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KMID : 0923620140140050249
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Immune Network
2014 Volume.14 No. 5 p.249 ~ p.254
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TRIF Deficiency does not Affect Severity of Ovalbumin-induced Airway Inflammation in Mice
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Kim Tae-Hyoun
Kim Dong-Jae
Park Jae-Hak
Park Jong-Hwan
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Abstract
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Allergic asthma is a chronic pulmonary inflammatory disease characterized by reversible airway obstruction, hyper-responsiveness and eosinophils infiltration. Toll-like re-ceptors (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 in-flammation have been studied; however, the precise role of TIR-domain-containing adapter-inducing interferon-β (TRIF), the adaptor molecule for both TLR3 and TLR4, is not yet fully understood. To investigate this, we developed a mouse mod-el of OVA-induced allergic airway inflammation and com-pared 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 cyto-kine 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 de-velopment of allergic airway inflammation.
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KEYWORD
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TRIF, Allergic airway inflammation, Th2
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