A central role for the mast cell in early phase vasculitis in the Brown Norway rat model of vasculitis: a histological study.
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 alpha beta 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.
Vinen
Catherine S
CS
Department of Renal Medicine, St George's Hospital Medical School, Cranmer Terrace, London, UK.
Turner
David R
DR
Oliveira
David B G
DB
D000818:Animals; D001327:Autoimmune Diseases / Q000473:pathology*; D002432:Cecum / Q000098:blood supply; D015550:Cell Degranulation; D008297:Male; D008407:Mast Cells / Q000473:pathology / Q000502:physiology*; D008627:Mercuric Chloride; D023421:Models, Animal; D051381:Rats; D011914:Rats, Inbred BN; D013997:Time Factors; D014657:Vasculitis / Q000473:pathology*
D008627:Mercuric Chloride