BCG-induced enhancement of endotoxin sensitivity in C3H/HeJ mice. I. In vivo studies

S. N. Vogel, R. N. Moor, J. D. Sipe, David L. Rosenstreich

Research output: Contribution to journalArticle

68 Citations (Scopus)

Abstract

C3H/HeJ mice exhibit a marked insensitivity to bacterial lipopolysaccharide (LPS) in vivo. Pretreatment of these mice with viable BCG organisms 11 days before LPS administration renders them sensitive to the lethal effects of a highly purified, phenol-extracted LPS. Other in vivo responses to LPS are increased in BCG-infected C3H/HeJ mice in parallel with enhanced lethality. These include 1) the elevation of serum interferon, 2) the production of the acute phase reactant, serum amyloid A (SAA), and 3) hypoglycemia. However, BCG infection has only a minimal effect on anti-LPS antibody production. BCG-infected C3H/HeJ mice approach the LPS sensitivity of normal C3H/HeN mice, but the enhanced LPS sensitivity is transient and decreases over a 2-month period. The ability of BCG to induce LPS sensitivity in C3H/HeJ mice demonstrates that LPS unresponsiveness is not due to an absolute defect in this strain, but rather, a partially reversible state of hyporesponsiveness. In addition, these findings, in conjunction with other observations, suggest that the enhancement of LPS sensitivity induced by BCG infection is mediated primarily through an effect on T cells and/or macrophages rather than B lymphocytes.

Original languageEnglish (US)
Pages (from-to)2004-2009
Number of pages6
JournalJournal of Immunology
Volume124
Issue number4
StatePublished - 1980
Externally publishedYes

Fingerprint

Inbred C3H Mouse
Mycobacterium bovis
Endotoxins
Lipopolysaccharides
Serum Amyloid A Protein
Acute-Phase Proteins
Phenol
Infection
Hypoglycemia
Interferons
Antibody Formation
Anti-Idiotypic Antibodies
B-Lymphocytes
Macrophages
T-Lymphocytes

ASJC Scopus subject areas

  • Immunology

Cite this

BCG-induced enhancement of endotoxin sensitivity in C3H/HeJ mice. I. In vivo studies. / Vogel, S. N.; Moor, R. N.; Sipe, J. D.; Rosenstreich, David L.

In: Journal of Immunology, Vol. 124, No. 4, 1980, p. 2004-2009.

Research output: Contribution to journalArticle

Vogel, S. N. ; Moor, R. N. ; Sipe, J. D. ; Rosenstreich, David L. / BCG-induced enhancement of endotoxin sensitivity in C3H/HeJ mice. I. In vivo studies. In: Journal of Immunology. 1980 ; Vol. 124, No. 4. pp. 2004-2009.
@article{0e9e055aff4b4389960da2bb3dfe21b4,
title = "BCG-induced enhancement of endotoxin sensitivity in C3H/HeJ mice. I. In vivo studies",
abstract = "C3H/HeJ mice exhibit a marked insensitivity to bacterial lipopolysaccharide (LPS) in vivo. Pretreatment of these mice with viable BCG organisms 11 days before LPS administration renders them sensitive to the lethal effects of a highly purified, phenol-extracted LPS. Other in vivo responses to LPS are increased in BCG-infected C3H/HeJ mice in parallel with enhanced lethality. These include 1) the elevation of serum interferon, 2) the production of the acute phase reactant, serum amyloid A (SAA), and 3) hypoglycemia. However, BCG infection has only a minimal effect on anti-LPS antibody production. BCG-infected C3H/HeJ mice approach the LPS sensitivity of normal C3H/HeN mice, but the enhanced LPS sensitivity is transient and decreases over a 2-month period. The ability of BCG to induce LPS sensitivity in C3H/HeJ mice demonstrates that LPS unresponsiveness is not due to an absolute defect in this strain, but rather, a partially reversible state of hyporesponsiveness. In addition, these findings, in conjunction with other observations, suggest that the enhancement of LPS sensitivity induced by BCG infection is mediated primarily through an effect on T cells and/or macrophages rather than B lymphocytes.",
author = "Vogel, {S. N.} and Moor, {R. N.} and Sipe, {J. D.} and Rosenstreich, {David L.}",
year = "1980",
language = "English (US)",
volume = "124",
pages = "2004--2009",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "4",

}

TY - JOUR

T1 - BCG-induced enhancement of endotoxin sensitivity in C3H/HeJ mice. I. In vivo studies

AU - Vogel, S. N.

AU - Moor, R. N.

AU - Sipe, J. D.

AU - Rosenstreich, David L.

PY - 1980

Y1 - 1980

N2 - C3H/HeJ mice exhibit a marked insensitivity to bacterial lipopolysaccharide (LPS) in vivo. Pretreatment of these mice with viable BCG organisms 11 days before LPS administration renders them sensitive to the lethal effects of a highly purified, phenol-extracted LPS. Other in vivo responses to LPS are increased in BCG-infected C3H/HeJ mice in parallel with enhanced lethality. These include 1) the elevation of serum interferon, 2) the production of the acute phase reactant, serum amyloid A (SAA), and 3) hypoglycemia. However, BCG infection has only a minimal effect on anti-LPS antibody production. BCG-infected C3H/HeJ mice approach the LPS sensitivity of normal C3H/HeN mice, but the enhanced LPS sensitivity is transient and decreases over a 2-month period. The ability of BCG to induce LPS sensitivity in C3H/HeJ mice demonstrates that LPS unresponsiveness is not due to an absolute defect in this strain, but rather, a partially reversible state of hyporesponsiveness. In addition, these findings, in conjunction with other observations, suggest that the enhancement of LPS sensitivity induced by BCG infection is mediated primarily through an effect on T cells and/or macrophages rather than B lymphocytes.

AB - C3H/HeJ mice exhibit a marked insensitivity to bacterial lipopolysaccharide (LPS) in vivo. Pretreatment of these mice with viable BCG organisms 11 days before LPS administration renders them sensitive to the lethal effects of a highly purified, phenol-extracted LPS. Other in vivo responses to LPS are increased in BCG-infected C3H/HeJ mice in parallel with enhanced lethality. These include 1) the elevation of serum interferon, 2) the production of the acute phase reactant, serum amyloid A (SAA), and 3) hypoglycemia. However, BCG infection has only a minimal effect on anti-LPS antibody production. BCG-infected C3H/HeJ mice approach the LPS sensitivity of normal C3H/HeN mice, but the enhanced LPS sensitivity is transient and decreases over a 2-month period. The ability of BCG to induce LPS sensitivity in C3H/HeJ mice demonstrates that LPS unresponsiveness is not due to an absolute defect in this strain, but rather, a partially reversible state of hyporesponsiveness. In addition, these findings, in conjunction with other observations, suggest that the enhancement of LPS sensitivity induced by BCG infection is mediated primarily through an effect on T cells and/or macrophages rather than B lymphocytes.

UR - http://www.scopus.com/inward/record.url?scp=0018876276&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018876276&partnerID=8YFLogxK

M3 - Article

VL - 124

SP - 2004

EP - 2009

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 4

ER -