Murine strain differences in airway inflammation induced by diesel exhaust particles and house dust mite allergen

Background. Differences in allergic airway inflammation induced by ovalbumin (OVA) + diesel exhaust particles (DEP) in various murine strains have already been reported. However, there is no report that different murine strains respond differently towards house dust mites or DEP, which are known to aggravate allergic asthma. Methods:The Dermatophagoides farinae allergens Der f (1 mug) or Der f (1 mug) + DEP (50 mug) were administered intratracheally to two different mouse strains (CBA/JN and C57BL/6N). Histological changes in the lung tissues, asthma-relevant cytokines in the lungs, and allergen-specific immunoglobulins in plasma were investigated. Results: Der f treatment led to the proliferation of goblet cells, production of mucus plugs, and the recruitment of eosinophils and lymphocytes to the airways of the mice. The manifestation of the airway inflammation in the C57BL/6N mouse was much greater than in the CBA/JN mouse. The protein levels of interleukin (IL)-4 and IL-5, regulated on activation, normal T cell expressed, and presumably secreted (RANTES), and eotaxin in the lung tissue of C57BL/6N mice were higher than those in CBA/JN mice by a factor of 1.26 (IL-4), 5.26 (IL-5), 2.07 (RANTES) and 3.27 (eotaxin). DEP aggravated the manifestations of the eosinophilic inflammation in CBA/JN mice through goblet cell proliferation. However, the exact effect of DEP could not be evaluated in C57BL/6N because of its severe enhancement of the inflammation. DEP enhanced the local expression of IL-5, RANTES, and eotaxin in the CBA/JN mouse, and consequently triggered an increased IgG1 production in both strains. Allergen-specific IgE antibodies were lower than 1 titer in both mice. Conclusion: The murine strain differences in the pathogenesis of allergic airway disease caused by mite allergen might be related to the local expression of the cytokines we screened. The aggravating effect of DEP may be mediated by an increase in the local expression of IL-5, RANTES, eotaxin, and the production of an antigen specific to IgG1. Copyright (C) 2002 S. Karger AG, Basel.