Inflammation plays a key role in
lung injury and in the pathogenesis of
asthma. Two murine models of allergic airway
inflammation-sensitization and challenge to
ovalbumin (OVA) and intratracheal exposure to
interleukin-13 (IL13)-were used to evaluate the expression of
poly(ADP-ribose) polymerase-1 (PARP-1) in allergic airway
inflammation.
Inflammation is prominent in OVA-induced allergic
asthma, but this
inflammation is greatly reduced by a PARP-1 inhibitor and almost eliminated when PARP-1 knockout mice are subjected to the OVA model. The present study temporally evaluated
PARP-1 protein expression, localization, and activity, as well as
inflammation and goblet cell
metaplasia (GCM), in murine lungs following a single OVA challenge or
IL13 exposure. Following OVA challenge
PARP-1 protein expression and activity were greatly increased, being maximal at 3 to 5 days following OVA exposure and beginning to decrease by day 8. These changes correlated with the timing and degree of
inflammation and GCM. In contrast,
PARP-1 protein or activity did not change following single
IL13 exposure, though GCM was manifested without
inflammation. This study demonstrates that both
PARP-1 protein and activity are increased by
allergen-activated inflammatory mediators, excluding
IL13, and that PARP-1 increase does not appear necessary for GCM, one of the characteristic markers of allergic airway
inflammation in murine models.