Abstract
Background: IL-6 is a unique cytokine that has pro- and anti-inflammatory property. The purpose of this study was to clarify the role of IL-6 in the allergic airway inflammation.
Methods: We challenged wild-type and IL-6-deficient mice with ovalbumin (OVA) inhalation after sensitization to OVA.
Results: OVA challenge induced an intrapulmonary eosinophil infiltration and airway hyperresponsiveness in wild-type mice with increased serum IgE levels and enhanced intrapulmonary mRNA expression of T helper type 2 (Th2) cytokines, IL-5 and IL-13. IL-6-deficient mice developed a similar level of airway hyperresponsiveness despite an attenuated eosinophil infiltration and reduced elevation in serum IgE levels after OVA challenge. After OVA challenge, intrapulmonary IL-5 and IL-13 mRNA expression was less evident in IL-6-deficient mice than wild-type mice, while intrapulmonary IFN-γ mRNA expression was more enhanced. Intravenous administration of anti-IL-6 antibodies during sensitization period in wild-type mice caused similar effects as observed in IL-6 deficient mice.
Conclusions: Endogenous IL-6 may have important roles in Th2 polarization in sensitization period accompanied by eosinophil infiltration after acute exposure to aerosolized antigen.
