Heme oxygenase 1 attenuates cockroach allergen-induced airway inflammation
Sunday, March 4, 2018
South Hall A2 (Convention Center)
Lipeng Qiu, PhD, Qi Tang, Guohui Li
RATIONALE: Cockroach allergen is a strong risk factor of developing asthma. Oxidative stress was an important mechanism by which environmental pollutant/ allergen exposure induce adverse health effects. We sought to investigate whether cockroach allergen can induce oxidative stress in airway epithelium, and whether antioxidant defense pathways play a role in preventing the progression of allergic asthma.

METHODS: The induction of reactive oxygen species (ROS) by cockroach allergen extract (CRE) was detected using flow cytometry and immunofluorescence. The up-regulation of heme oxygenase 1 (HO-1) in CRE treated epithelial cells and lung tissues of CRE-challenged mouse asthmatic model were detected by real-time PCR. The effect of Nrf2 on HO-1 and the regulatory mechanism of Nrf2 by CRE were also investigated.

RESULTS: CRE induced reactive oxygen species production in airway epithelial cells. HO-1, an important anti-inflammatory enzyme, was significantly up-regulated in cockroach allergen-treated mouse MLE-12 epithelial cells. This increased HO-1 was further validated in lung tissues of CRE-induced mouse asthmatic model. In CRE-challenged mice, HO-1 inducer hemin attenuated airway inflammation and decreased eosinophils infiltration in bronchial alveolar lavage fluid, whereas its inhibitor tin protoporphyrin IX reversed these effects. CRE up-regulated HO-1 by activating transcription factor Nrf2.

CONCLUSIONS: These results suggest that HO-1 was an important gene related to CRE-induced oxidative stress, and may play a role in reducing airway inflammation of asthma.