Acute episodes of wheeze in children of preschool age are frequently triggered by viral upper respiratory tract infections and result in a significant burden to health services . However, to date, the inflammatory mechanisms underlying preschool wheeze remain unclear. Mediators that have not been studied in preschool wheeze, but are implicated in the pathogenesis of wheeze in adults with asthma, include the pro-inflammatory prostanoid prostaglandin D2 (PGD2)  and the anti-inflammatory prostanoid PGE2 [3, 4]. In this study, we sought evidence for either increased PGD2 biosynthesis or reduced PGE2 biosynthesis, or a combination of both in children with preschool wheeze. To achieve this, we measured the major metabolites of PGD2 and PGE2 in the urine: 9α-hydroxy-11,15-dioxo-2,3,4,5-tetranor-prostan-1,20-dioic acid (tetranor-PGDM) and 9,15-dioxo-11α-hydroxy-13,14-dihydro-2,3,4,5-tetranor-prostan-1,20-dioic acid (tetranor-PGEM), respectively [5, 6].