Abstract
Dietary nitrite (DN) generates NO that lowers blood pressure in vivo. Nitrated fatty acids (NO2-FAs) are formed endogenously from NO and nitrite and display broad anti-inflammatory effects including protection in an in vivo model of inflammatory bowel disease.
Our aim was to investigate if DN or NO2-FAs affect airway hyperresponsiveness and inflammation in a mouse model of asthma.
Female BALB/c mice were sensitized with OVA+Al(OH)3 on day 0 and 7 and challenged with OVA or PBS i.n. on day 14-16. DN was administered day 10-17 by nitrite-enriched drinking water. NO2-FAs (5 mg/kg/day) were administrated day 10-17 by a s.c. placed osmotic pump. Airway resistance (RN) to metacholine and inflammatory cells in bronchoalveolar lavage (BAL) were determined on day 17.
OVA induced an increase in RN compare to ctrl in all groups (OVA vs. PBS; 5.3±0.2 vs. 2.3±0.1, OVA-DN vs. PBS; 5.6±0.2 vs. 2.5±0.1, OVA-NO2-FAs vs. PBS; 5.4±0.2 vs. 2.2±0.1 (cmH20/mL), all p<0.001). No differences in RN were observed between the OVA groups with or without administration of DN or NO2-FAs (p>0.05). OVA induced an increase in BAL eosinophils (EOS) compared to ctrl in all groups (OVA vs. PBS; 25±5.5 vs. 0±0, OVA-DN vs. PBS; 21±4 vs. 0±0, OVA-NO2-FAs vs. PBS; 45±7 vs. 0.1±0 (10,000 cells/mL), all p<0.001). No difference in EOS were observed between OVA with or without administration of DN or NO2-FAs (p>0.05). The number of EOS were higher in OVA- NO2-FAs treated animals versus OVA alone (p<0.001).
To conclude, neither DN nor NO2-FAs displayed anti-inflammatory effects in this asthma model, indicating that there is tissue specificity in the actions of these reactive nitrogen oxide species.
- © 2011 ERS