TRIF Deficiency does not Affect Severity of Ovalbumin-induced Airway Inflammation in Mice
Immune Network
;
: 249-254, 2014.
Article
in English
| WPRIM
| ID: wpr-50688
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Asthma
/
Immunoglobulin E
/
Immunoglobulin G
/
Bronchoalveolar Lavage Fluid
/
Interferon-beta
/
Airway Obstruction
/
Eosinophils
/
Toll-Like Receptors
/
Inflammation
/
Lung
Limits:
Animals
Language:
English
Journal:
Immune Network
Year:
2014
Type:
Article
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