Nitric oxide contributes to tissue injury in mercuric chloride-induced autoimmunity.

Abstract:

:Recent data has suggested a role for nitric oxide (NO) both in the induction of immunity and as an effector of tissue injury in experimental models of inflammation. In this study, we have tested the efficacy of two inhibitors of NO synthase, NG-monomethyl-L-arginine (L-NMMA) and aminoguanidine (AG), to modify the autoimmune leucocytoclastic necrotizing vasculitis which develops following the administration of mercuric chloride (HgCl2) to the Brown Norway rat. Neither agent affected the induction of autoimmunity as judged by plasma IgE titres or the degree of tissue neutrophil infiltration; however, L-NMMA did significantly attenuate tissue injury scores. We conclude that inhibition of NO synthase does not influence the induction of autoimmunity by HgCl2, but that NO does contribute to the development of tissue injury in this experimental model.

authors

Woolfson RG,Qasim FJ,Thiru S,Oliveira DB,Neild GH,Mathieson PW

doi

10.1006/bbrc.1995.2806

subject

Has Abstract

pub_date

1995-12-14 00:00:00

pages

515-21

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(85)72806-9

journal_volume

217

pub_type

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