Abstract
Our lab focuses on the role of poly(ADP‐ribose)polymermase‐1(PARP‐1) in the pathogenesis of pulmonary inflammation. We have recently shown that PARP‐1 inhibition through genetic or pharmacological means in the OVA‐challenge mouse model of asthma results in a reduction in eosinophilia in comparison to mice with normal PARP‐1. Furthermore, there is a reduction in the inflammatory cytokines IL‐4 and IL‐5. We show the reduction in eosinophilia may be associated with an interruption in the IL‐4 receptor signal transduction pathway. The expression of GATA3, a critical transcription factor for IL‐5 expression is decreased in IL‐4 treated splenocytes derived from PARP‐1‐/‐ mice. Such an effect was associated with a decrease in the expression of STAT6, a transcription factor for GATA3. Such a decrease was not associated with a decrease in the pathway components JAK1 and JAK3. These findings suggest that PARP‐1 plays an important role in the expression of STAT6 and that the reduction of STAT6 expression in PARP‐1‐/‐ mice leads to a decrease in GATA3 expression in these mice. This may explain the reduction in IL‐5 production when PARP‐1 is inhibited in the OVA‐challenge mouse model.
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