Abstract
Inflammation plays a key role in lung injury and in the pathogenesis of asthma. Two murine models of allergic airway inflammationsensitization 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.
Original language | English (US) |
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Pages (from-to) | 381-389 |
Number of pages | 9 |
Journal | Experimental Lung Research |
Volume | 36 |
Issue number | 7 |
DOIs | |
State | Published - Aug 2010 |
Externally published | Yes |
Keywords
- Asthma
- Goblet cell metaplasia
- Inflammation
- Interleukin-13
- Ovalbumin
- Poly(ADP-ribose) polymerase
ASJC Scopus subject areas
- Molecular Biology
- Pulmonary and Respiratory Medicine
- Clinical Biochemistry