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A central role for the mast cell in early phase vasculitis in the Brown Norway rat model of vasculitis: a histological study
Author(s) -
Vinen Catherine S.,
Turner David R.,
Oliveira David B. G.
Publication year - 2004
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1111/j.0959-9673.2004.00382.x
Subject(s) - degranulation , vasculitis , mast cell , immunology , autoimmunity , pathology , medicine , antibody , disease , receptor
Summary Administration of mercuric chloride (HgCl 2 ) to Brown Norway rats causes Th2‐dominated autoimmunity with raised immunoglobulin E concentrations and gut vasculitis, both of which are T‐cell dependent, peak at 14 days after starting HgCl 2 and then spontaneously resolve. If animals are re‐challenged with HgCl 2 6 weeks after initial exposure, they are resistant to autoimmunity, developing only attenuated disease. Recently, a separate phase of early caecal vasculitis was described beginning 24 h after initiating HgCl 2 and prior to caecal entry of T cells. Previous work suggested this early vasculitis was αβ T‐cell independent and implied a role for mast cells. We further tested this hypothesis by performing a histological study during the first 93 h following HgCl 2 challenge defining the precise relationship between gut mast cell degranulation and appearing caecal vasculitis. We also studied whether early caecal vasculitis enters a resistant phase upon re‐challenge with HgCl 2 . We show a direct correlation between mast cell degranulation and early caecal vasculitis following initial HgCl 2 challenge. We demonstrate resistance to re‐challenge in this phase of injury, with results at re‐challenge also showing a correlation between mast cell degranulation and early caecal injury.