| 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.
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| 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.
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