Therapeutic effect of surfactant protein D in allergic inflammation of mite-sensitized mice
Article first published online: 11 APR 2005
Clinical & Experimental Allergy
Volume 35, Issue 4, pages 515–521, April 2005
How to Cite
Liu, C.-F., Chen, Y.-L., Shieh, C.-C., Yu, C.-K., Reid, K. B. M. and Wang, J.-Y. (2005), Therapeutic effect of surfactant protein D in allergic inflammation of mite-sensitized mice. Clinical & Experimental Allergy, 35: 515–521. doi: 10.1111/j.1365-2222.2005.02205.x
- Issue published online: 11 APR 2005
- Article first published online: 11 APR 2005
- Submitted 19 April 2004; revised 6 December 2004; accepted 17 December 2004
- alveolar macrophage;
- asthma murine model;
- surfactant protein D
Background Surfactant protein D (SP-D) is involved in the innate immunity within the lung and may have important roles in modulating the inflammatory process of asthma.
Objective To examine the potential immunomodulating role of SP-D on the allergic response in mice, and its interaction with the alveolar macrophages (AMs) during allergic inflammation.
Methods A recombinant 60 kDa fragment of human SP-D (rfh SP-D), Survanta, and budesonide were administrated, respectively, to Der p-sensitive BALB/c mice before or after allergen challenge (AC). Total and differential cell counts, levels of cytokines in bronchoalveolar lavage fluids(BALFs), and levels of Der p-specific IgE and IgG1 antibodies in sera, were assayed. The production of nitric oxide (NO), and inducible NO synthase (iNOS) expression, in AMs, were determined by ELISA and RT-PCR, respectively.
Results Instillation of rfh SP-D to sensitized mice 6 h after AC (therapeutic), but not 24 h before AC (preventive), markedly reduced infiltration of eosinophils, and also reduced levels of IL-4, IL-5, eotaxin, and TNF-α but elevated levels of IFN-γ in the BALF. These effects were comparable with those obtained with budesonide treatment, whereas Survanta did not have a suppressive effect, either before or after AC. There was significant inhibition of NO production in the rfh SP-D pre-treated AMs of allergen-sensitized mice, but not in naïve mice.
Conclusions These results indicate that rfh SP-D has a therapeutic effect on allergen-induced bronchial inflammation, and that this might be because of its inhibitory effect on NO and TNF-α production by AMs, and it thus prevents the development of T-helper type 2 cytokine response.