IL-13 suppresses in vitro production of many proinflammatory factors. Initial in vivo experiments indicate that intratracheally administered IL-13 attenuates the increased vascular permeability that is observed in IgGimmune complex-mediated lung injury. To elucidate whether endogenous IL-13 is generated in the course of the inflammatory response in vivo, we sought to determine whether IL-13 was transcriptionally expressed during IgG-immune complex-induced lung injury. Rat IL-13 was PCR cloned from cDNA templates generated by the reverse transcription of mRNA isolated from injured rat lungs. Using a sequential PCR strategy that employed two sets of primers constructed according to the published rat IL-13 sequence, a PCR product was obtained and ligated into a pCR II vector, sequenced and confirmed to be rat IL-13. This clone was then utilized to generate a 32p probe for IL13 for use in Northern blot analysis of whole lung RNA obtained over the time course of IgG-immune complex-induced injury. The results demonstrated that IL-13 message increased 10% to 75% above baseline expression during the first 24 hours following injury. These findings suggest that IL-13 may function as an endogenous regulator of the in vivo inflammatory response during IgG-immune complex-induced lung njury.
|Original language||English (US)|
|State||Published - 1996|
ASJC Scopus subject areas
- Molecular Biology