TRIF Deficiency does not Affect Severity of Ovalbumin-induced Airway Inflammation in Mice.
- Author:
Tae Hyoun KIM
1
;
Dong Jae KIM
;
Jae Hak PARK
;
Jong Hwan PARK
Author Information
- Publication Type:Original Article
- Keywords: TRIF; Allergic airway inflammation; Th2
- MeSH: Airway Obstruction; Animals; Asthma; Bronchoalveolar Lavage Fluid; Eosinophils; Immunoglobulin E; Immunoglobulin G; Inflammation*; Interferon-beta; Lung; Mice*; Toll-Like Receptors
- From:Immune Network 2014;14(5):249-254
- CountryRepublic of Korea
- Language:English
- Abstract: Allergic asthma is a chronic pulmonary inflammatory disease characterized by reversible airway obstruction, hyperresponsiveness and eosinophils infiltration. Toll-like receptors (TLRs) signaling are closely associated with asthma and have emerged as a novel therapeutic target in allergic disease. The functions of TLR3 and TLR4 in allergic airway inflammation have been studied; however, the precise role of TIR-domain-containing adapter-inducing interferon-beta (TRIF), the adaptor molecule for both TLR3 and TLR4, is not yet fully understood. To investigate this, we developed a mouse model of OVA-induced allergic airway inflammation and compared the severity of allergic airway inflammation in WT and TRIF-/- mice. Histopathological assessment revealed that the severity of inflammation in airway inflammation in TRIF-deficient mice was comparable to that in WT mice. The total number of cells recovered from bronchoalveolar lavage fluid did not differ between WT and TRIF-deficient mice. Moreover, TRIF deficiency did not affect Th1 and Th2 cytokine production in lung tissue nor the level of serum OVA-specific IgE, IgG1 and IgG2c. These findings suggest that TRIF-mediated signaling may not be critical for the development of allergic airway inflammation.
