miller JN, Johnson RE, O'Banion MK (2007 Jun 05). Sustained hippocampal IL-1 beta overexpression mediates chronic neuroinflammation and ameliorates Alzheimer plaque pathology. J Clin Invest. 117, 1595-604.
This is the second post of a series: Inflammatory Language.The series will briefly emphasize aspects of inflammation, mainly in response to microorganisms, but not always. You can contribute to this column by submitting 300 serious, political, scientific, or funny words (as long as they have something to do with inflammation) to me by email, along with byline. If deemed appropriate, we'll publish it here--thank you. At some point, I may be able to offer gifts, but not yet.
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