R. Kleemann et al., SEPHADEX INDUCED BRONCHIAL HYPERREACTIVITY IN THE RAT - HEMATOLOGY, HISTOLOGY, HISTOCHEMISTRY AND IMMUNOHISTOLOGY OF THE LUNG, Experimental and toxicologic pathology, 48(4), 1996, pp. 233-241
24 hours after an i.v. injection of 2 mg Sephadex G 200(R) particels o
valbumin sensitized Sprague Dawley rats show an antigen specific bronc
hial hyperreactivity and an unspecific hyperreactivity against seroton
in. The aim of this study was to investigate the effects of Sephadex o
n blood parameters and lung pathology to find the morphological substr
ate of bronchial hyperreactivity in this animal model. In the blood ne
utrophilia (p < 0.01) but no eosinophilia was present. We conclude tha
t a blood eosinophilia needs not to be necessarily correlated with hyp
erreactivity of the airways like claimed by other investigators for th
is animal model. Histologically we found that Sephadex particels are t
rapped in smaller-diameter arteries of the lung and lead to a granulom
atous arteritis consisting mainly of ED1 positive and widely ED2 negat
ive macrophages interspersed with eosinophils and neutrophils. Larger
vessels not occluded by particels showed perivascular oedema with infi
ltration of eosinophils. We report here for the first time a significa
nt hypertrophy of PAS positive goblet cells (p < 0.01) accompanied by
a peribronchial infiltration with eosinophils (p < 0.01) and macrophag
es positive for ED1, ED2 and Ox-6 (p < 0.01) but not Ox-19 positive T-
lymphocytes. The authors suggest that the peribronchial inflammation c
ontributes importantly to the onset of bronchial hyperreactivity in th
is animal model and that the hypertrophy of goblet cells indicates the
pathophysiological importance of peribronchial leukocytes.