Mouse strain differences in eosinophilic airway inflammation caused by intratracheal instillation of mite allergen and diesel exhaust particles.
Response differences by different strains of mice towards house dust mites (Dermatophagoides farinae) or diesel exhaust particles (DEP) were investigated. Mouse strains BALB/c, ICR and C3H/He received 1 micro g of D. farinae or 1 microg of D. farinae + 50 microg of DEP intratracheally four times at 2-week intervals. Dermatophagoides farinae treatment caused the recruitment of eosinophils and lymphocytes. The order of magnitude of the eosinophilic airway inflammation was BALB/c < ICR < C3H/He mice. The protein levels of eotaxin and IL-5 in lung tissues correlated with the manifestations of eosinophilic airway inflammation by D. farinae administration. Diesel exhaust particles aggravated the manifestation of the eosinophilic inflammation through goblet cell proliferation in the airway and enhanced the local expression of eotaxin and IL-5 in all three strains of mice. The levels of eotaxin and IL-5 in lung tissues corresponded to the pathological changes caused by D. farinae + DEP. The increasing order of production levels of antigen-specific IgG1 by D. farinae or D. farinae + DEP was BALB/c < ICR < C3H/He mice. The significant adjuvant effect of DEP on IgG1 production was observed in the C3H/He mice (P < 0.05). These results suggest that the murine strain differences in the production of eosinophilic airway inflammation by D. farinae + DEP are related to differences in local expression of IL-5 and eotaxin. The enhancing effects of DEP may be mediated by a cytokine increase in the local expression. Antigen-specific IgG1 may be an important immunoglobulin in the pathogenesis of allergic asthma enhanced by DEP.
Ichinose
Takamichi
T
Department of Health Sciences, Oita University of Nursing and Health Sciences, 2944-9 Notsuharu, Oita 870-1201, Japan.
Takano
Hirohisa
H
Sadakane
Kaori
K
Yanagisawa
Rie
R
Yoshikawa
Toshikazu
T
Sagai
Masaru
M
Shibamoto
Takayuki
T
D000485:Allergens / Q000009:adverse effects*; D000818:Animals; D039741:Antigens, Dermatophagoides / Q000008:administration & dosage / Q000009:adverse effects*; D001249:Asthma / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000378:metabolism; D002631:Chemotactic Factors, Eosinophil / Q000378:metabolism; D004195:Disease Models, Animal; D004306:Dose-Response Relationship, Immunologic; D004359:Drug Therapy, Combination; D004391:Dust; D007124:Immunoenzyme Techniques; D015848:Interleukin-5 / Q000378:metabolism; D007442:Intubation, Intratracheal; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008813:Mice, Inbred ICR; D011657:Pulmonary Eosinophilia / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D039981:Pyroglyphidae / Q000276:immunology*; D013045:Species Specificity; D001335:Vehicle Emissions / Q000009:adverse effects*
D000485:Allergens; D039741:Antigens, Dermatophagoides; C515457:Ccl11 protein, mouse; D054413:Chemokine CCL11; D019742:Chemokines, CC; D002631:Chemotactic Factors, Eosinophil; D004391:Dust; D015848:Interleukin-5; D001335:Vehicle Emissions