We are going to put everyone to sleep here! 
Can you tell that I did a Pharmacology B.Sc. in an added year at medical school? One of the major courses in it was âMediators of Inflammationâ. OK, you asked for it, so here goes. At the top of this particular pathway is Arachidonic Acid. This is the product of Phospholipase A2 (PLA-2) acting on membrane phospholipids. PLA-2 happens to be one of the major components of bee venom. The following article is nothing to do with bee stings, but it does have a very nice summary diagram of the biochemical pathway:
http://www.cvphysiology.com/Blood%20Flow/BF013.htm
So once PLA-2 has released Arachidonic Acid (AA), the AA is available to go either down the Leukotriene (LT), or the Prostaglandin (PG) pathway. To make PG, you need to have Cyclo-Oxygenase (COX) enzyme activity. If you take NSAIDs, including ibuprofen, naproxen and aspirin, you will block COX activity, which creates a backup of upstream AA. This excess AA will then get shunted down to Lipo-oxygenase in the LT pathway instead. The problem with that is that Leukotrienes tend to cause a much more prolonged and more allergic-type (rather than inflammatory) response than Prostaglandins do, including wheezing and a sustained oedematous local inflammatory reaction. The treatment for this would be either a Lipo-oxygenase inhibitor, or a Leukotriene receptor antagonist. Not sure what is available in the UK, but there are certainly approved medications which have this kind of activity.
Still awake?