Interleukin, schminterleukin: Inflammatory Language No.2

Flasks by Skycaptaintwo 2006

There are many chemicals involved in inflammation. Some chemicals are released by injured cells and travel through the body causing immune cells to “come-on-over” or take action. The immune cells either navigate to the site of injury or act by releasing more chemicals, called cytokines. A cytokine (chemical from a cell) like interleukin is released from various cells such as leukocytes, monocytes, B cells, T cells, and etcetera. It acts by causing many reactions such as inflammation, neutrophil maturation, fever, or may try to inhibit further reactions. The interleukin may act by recruiting other cells to join in the perceived “fight,” or try to slow-down or stop the reactions all-together.

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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