Background Although many studies have examined chronic asthma, limited data
exist on acute immunopathogenic events induced by allergens. The aim of th
e study was to investigate the acute cellular, serologic and histopathologi
c events in airway inflammation produced by intranasal challenge of mice se
nsitised to the major house dust mite allergen Der p 1. Methods: C57BL/6 mi
ce were immunised subcutaneously with Der p 1 in alum. Mice were bled and c
hallenged intranasally with Der p 1 on day 14 and killed on day 17. Lungs w
ere fixed in situ, processed and stained with haematoxylin and eosin. The d
egree of inflammation and eosinophil infiltration was quantified by image a
nalysis. Specific IgE was determined by passive cutaneous anaphylaxis. Cell
s from spleen and draining lymph nodes were cultured for 24 h with Der p 1,
and IL-3/GM-CSF released into supernatants was measured by bioassay. Resul
ts: Intranasal challenge of sensitised mice induced eosinophilic influx int
o the large and small airways and the alveolar regions of the lung, mucus p
lugging and in severe cases numerous Charcot-Leyden crystals. The quantitat
ion of the inflammation induced by different sensitisation and challenge do
ses showed that optimal inflammation could be produced using only 1 mu g of
allergen for both sensitisation and challenge. The degree of inflammation
was not related to the titre of IgE antibody and was indeed produced in its
absence. T cell reactivity of spleen cells to the allergen was decreased s
uggesting cell migration or inactivation. Conclusions: Mice sensitised and
challenged intranasally with as little as 1 mu g of Der p 1 produced an ext
ensive pulmonary eosinophilic inflammation which shared many of the feature
s of the inflammation found in asthma. The small amount of allergens requir
ed and the use of intranasal challenge should provide a useful model.