Literature DB >> 10753497

Increased burn-induced immunosuppression in lipopolysaccharide-resistant mice.

N Jobin1, D R Garrel, J Bernier.   

Abstract

Severe burns induce a state of immunosuppression, and the inflammatory response after burn injury may play a role in this phenomenon. This study examined the effect of the inflammatory response to endotoxin on burn-induced immunosuppression and oxidative stress. An endotoxin-resistant mouse strain (C3H/HeJ) and a normally responding mouse strain (C3H/HeN) were compared. The mice were separated into three groups of five animals for each experimental day: (1) saline, (2) buprenorphine, and (3) buprenorphine and 20% total body surface area burn. All animals were fed ad libitum. The inflammatory response was studied at 1, 4, 7, 10, and 14 days postburn. Proliferation of activated splenocytes in burn mice was significantly lower on days 7, 10, and 14 for the C3H/HeJ strain and on days 4 and 10 for the C3H/HeN strain. Globally, C3H/HeJ presented stronger immune suppression than C3H/HeN. Oxidative stress parameters (liver malonaldehyde, spleen metabolic activity, and thiol concentrations) were higher in endotoxin-resistant mice than in the control strain. Impairment of the inflammatory response was more pronounced and oxidative stress was greater in endotoxin-resistant burn mice than in normal burn controls. Buprenorphine administration was not related to depression of these immune parameters. The inflammatory response following burn injury may be beneficial to the immune system. Copyright 2000 Academic Press.

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Year:  2000        PMID: 10753497     DOI: 10.1006/cimm.2000.1619

Source DB:  PubMed          Journal:  Cell Immunol        ISSN: 0008-8749            Impact factor:   4.868


  9 in total

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2.  Selective effect of burn injury on splenic CD11c(+) dendritic cells and CD8alpha(+)CD4(-)CD11c(+) dendritic cell subsets.

Authors:  Julie Patenaude; Michele D'Elia; Claudine Hamelin; Jacques Bernier
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Journal:  Results Immunol       Date:  2013-06-29

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Review 5.  To Treat or Not to Treat: The Effects of Pain on Experimental Parameters.

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7.  Platelet depletion in mice increases mortality after thermal injury.

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8.  Toll-Like Receptor 4 on both Myeloid Cells and Dendritic Cells Is Required for Systemic Inflammation and Organ Damage after Hemorrhagic Shock with Tissue Trauma in Mice.

Authors:  Kent Zettel; Sebastian Korff; Ruben Zamora; Adrian E Morelli; Sophie Darwiche; Patricia A Loughran; Greg Elson; Limin Shang; Susana Salgado-Pires; Melanie J Scott; Yoram Vodovotz; Timothy R Billiar
Journal:  Front Immunol       Date:  2017-11-28       Impact factor: 7.561

9.  Toll-like receptor 4 has an essential role in early skin wound healing.

Authors:  Lin Chen; Shujuan Guo; Matthew J Ranzer; Luisa A DiPietro
Journal:  J Invest Dermatol       Date:  2012-09-06       Impact factor: 8.551

  9 in total

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