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

Abstract:

: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.

journal_name

Int J Exp Pathol

authors

Vinen CS,Turner DR,Oliveira DB

doi

10.1111/j.0959-9673.2004.00382.x

subject

Has Abstract

pub_date

2004-06-01 00:00:00

pages

165-74

issue

3

eissn

0959-9673

issn

1365-2613

pii

IEP382

journal_volume

85

pub_type

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