Open AccessInhibition of TLR4 inhibits allergic responses in murine allergic rhinitis by regulating the NF‑κB pathway
Author(s) -
Haitian Xu,
Hai-Rong Shu,
Jie Zhu,
Jukun Song
Publication year - 2019
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2019.7631
Subject(s) - oncogene , molecular medicine , tlr4 , apoptosis , nf κb , immunology , medicine , cell cycle , allergic response , cancer research , biology , immune system , inflammation , immunoglobulin e , genetics , antibody
The present study investigated the underlying mechanisms and effects of toll-like receptor 4 (TLR4) on a mouse model of allergic rhinitis (AR). An ovalbumin (OVA)-induced mouse model of AR was treated with TLR4-short hairpin RNA (shRNA). Allergic symptoms were then subsequently assessed. Protein levels of OVA-specific immunoglobulin E (IgE), eosinophil cation protein (ECP), leukotriene C4 (LTC4) and prostaglandin D2 (PGD2) in mice serum and nasal lavage fluid, as well as various inflammatory cytokine mediators in mice serum, were determined by ELISA. Protein level detection was performed using reverse transcription-quantitative PCR and western blot analysis. The results revealed that TLR4 was highly expressed in the nasal mucosa of AR mice. TLR4 inhibition significantly relieved OVA-induced AR symptoms. Relief of symptoms was evidenced by a decreased frequency of sneezing and nose friction, reduced levels of OVA-specific IgE, ECP, LTC4, PGD2, less inflammatory cells and decreased levels of T-helper 2 type cytokines. In addition, the data indicated that OVA-induced activation of the NF-κB pathway was repressed by TLR4-shRNA. The results of the current study indicate that TLR4 may be a promising therapeutic target of AR.