Bacterial Lipoprotein and Lipopolysaccharide Act Synergistically to Induce Lethal Shock and Proinflammatory Cytokine Production

Hongwei Zhang, Johnny Peterson, David Niesel, Gary R. Klimpel

Research output: Contribution to journalArticle

94 Citations (Scopus)

Abstract

Septic shock is a major cause of death in the world. Although much is known about the role of LPS in septic shock, little is known about the role of other bacterial components. Lipoprotein (LP) is a major component of bacteria in the family Enterobacteriaceae. LP purified from Escherichia coli was shown to induce TNF-α and IL-6 production in peritoneal exudate macrophages obtained from LPS-responsive (C3H/HeOuJ) and LPS-nonresponsive (C3H/HeJ) mice. LP and LPS acted synergistically to induce cytokine production not only in C3H/HeOuJ macrophages but also in C3H/HeJ macrophages. These results suggest that LPS can induce cellular signaling in C3H/HeJ macrophages, and that LPS and LP activate macrophages via different receptors and/or signaling pathways. The role LP plays in septic shock was investigated using the mouse D-galactosamine model. LP induced lethal shock and in vivo production of TNF-α and IL-6 in both LPS-responsive and LPS-nonresponsive mice. LPS failed to induce lethal shock or in vivo cytokine production in C3H/HeJ mice. However, LP and LPS acted synergistically in inducing lethal shock and in vivo cytokine production in both LPS-responsive and LPS-nonresponsive mice. Finally, a heat-killed preparation of an E. coli mutant strain that lacked LP was shown to be less efficient than heat-killed wild-type E. coli at inducing lethal shock in C3H/HeJ mice. Collectively, these results suggest that LP and LPS induce cytokine production via different mechanisms and that LP plays an important role in septic shock induced by bacteria in the family Enterobacteriaceae.

Original languageEnglish (US)
Pages (from-to)4868-4878
Number of pages11
JournalJournal of Immunology
Volume159
Issue number10
StatePublished - Nov 15 1997

Fingerprint

Lipoproteins
Lipopolysaccharides
Shock
Cytokines
Septic Shock
Macrophages
Enterobacteriaceae
Escherichia coli
Interleukin-6
Hot Temperature
Bacteria
Galactosamine
Peritoneal Macrophages
Exudates and Transudates
Cause of Death

ASJC Scopus subject areas

  • Immunology

Cite this

Bacterial Lipoprotein and Lipopolysaccharide Act Synergistically to Induce Lethal Shock and Proinflammatory Cytokine Production. / Zhang, Hongwei; Peterson, Johnny; Niesel, David; Klimpel, Gary R.

In: Journal of Immunology, Vol. 159, No. 10, 15.11.1997, p. 4868-4878.

Research output: Contribution to journalArticle

@article{0e748b3334004434b10394aabe4c0417,
title = "Bacterial Lipoprotein and Lipopolysaccharide Act Synergistically to Induce Lethal Shock and Proinflammatory Cytokine Production",
abstract = "Septic shock is a major cause of death in the world. Although much is known about the role of LPS in septic shock, little is known about the role of other bacterial components. Lipoprotein (LP) is a major component of bacteria in the family Enterobacteriaceae. LP purified from Escherichia coli was shown to induce TNF-α and IL-6 production in peritoneal exudate macrophages obtained from LPS-responsive (C3H/HeOuJ) and LPS-nonresponsive (C3H/HeJ) mice. LP and LPS acted synergistically to induce cytokine production not only in C3H/HeOuJ macrophages but also in C3H/HeJ macrophages. These results suggest that LPS can induce cellular signaling in C3H/HeJ macrophages, and that LPS and LP activate macrophages via different receptors and/or signaling pathways. The role LP plays in septic shock was investigated using the mouse D-galactosamine model. LP induced lethal shock and in vivo production of TNF-α and IL-6 in both LPS-responsive and LPS-nonresponsive mice. LPS failed to induce lethal shock or in vivo cytokine production in C3H/HeJ mice. However, LP and LPS acted synergistically in inducing lethal shock and in vivo cytokine production in both LPS-responsive and LPS-nonresponsive mice. Finally, a heat-killed preparation of an E. coli mutant strain that lacked LP was shown to be less efficient than heat-killed wild-type E. coli at inducing lethal shock in C3H/HeJ mice. Collectively, these results suggest that LP and LPS induce cytokine production via different mechanisms and that LP plays an important role in septic shock induced by bacteria in the family Enterobacteriaceae.",
author = "Hongwei Zhang and Johnny Peterson and David Niesel and Klimpel, {Gary R.}",
year = "1997",
month = "11",
day = "15",
language = "English (US)",
volume = "159",
pages = "4868--4878",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "10",

}

TY - JOUR

T1 - Bacterial Lipoprotein and Lipopolysaccharide Act Synergistically to Induce Lethal Shock and Proinflammatory Cytokine Production

AU - Zhang, Hongwei

AU - Peterson, Johnny

AU - Niesel, David

AU - Klimpel, Gary R.

PY - 1997/11/15

Y1 - 1997/11/15

N2 - Septic shock is a major cause of death in the world. Although much is known about the role of LPS in septic shock, little is known about the role of other bacterial components. Lipoprotein (LP) is a major component of bacteria in the family Enterobacteriaceae. LP purified from Escherichia coli was shown to induce TNF-α and IL-6 production in peritoneal exudate macrophages obtained from LPS-responsive (C3H/HeOuJ) and LPS-nonresponsive (C3H/HeJ) mice. LP and LPS acted synergistically to induce cytokine production not only in C3H/HeOuJ macrophages but also in C3H/HeJ macrophages. These results suggest that LPS can induce cellular signaling in C3H/HeJ macrophages, and that LPS and LP activate macrophages via different receptors and/or signaling pathways. The role LP plays in septic shock was investigated using the mouse D-galactosamine model. LP induced lethal shock and in vivo production of TNF-α and IL-6 in both LPS-responsive and LPS-nonresponsive mice. LPS failed to induce lethal shock or in vivo cytokine production in C3H/HeJ mice. However, LP and LPS acted synergistically in inducing lethal shock and in vivo cytokine production in both LPS-responsive and LPS-nonresponsive mice. Finally, a heat-killed preparation of an E. coli mutant strain that lacked LP was shown to be less efficient than heat-killed wild-type E. coli at inducing lethal shock in C3H/HeJ mice. Collectively, these results suggest that LP and LPS induce cytokine production via different mechanisms and that LP plays an important role in septic shock induced by bacteria in the family Enterobacteriaceae.

AB - Septic shock is a major cause of death in the world. Although much is known about the role of LPS in septic shock, little is known about the role of other bacterial components. Lipoprotein (LP) is a major component of bacteria in the family Enterobacteriaceae. LP purified from Escherichia coli was shown to induce TNF-α and IL-6 production in peritoneal exudate macrophages obtained from LPS-responsive (C3H/HeOuJ) and LPS-nonresponsive (C3H/HeJ) mice. LP and LPS acted synergistically to induce cytokine production not only in C3H/HeOuJ macrophages but also in C3H/HeJ macrophages. These results suggest that LPS can induce cellular signaling in C3H/HeJ macrophages, and that LPS and LP activate macrophages via different receptors and/or signaling pathways. The role LP plays in septic shock was investigated using the mouse D-galactosamine model. LP induced lethal shock and in vivo production of TNF-α and IL-6 in both LPS-responsive and LPS-nonresponsive mice. LPS failed to induce lethal shock or in vivo cytokine production in C3H/HeJ mice. However, LP and LPS acted synergistically in inducing lethal shock and in vivo cytokine production in both LPS-responsive and LPS-nonresponsive mice. Finally, a heat-killed preparation of an E. coli mutant strain that lacked LP was shown to be less efficient than heat-killed wild-type E. coli at inducing lethal shock in C3H/HeJ mice. Collectively, these results suggest that LP and LPS induce cytokine production via different mechanisms and that LP plays an important role in septic shock induced by bacteria in the family Enterobacteriaceae.

UR - http://www.scopus.com/inward/record.url?scp=0031573217&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031573217&partnerID=8YFLogxK

M3 - Article

C2 - 9366412

AN - SCOPUS:0031573217

VL - 159

SP - 4868

EP - 4878

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 10

ER -