Naked Science Forum
Life Sciences => Physiology & Medicine => Topic started by: Rokitansky on 16/05/2004 00:56:16
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Here is a tough question. Once I was ill my microbiology teacher noticed that, and I told her that I took an aspirin, and that otherwise I wouldn`t make to come on the class. And, then She told me that the aspirin suppresses my immune system, and that I shouldn`t take it unless I have a really high temperature.
Aspirin inhibits cyclooxigenase that transforms arachidonic acid into PGG 2 and thus inhibits the prostaglandin production. Prostaglandins are increasing the body temperature by acting on the regulation center in hypothalamus. IL1, cytokine, released by leukocytes during an immune response, activates enzymes responsible for prostaglandin production. Since cytokine production is not affected (I think) by aspirin, I do not understand how it can suppress immune cells. She was implying that it inhibits IL1 production but I think she was wrong.
The only idea I have is that PGs may play a role in regulation of immune response, but that`s not what she told me. I know that LTB4 acts as chemotaxin, but it is created by other metabolic route than PGs.
Does aspirin suppress our immune system and if yes, by which mechanism does it do that?
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ok long shot, i'm probably wrong;
amongst other prostaglandins that are produced though the cyclo oxygenase pathway, are the prostaglandins PGE2 and PGI2. They are vasodilators. Their effect may facilitate the action of other substances like the C5a complement element and LTB4, thus making LTB4 easier to attract more neutrophils.
However, it's not as if you've been taking glucocorticosteroids! I would say asprin has a negligable effect on the immune system.
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Actually the thinking behind her statement is a bit more complicated than that.
Aspirin, and other NSAIDs like ibuprofen, ketoprofen, voltarol or indomethacin, work through inhibition of the inducible form of cyclooxygenase (COX-2), the rate-limiting step in prostaglandin synthesis. This discovery in the 1970's won British scientist John Vane the 1982 Nobel Prize and a Knighthood.
Prostaglandins are produced at sites of infection to promote inflammation; they dilate blood vessels to help blood-bourne components of the immune system to arrive quickly; they sensitise local nerves, producing pain, to alert you to the problems going on in the affected part of the body, they activate inflammatory cells (which produce cytokines) and can help to attract other immune components to the site of infection. They also act as pyrogens (which push up temperature).
By blocking the production of prostaglandins aspirin can stop some of these processes from occurring. We also now know that, in addition to inhibiting the synthesis of prostaglandins, aspirin can also block the activation of NF-KB (NF-kappa beta), a potent pro-inflammatory agent, and it can also block the production of IL-4, another inflammatory cytokine involved in recruiting inflammatory cells from the bloodstream. These findings probably help to explain the powerful benefit of aspirin-like drugs in heart disease and rheumatoid arthritis. Even more recently, scientists have found that aspirin can activate a receptor called PPAR-gamma which can suppress the action of genes encoding inflammatory cytokines.
Therefore, if you take aspirin and suppress these mechanisms, you are potentially affecting the processes which help the body to fight infection. Paracetamol (acetaminophen) might therefore be a better alternative since this seems to have a preominantly anti-pyretic (temperature lowering) effect.
As an aside, aspirin itself (acetylsalicylate ASA) dates from 1897 when it was first made by Bayer scientist Felix Hoffman as an alternative to salicylate. Salicylate was very good at relieving pain but played havoc with peoples' stomachs. ASA was found to be much kinder, and now over 80 billion aspirin pills are popped each year around the world.
Chris
"I never forget a face, but in your case I'll make an exception"
- Groucho Marx