A central role for the mast cell in early phase vasculitis in the Brown Norway rat model of vasculitis: a histological study

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.