Lipopolysaccharide Induced Th1 Immune Responses and CD14 Mediated Airway Inflammatory Response in the Asthma Model of Mice / 소아알레르기및호흡기학회지

ABSTRACT

PURPOSE: CD14 is a major factor that mediate the inflammatory response upon lipopolysaccharides (LPS) in vivo. Although it is considered that LPS increases neutrophils upon allergic inflammation and induces aggravation of allergic immune response, there is no explicit study on the role of CD14. In this study, we investigated the effect of membrane-bound CD14 (mCD14), appears on the lung tissue after exposing LPS to asthmatic mice upon inflammatory response of asthmatic lung. METHODS: Twenty mice with athme and 20 control mice were challenged via intratracheally, with saline and LPS, respectively. Bronchoalveolar lavage (BAL) fluid was collected 0, 6 and 12 hours after challenger. BAL fluid was analyzed for total and differential cell counts and soluble markers (IL-4, IL-10, TNF-alpha and IFN-gamma). Immunohistochemistry for confocal localization of CD14 in the lung specimens was used to analyze mCD14 expression. RESULTS: Asthmatic lungs demonstrated significantly lower levels of mCD14 expression than controls before intratracheal challenge with LPS (35.38+/-12.5 vs. 63.55+/-24.1 cell/HPF, P<0.05). LPS-induced PMN responses reach the peak 6 hours after LPS in the asthma group and was correlated with mCD14 expression. The level of Interferon-gamma was markedly increased at 24 hours after intratracheal challenge of LPS in asthma group (515.13+/-12.5 vs. 62.82+/-23.7, P<0.05). CONCLUSION: mCD14 of inside airway is expected to act an important role on controlling allergic inflammation as a mediator of allergic immune cascades of lung. And it is also believed that the increase of Th1 response by LPS exposing on asthmatic airway is related with the increase of CD14.