TRIF Deficiency does not Affect Severity of Ovalbumin-induced Airway Inflammation in Mice
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Allergic asthma is a chronic pulmonary inflammatory diseasecharacterized by reversible airway obstruction, hyperresponsivenessand eosinophils infiltration. Toll-like receptors(TLRs) signaling are closely associated with asthmaand have emerged as a novel therapeutic target in allergicdisease. The functions of TLR3 and TLR4 in allergic airway inflammationhave been studied; however, the precise role ofTIR-domain-containing adapter-inducing interferon-β (TRIF),the adaptor molecule for both TLR3 and TLR4, is not yet fullyunderstood. To investigate this, we developed a mouse modelof OVA-induced allergic airway inflammation and comparedthe severity of allergic airway inflammation in WT andTRIF−/− mice. Histopathological assessment revealed thatthe severity of inflammation in airway inflammation inTRIF-deficient mice was comparable to that in WT mice. Thetotal number of cells recovered from bronchoalveolar lavagefluid did not differ between WT and TRIF-deficient mice. Moreover, TRIF deficiency did not affect Th1 and Th2 cytokineproduction in lung tissue nor the level of serumOVA-specific IgE, IgG1 and IgG2c. These findings suggestthat TRIF-mediated signaling may not be critical for the developmentof allergic airway inflammation.
Abstract
Allergic asthma is a chronic pulmonary inflammatory diseasecharacterized by reversible airway obstruction, hyperresponsivenessand eosinophils infiltration. Toll-like receptors(TLRs) signaling are closely associated with asthmaand have emerged as a novel therapeutic target in allergicdisease. The functions of TLR3 and TLR4 in allergic airway inflammationhave been studied; however, the precise role ofTIR-domain-containing adapter-inducing interferon-β (TRIF),the adaptor molecule for both TLR3 and TLR4, is not yet fullyunderstood. To investigate this, we developed a mouse modelof OVA-induced allergic airway inflammation and comparedthe severity of allergic airway inflammation in WT andTRIF−/− mice. Histopathological assessment revealed thatthe severity of inflammation in airway inflammation inTRIF-deficient mice was comparable to that in WT mice. Thetotal number of cells recovered from bronchoalveolar lavagefluid did not differ between WT and TRIF-deficient mice. Moreover, TRIF deficiency did not affect Th1 and Th2 cytokineproduction in lung tissue nor the level of serumOVA-specific IgE, IgG1 and IgG2c. These findings suggestthat TRIF-mediated signaling may not be critical for the developmentof allergic airway inflammation.
참고문헌 (40)
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