Demonstration of a mechanism of anti-inflammatory effect of erythromycin on allergic airway inflammation in rat

Abstract

To investigate whether erythromycin exerts anti-inflammatory effect on allergic airway inflammation and whether erythromycin modulate allergic airway inflammation by inhibiting nuclear factor kappa B (NF-kappa B) activation. Ovalbumin (OVA) together with aluminum hydroxide and Bordetella Pertussis was injected intraperitoneally to immunize SD rats and two weeks later 1% OVA was inhaled to challenge them for consecutive 7 days to mimic allergic airway inflammation. In treatment group, erythromycin was given orally (180 mg/kg.d) during the course of allergen exposure. WBC counts in bronchoalveolar lavage fluid (BALF) and lung specimen analysis were used to describe lung tissue inflammation. The expression of NF-kappa B subunit p65 in cell nucleus of lung tissue was measured by immunohistochemistry and NF-kappa B binding activation in lung tissue by electrophoresis mobility shift assay (EMSA). Lung tissue specimen analysis indicated that the severity of allergic inflammation was reduced in treatment group. The number of total WBC in BALF (x 10(8)/L) (31 +/- 22) was lower than that in model group animals (66 +/- 28), P < 0.01. The number (x 10(3)/mm(2)) of cells with nuclear staining of NF-kappa B per square millimeter of submucosal region around large bronchus (1.4 +/- 0.4) was lower than that in model group animals (2.6 +/- 0.6), P < 0.01. NF-kappa B binding activity (32 +/- 14) was lower than that of model group (46 +/- 17), P < 0.05. Erythromycin had an obvious protective role in allergic airway inflammation. Erythromycin inhibited NF-kappa B transcriptional activity to exert anti-inflammatory effect.