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Article: Low-dose mercuric chloride induces resistance in brown norway rats to further mercuric chloride by up-regulation of interferon-γ

TitleLow-dose mercuric chloride induces resistance in brown norway rats to further mercuric chloride by up-regulation of interferon-γ
Authors
Issue Date1999
Citation
Scandinavian Journal of Immunology, 1999, v. 50 n. 2, p. 195-201 How to Cite?
AbstractMercuric chloride induces autoimmunity in Brown Norway rats with polyclonal B-cell activation, hyper-IgE and multiple autoantibodies. Pre- treatment with low-dose HgCl 2 (one-tenth of the standard dose) induces resistance to later full-dose HgCl 2; we have studied the mechanism of this resistance. Brown Norway rats given low-dose HgCl 2 showed only a modest increase in serum IgE level, three logs lower than rats given standard-dose HgCl 2, and no up-regulation of splenic interleukin (IL)-4 mRNA. There was up-regulation of splenic interferon (IFN)-γ gene expression and a progressive rise in serum IFN-γ. Neither IL-12 nor IL-18 were induced, but there was up-regulation of IL-12 receptor β2-chain (IL-12Rβ2) expression. IL-10 and transforming growth factor (TGF)-β expression did not change. Serum IgE and splenic IL-4 mRNA expression remained static when these rats were rechallenged, confirming resistance. Thereafter IFN-γ expression gradually fell, after which IL-4 expression and serum IgE rose slightly. Our observations suggest that low-dose HgCl 2 confers protection in Brown Norway rats to further HgCl 2 by up-regulation of IFN-γ, associated with enhanced IL-12Rβ2 expression. The immunological response to HgCl2 in susceptible rat strains is more complex than previously appreciated and is dose dependent, with low doses inducing a T helper '(Th)1' type of response in contrast to the 'Th2' type response associated with standard doses.
Persistent Identifierhttp://hdl.handle.net/10722/195379
ISSN
2015 Impact Factor: 2.27
2015 SCImago Journal Rankings: 0.934

 

DC FieldValueLanguage
dc.contributor.authorSzeto, C-C-
dc.contributor.authorGillespie, KM-
dc.contributor.authorMathieson, PW-
dc.date.accessioned2014-02-28T06:12:04Z-
dc.date.available2014-02-28T06:12:04Z-
dc.date.issued1999-
dc.identifier.citationScandinavian Journal of Immunology, 1999, v. 50 n. 2, p. 195-201-
dc.identifier.issn0300-9475-
dc.identifier.urihttp://hdl.handle.net/10722/195379-
dc.description.abstractMercuric chloride induces autoimmunity in Brown Norway rats with polyclonal B-cell activation, hyper-IgE and multiple autoantibodies. Pre- treatment with low-dose HgCl 2 (one-tenth of the standard dose) induces resistance to later full-dose HgCl 2; we have studied the mechanism of this resistance. Brown Norway rats given low-dose HgCl 2 showed only a modest increase in serum IgE level, three logs lower than rats given standard-dose HgCl 2, and no up-regulation of splenic interleukin (IL)-4 mRNA. There was up-regulation of splenic interferon (IFN)-γ gene expression and a progressive rise in serum IFN-γ. Neither IL-12 nor IL-18 were induced, but there was up-regulation of IL-12 receptor β2-chain (IL-12Rβ2) expression. IL-10 and transforming growth factor (TGF)-β expression did not change. Serum IgE and splenic IL-4 mRNA expression remained static when these rats were rechallenged, confirming resistance. Thereafter IFN-γ expression gradually fell, after which IL-4 expression and serum IgE rose slightly. Our observations suggest that low-dose HgCl 2 confers protection in Brown Norway rats to further HgCl 2 by up-regulation of IFN-γ, associated with enhanced IL-12Rβ2 expression. The immunological response to HgCl2 in susceptible rat strains is more complex than previously appreciated and is dose dependent, with low doses inducing a T helper '(Th)1' type of response in contrast to the 'Th2' type response associated with standard doses.-
dc.languageeng-
dc.relation.ispartofScandinavian Journal of Immunology-
dc.titleLow-dose mercuric chloride induces resistance in brown norway rats to further mercuric chloride by up-regulation of interferon-γ-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j.1365-3083.1999.00584.x-
dc.identifier.pmid10447925-
dc.identifier.scopuseid_2-s2.0-0032802350-
dc.identifier.volume50-
dc.identifier.issue2-
dc.identifier.spage195-
dc.identifier.epage201-

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