Overexpression of toll-like receptor 4 amplifies the host response to lipopolysaccharide and provides a survival advantage in transgenic mice

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Overexpression of toll-like receptor 4 amplifies the host response to lipopolysaccharide and provides a survival advantage in transgenic mice. / Bihl, Franck; Salez, Laurent; Beaubier, Magali et al.
In: Journal of Immunology, Vol. 170, No. 12, 15.06.2003, p. 6141-6150.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Bihl, F, Salez, L, Beaubier, M, Torres, D, Larivière, L, Laroche, L, Benedetto, A, Martel, D, Lapointe, J-M, Ryffel, B & Malo, D 2003, 'Overexpression of toll-like receptor 4 amplifies the host response to lipopolysaccharide and provides a survival advantage in transgenic mice', Journal of Immunology, vol. 170, no. 12, pp. 6141-6150. https://doi.org/10.4049/jimmunol.170.12.6141

APA

Bihl, F., Salez, L., Beaubier, M., Torres, D., Larivière, L., Laroche, L., Benedetto, A., Martel, D., Lapointe, J-M., Ryffel, B., & Malo, D. (2003). Overexpression of toll-like receptor 4 amplifies the host response to lipopolysaccharide and provides a survival advantage in transgenic mice. Journal of Immunology, 170(12), 6141-6150. https://doi.org/10.4049/jimmunol.170.12.6141

Vancouver

Bihl F, Salez L, Beaubier M, Torres D, Larivière L, Laroche L et al. Overexpression of toll-like receptor 4 amplifies the host response to lipopolysaccharide and provides a survival advantage in transgenic mice. Journal of Immunology. 2003 Jun 15;170(12):6141-6150. doi: 10.4049/jimmunol.170.12.6141

Author

Bihl, Franck ; Salez, Laurent ; Beaubier, Magali et al. / Overexpression of toll-like receptor 4 amplifies the host response to lipopolysaccharide and provides a survival advantage in transgenic mice. In: Journal of Immunology. 2003 ; Vol. 170, No. 12. pp. 6141-6150.

Bibtex

@article{d6cb22e236054521904c1860b1972607,

title = "Overexpression of toll-like receptor 4 amplifies the host response to lipopolysaccharide and provides a survival advantage in transgenic mice",

abstract = "Toll-like receptors are transmembrane proteins that are involved in the innate immune recognition of microbial constituents. Among them, Toll-like receptor 4 (Tlr4) is a crucial signal transducer for LPS, the major component of Gram-negative bacteria outer cell membrane. The contribution of Tlr4 to the host response to LPS and to infection with virulent Salmonella typhimurium was studied in four transgenic (Tg) strains including three overexpressing Tlr4. There was a good correlation between the level of Tlr4 mRNA expression and the sensitivity to LPS both in vitro and in vivo: Tg mice possessing the highest number of Tlr4 copies respond the most to LPS. Overexpression of Tlr4 by itself appears to have a survival advantage in Tg mice early during infection: animals possessing more than two copies of the gene survived longer and in a greater percentage to Salmonella infection. The beneficial effect of Tlr4 overexpression is greatly enhanced when the mice present a wild-type allele at natural resistance-associated macrophage protein 1, another critical innate immune gene involved in resistance to infection with Salmonella. Tlr4 and natural resistance-associated macrophage protein 1 exhibit functional epistatic interaction to improve the capacity of the host to control bacterial replication. However, this early improvement in disease resistance is not conducted later during infection, because mice overexpressing Tlr4 developed an excessive inflammatory response detrimental to the host.",

keywords = "Adjuvants, Immunologic, Animals, Cell Membrane, Cells, Cultured, Crosses, Genetic, Flow Cytometry, Gene Dosage, Gene Expression Regulation, Injections, Intraperitoneal, Lipopolysaccharides, Lymphocyte Activation, Membrane Glycoproteins, Mice, Mice, Inbred C3H, Mice, Inbred C57BL, Mice, Transgenic, Receptors, Cell Surface, Reverse Transcriptase Polymerase Chain Reaction, Salmonella Infections, Animal, Shock, Septic, Survival Rate, Toll-Like Receptor 4, Toll-Like Receptors, Transgenes, Journal Article, Research Support, Non-U.S. Gov't",

author = "Franck Bihl and Laurent Salez and Magali Beaubier and David Torres and Line Larivi{\`e}re and Line Laroche and Alexandre Benedetto and Dominic Martel and Jean-Martin Lapointe and Bernhard Ryffel and Danielle Malo",

year = "2003",

month = jun,

day = "15",

doi = "10.4049/jimmunol.170.12.6141",

language = "English",

volume = "170",

pages = "6141--6150",

journal = "Journal of Immunology",

issn = "0022-1767",

publisher = "American Association of Immunologists",

number = "12",

}

RIS

TY - JOUR

T1 - Overexpression of toll-like receptor 4 amplifies the host response to lipopolysaccharide and provides a survival advantage in transgenic mice

AU - Bihl, Franck

AU - Salez, Laurent

AU - Beaubier, Magali

AU - Torres, David

AU - Larivière, Line

AU - Laroche, Line

AU - Benedetto, Alexandre

AU - Martel, Dominic

AU - Lapointe, Jean-Martin

AU - Ryffel, Bernhard

AU - Malo, Danielle

PY - 2003/6/15

Y1 - 2003/6/15

N2 - Toll-like receptors are transmembrane proteins that are involved in the innate immune recognition of microbial constituents. Among them, Toll-like receptor 4 (Tlr4) is a crucial signal transducer for LPS, the major component of Gram-negative bacteria outer cell membrane. The contribution of Tlr4 to the host response to LPS and to infection with virulent Salmonella typhimurium was studied in four transgenic (Tg) strains including three overexpressing Tlr4. There was a good correlation between the level of Tlr4 mRNA expression and the sensitivity to LPS both in vitro and in vivo: Tg mice possessing the highest number of Tlr4 copies respond the most to LPS. Overexpression of Tlr4 by itself appears to have a survival advantage in Tg mice early during infection: animals possessing more than two copies of the gene survived longer and in a greater percentage to Salmonella infection. The beneficial effect of Tlr4 overexpression is greatly enhanced when the mice present a wild-type allele at natural resistance-associated macrophage protein 1, another critical innate immune gene involved in resistance to infection with Salmonella. Tlr4 and natural resistance-associated macrophage protein 1 exhibit functional epistatic interaction to improve the capacity of the host to control bacterial replication. However, this early improvement in disease resistance is not conducted later during infection, because mice overexpressing Tlr4 developed an excessive inflammatory response detrimental to the host.

AB - Toll-like receptors are transmembrane proteins that are involved in the innate immune recognition of microbial constituents. Among them, Toll-like receptor 4 (Tlr4) is a crucial signal transducer for LPS, the major component of Gram-negative bacteria outer cell membrane. The contribution of Tlr4 to the host response to LPS and to infection with virulent Salmonella typhimurium was studied in four transgenic (Tg) strains including three overexpressing Tlr4. There was a good correlation between the level of Tlr4 mRNA expression and the sensitivity to LPS both in vitro and in vivo: Tg mice possessing the highest number of Tlr4 copies respond the most to LPS. Overexpression of Tlr4 by itself appears to have a survival advantage in Tg mice early during infection: animals possessing more than two copies of the gene survived longer and in a greater percentage to Salmonella infection. The beneficial effect of Tlr4 overexpression is greatly enhanced when the mice present a wild-type allele at natural resistance-associated macrophage protein 1, another critical innate immune gene involved in resistance to infection with Salmonella. Tlr4 and natural resistance-associated macrophage protein 1 exhibit functional epistatic interaction to improve the capacity of the host to control bacterial replication. However, this early improvement in disease resistance is not conducted later during infection, because mice overexpressing Tlr4 developed an excessive inflammatory response detrimental to the host.

KW - Adjuvants, Immunologic

KW - Animals

KW - Cell Membrane

KW - Cells, Cultured

KW - Crosses, Genetic

KW - Flow Cytometry

KW - Gene Dosage

KW - Gene Expression Regulation

KW - Injections, Intraperitoneal

KW - Lipopolysaccharides

KW - Lymphocyte Activation

KW - Membrane Glycoproteins

KW - Mice

KW - Mice, Inbred C3H

KW - Mice, Inbred C57BL

KW - Mice, Transgenic

KW - Receptors, Cell Surface

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Salmonella Infections, Animal

KW - Shock, Septic

KW - Survival Rate

KW - Toll-Like Receptor 4

KW - Toll-Like Receptors

KW - Transgenes

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.4049/jimmunol.170.12.6141

DO - 10.4049/jimmunol.170.12.6141

M3 - Journal article

C2 - 12794144

VL - 170

SP - 6141

EP - 6150

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 12

ER -

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