LPS response and tolerance in the zebrafish ( Danio rerio)

Zebrafish ( Danio rerio) has been used in the present work to study the fish response to bacterial lipopolysaccharide (LPS) exposure and LPS tolerance. These mechanisms are not completely understood in mammals and, presently, are totally unknown in fish. Zebrafish larval survival was assessed follow...

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Bibliographic Details
Published in:Fish & shellfish immunology 2009-02, Vol.26 (2), p.326-331
Main Authors: Novoa, B., Bowman, T.V., Zon, L., Figueras, A.
Format: Article
Language:English
Subjects:
Animals
CXCR4
Danio rerio
Drug Tolerance
Endotoxin
Freshwater
Gene Expression Regulation - drug effects
Immune System - drug effects
Larva - drug effects
Lipopolysaccharides - pharmacology
Lipopolysaccharides - toxicity
LPS
LPS tolerance
Mortality
Receptors, CXCR4 - immunology
Survival Analysis
Time Factors
Zebrafish
Zebrafish - immunology
Zebrafish - physiology
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Summary:Zebrafish ( Danio rerio) has been used in the present work to study the fish response to bacterial lipopolysaccharide (LPS) exposure and LPS tolerance. These mechanisms are not completely understood in mammals and, presently, are totally unknown in fish. Zebrafish larval survival was assessed following treatment with various types of LPS at a variety of concentrations to determine the sensitivity of zebrafish to LPS-induced immune activation. In addition, fish pretreated with a sublethal concentration of LPS did not die after exposure to a lethal concentration of LPS demonstrating, for the first time that LPS tolerance also happens in fish. The time interval between pretreatment and secondary exposure as well as the type of pretreatment dictated the strength of protection. Since zebrafish are in intimate contact with microorganisms, the high resistance of fish to LPS suggests that there must be a tight control of the LPS receptor cluster in order to avoid an excess of inflammation. One of these components is CXCR4, which has previously been shown to regulate the signal transduced by TLR4. Treating fish with AMD3100, a specific inhibitor of CXCR4, increased LPS treatment associated mortality. Blocking CXCR4 via chemical or genetic inhibition resulted in a reversion of LPS tolerance, thus further supporting the negative regulatory role of CXCR4 in this inflammatory response. In support of an inhibitory role for CXCR4 in the inflammatory cascade, IL-1 transcript levels were elevated in both unstimulated and LPS stimulated zebrafish Odysseus (CXCR4 deficient mutant) larvae.
ISSN:1050-4648
1095-9947
DOI:10.1016/j.fsi.2008.12.004