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Prostaglandin D2 is a useful in vivo marker of mast cell activation in humans
While the pro-inflammatory role of eosinophilic granulocytes in asthma is currently under debate, an increasing body of evidence suggests that mast cells may indeed orchestrate many of the characteristic pathophysiological changes in asthma.1 There are also indications that the mast cell may be an effector cell in other lung diseases such as chronic obstructive pulmonary disease2–4 and lung fibrosis.5 Given the location of mast cells at multiple sites within the airways,1 they clearly have the potential to function as sensors of alterations in the microenvironment—be it to inhaled or bloodborne substances, microbes, or other insults that require a prompt host defence reaction. Their versatility is demonstrated by the great number of stimuli that trigger mast cell activation (fig 1). In addition to classical IgE dependent degranulation of mast cells, transduction pathways resulting in mast cell activation may be triggered by, for example, adenosine,6 hyperosmolarity,7 and lipopolysaccharide.8
Mast cells may produce a large number of mediators, enzymes, cytokines and other factors in response to allergic (IgE dependent) or non-allergic activation (adenosine, exercise, endotoxin, mannitol, non-steroidal anti-inflammatory drugs (NSAIDs) in NSAID intolerant subjects, etc). However, only tryptase and prostaglandin (PG) D2 (boxed) are specific markers of mast cell activation. As reported by Bochenek et al in this issue, measurement of PGD2 and its metabolites is currently the most sensitive strategy to monitor mast cell activation in human subjects. LTC4 = leukotriene C4.
MAST CELL MARKERS
Although many mast cell mediators or products serve as useful markers of mast cell activation in vitro, it has been notoriously difficult conclusively to establish mast cell activation in human studies. For example, it is difficult to catch the short lived increase in …