Interleukin-1
Aug 22, 2015
The term interleukin was first proposed in 1979 to describe two leukocyte products with similar molecular weights (15,000-17,000): Interleukin-1 (IL-1) was the name given to the macrophage product, called lymphocyte-activating factor, that activated T and B lymphocytes. Interleukin-2 (IL-2), known as T-cell groth factor, was the name given to the lymphocyte product that stimulated T-cell proliferation. The term interleukin was adopted since these substances were both produced by and acted on by leukocytes.
At the time the biological relationship was unclear. It is now clear that IL-2 is specific in its biological effect by being a direct growth factor for T lymphocytes, whereas IL-1 seems non specific and mediates several components of the systemic acute phase response. IL-1 is more than an interleukin because it affects several nonleukocytic targets such as the liver, pancreas, bone, cartilage, muscle, synovial fibroblasts and brain (1). Interleukin-1 is a family of polypeptides whereas IL-2 is a single substance.
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Interleukin 1[/caption]
Interleukin-1
Microbial invasion, injury, immunological reaction and inflammatory processes continually challenge the hosts ability to survive. The body's response to these challenges are often called acute-phase responses. These are characterized by alteration in metabolic, endocrinologic, neurologic, and immunlogic functions. Neurological changes are fever, increases in sleep and decreased appetite.
Perhaps the most fundamental event in the initiation of the response is the production of IL-1 (1). IL-1 is produced primarily from phagocytic cells, enters the circulation, and affects distant organ systems; int his regard IL-1 acts as a hormone mediating the responses to infection and inflammation. The primary sources of IL-1 are blood monocytes, phagocytic lining cells of the liver, spleen and other organs. In addition, keratinocytes, corneal epithelial cells, brain astrocytes and gingival cells also produce IL-1. The interleukin 1 produced by these latter cells exerts its primary effects within those tissues.
The best clinical example of the effects of IL-1 on the host is found in patients with a localized bacterial infection. At the onset of infection, blood monocytes and macrophages become activated by exposure to microbial toxins. This results in the synthesis of IL-1. IL-1 stimulates several distant tissues. These include the hypothalamus and production of fever (2). The release of neutrophils is due to the direct action of IL-1 on bone marrow (3).IL-1 stimulates PGE2 (Prostaglandin 2), fibroblast proliferation, and resorption of cartilage and bone matrices (4)(5). Interleukin 1 induces an influx of inflammatory cells into the skin and is a chemoattractant for neutrophils, monocytes, B and T.
In our next article we will cover how Interleukin 1 interacts with the skin and its role in inflammation, acne and the maintenance of the skin barrier.
1. Dinarello, C.A. 1984 Interleukin-1. Rev Infect. Dis. 6:51-95
2. Dinarello, C. A., Wolff, S. M. 1982. Molecular basis of fever in humans. Am. J. Med. 72:799-819.
3. Kampschmidt, R.f. 1984. Infection, inflammation and interleukin-1. Lymphokine Res. 2:987-110.
4. Saklatvala, J., Pilsworth, L.M.C., Sarsfield, S.J., Gavrilovic, J., Heath, J.K. 1984. Pig catabolin is a form of interleukin-1. Biochem. J. 224:461-66.
5. Krane, S. M.,Goldring, S. R., Dayer, J.M. 1982. Interactions among lymphocytes, monocytes and other synovial cells in the rheumatoid synovium. In Lymphokines. &: 75-95
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