Ovalbumin-induced experimental allergic asthma is Toll-like receptor 2 dependent
The role of Toll-like receptor (TLR) 2 in modulating allergy-induced asthma is contradictory. We investigated the effect of TLR2 gene deletion in a murine model of ovalbumin (OVA)-challenged asthma. TLR2 wild-type (TLR2+/+) and TLR2-deficient (TLR2−/−)
mice were sensitized to soluble OVA antigens and challenged with OVA, and the extent of allergic airways disease was analyzed in both groups of mice at day 8 after being challenged with OVA aerosol. At day 8 post-OVA, TLR2−/− mice exhibited significantly lower airway
hyperresponsiveness, airway inflammation, and whole lung T-helper type 2 (Th2) cytokine levels compared with the TLR2+/+ group. TLR2 deletion also significantly reduced mucus cell metaplasia and peribronchial fibrosis in mice at day 8 after challenged by OVA. The p38/AKT/nuclear
factor kappaB (NF-kappaB) p65 and phosphate extracellular signal‐regulated kinase (ERK)/p38/AKT was decreased in TLR2−/− mouse lungs. Thus, during OVA asthma in mice, TLR2 is a major contributor to the maintenance of the adaptive Th2-cytokine‐driven inflammatory
disorder and ERK/p38 as well as AKT/NF-κB playing a role in it.
Keywords: Akt; ERK; NF-κB; TLR2; allergic asthma; ovalbumin; p38
Document Type: Research Article
Affiliations: Soochow University Affiliated Children’s Hospital, Suzhou, People’s Republic of China
Publication date: 01 March 2014
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