Genetic Control of Endotoxic Responses in Mice

Overview

Journal J Exp Med

Specialties Allergy & Immunology
General Medicine

Date 1978 Jan 1

PMID 342667

Citations 22

Authors

J Watson

M Largen

K P McAdam

Affiliations

Soon will be listed here.

Abstract

A number of altered immunologic responses to lipopolysaccharide (LPS) in C3H/HeJ mice result from the expression in B lymphocytes of a defective genetic locus, termed Lps. Lps has been mapped to chromosome 4 between two loci, Mup-1 and Ps. As it is difficult to type individual mice for LPS responsiveness in more than one type of assay, we have utilized Mup-1 as a genetic marker to correlate LPS responses in mice to the expression of the Lps locus. Three nonlymphoid responses to LPS have been examined in 12 recombinant inbred strains of mice and in a backcross linkage analysis, and are all regulated by the expression of the Lps locus. These responses are hypothermal changes in body temperature, and the elevation in serum levels of a colony stimulating factor and the precursor of the secondary amyloid protein AA. Therefore, the initiation of LPS responses in different cell types in mice involve the expression of a common locus. These linkage studies provide a means for analyzing the genetic control of many of the diverse reactions of the endotoxic response to LPS.

Citing Articles

Toll-Like Receptor 4-Independent Carbon Tetrachloride-Induced Fibrosis and Lipopolysaccharide-Induced Acute Liver Injury in Mice: Role of Hepatic Stellate Cells.

Kumar S, Wang J, Shanmukhappa S, Gandhi C Am J Pathol. 2017; 187(6):1356-1367.

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Genetic basis for unresponsiveness to lipopolysaccharide in C57BL/10Cr mice.

Coutinho A, Meo T Immunogenetics. 2011; 7(1):17-24.

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Peptide nucleic acid antisense oligomer as a therapeutic strategy against bacterial infection: proof of principle using mouse intraperitoneal infection.

Tan X, Actor J, Chen Y Antimicrob Agents Chemother. 2005; 49(8):3203-7.

PMID: 16048926 PMC: 1196239. DOI: 10.1128/AAC.49.8.3203-3207.2005.

Lps(d)/Ran of endotoxin-resistant C3H/HeJ mice is defective in mediating lipopolysaccharide endotoxin responses.

Wong P, Kang A, Chen H, Yuan Q, Fan P, SULTZER B Proc Natl Acad Sci U S A. 1999; 96(20):11543-8.

PMID: 10500213 PMC: 18070. DOI: 10.1073/pnas.96.20.11543.

Secretory leukocyte protease inhibitor interferes with uptake of lipopolysaccharide by macrophages.

Ding A, Thieblemont N, Zhu J, Jin F, Zhang J, Wright S Infect Immun. 1999; 67(9):4485-9.

PMID: 10456890 PMC: 96768. DOI: 10.1128/IAI.67.9.4485-4489.1999.

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