Various immunological phenotypes are associated with increased airway responsiveness.
BACKGROUND
Bronchial asthma is characterized by a TH2 type immune response, chronic inflammation of the airways and increased airway responsiveness. The relationship between IgE- and inflammatory-dependent mechanisms that contribute to bronchial asthma are not well defined.


OBJECTIVE
The purpose of this study was to compare and analyse the immune pathways that resulted in development of allergen-induced and/or inflammatory dependent increased airways responsiveness.


RESULTS
BALB/c and C57BL/6 mice responded to OVA-sensitization with elevated allergen-specific IgE/IgG1 serum antibody-titres and the development of cutaneous immediate-type hypersensitivity reactions. Increased airway responsiveness was observed following airway allergen challenges. However, the inflammatory component of the lung differed between the strains. In OVA-sensitized BALB/c mice a marked increase in lymphocytes, eosinophils and neutrophils in BAL fluids was parallelled with elevated production of IL-4, IL-5 and TNFalpha in the lung. In contrast in OVA-sensitized C57BL/6 mice, the inflammatory immune response in the lung was much weaker. We postulate that two pathways can regulate the induction of increased airway responsiveness. One depends on the presence of allergen-specific IgE/IgG1 and allergen, and a second is mediated by allergen-independent inflammation of the lung. To test this hypothesis, BALB/c mice were treated nasally with low doses of bacterial superantigen (SEB) as a prototypical inducer of airway inflammation, following which influx of lymphocytes, eosinophils and neutrophils into the airways was parallelled by development of increased airway-responsiveness in the absence of allergen-specific IgE/IgG1 antibodies and allergen.


CONCLUSIONS
These results indicate that increased airway responsiveness is associated with different immunological phenotypes in BALB/c and C57BL/6 mice.
Herz
U
U
Department of Clinical Chemistry and Biochemistry, Virchow-Klinikum of the Humboldt-University Berlin, Germany.
Braun
A
A
Rückert
R
R
Renz
H
H
D000403:Airway Resistance / Q000276:immunology; D000485:Allergens / Q000276:immunology; D000818:Animals; D000942:Antigens, Bacterial / Q000276:immunology; D016535:Bronchial Hyperreactivity / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D016207:Cytokines / Q000096:biosynthesis; D006969:Hypersensitivity, Immediate / Q000276:immunology; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D007074:Immunoglobulin G / Q000097:blood; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D008168:Lung / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009130:Muscle, Smooth / Q000473:pathology; D010047:Ovalbumin / Q000276:immunology; D010641:Phenotype; D012867:Skin / Q000473:pathology; D018089:Superantigens / Q000276:immunology; D014132:Trachea / Q000473:pathology
D000485:Allergens; D000942:Antigens, Bacterial; D016207:Cytokines; D007074:Immunoglobulin G; D018089:Superantigens; D007073:Immunoglobulin E; D010047:Ovalbumin