In Vivo Effects of Lipopolysaccharide on Peroxisome Proliferator-Activated Receptor Expression in Juvenile Gilthead Seabream (Sparus Aurata).

Efthimia Antonopoulou,Nikolas Panteli,Dimitrios Kyriakis,Barbara Castellana,Yoryia Vraskou,Josep Planas,Elisavet Kaitetzidou

doi:10.3390/biology6040036

Efthimia Antonopoulou, Nikolas Panteli + Show 5 more

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https://doi.org/10.3390/biology6040036

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Abstract

Fish are constantly exposed to microorganisms in the aquatic environment, many of which are bacterial pathogens. Bacterial pathogens activate the innate immune response in fish involving the production of pro-inflammatory molecules that, in addition to their immune-related role, can affect non-immune tissues. In the present study, we aimed at investigating how inflammatory responses can affect metabolic homeostasis in the gilthead seabream (Sparus aurata), a teleost of considerable economic importance in Southern European countries. Specifically, we mimicked a bacterial infection by in vivo administration of lipopolysaccharide (LPS, 6 mg/kg body weight) and measured metabolic parameters in the blood and, importantly, the mRNA expression levels of the three isotypes of peroxisome proliferator activated receptors (PPARα, β, and γ) in metabolically-relevant tissues in seabream. PPARs are nuclear receptors that are important for lipid and carbohydrate metabolism in mammals and that act as biological sensors of altered lipid metabolism. We show here that LPS-induced inflammatory responses result in the modulation of triglyceride plasma levels that are accompanied most notably by a decrease in the hepatic mRNA expression levels of PPARα, β, and γ and by the up-regulation of PPARγ expression only in adipose tissue and the anterior intestine. In addition, LPS-induced inflammation results in an increase in the hepatic mRNA expression and protein activity levels of members of the mitogen-activated protein kinase (MAPK) family, known in mammals to regulate the transcription and activity of PPARs. Our results provide evidence for the involvement of PPARs in the metabolic response to inflammatory stimuli in seabream and offer insights into the molecular mechanisms underlying the redirection of metabolic activities under inflammatory conditions in vertebrates.

Highlights

Fish living in their natural marine environment, as well as those confined in sea cages, are exposed to the potential detrimental effects of Gram-negative bacterial pathogens
The results from this study indicated that LPS administration alters the expression of genes involved in carbohydrate, lipid, and protein metabolism, in muscle fiber contraction and in the immune system in white and red skeletal muscles of seabream [9], supporting the hypothesis that muscle growth in fish could be affected by infection by bacterial pathogens, as it has been described in mammals [17]
In this expression of PPARα, PPARβ, and PPARγ, key genes involved in metabolism and energy expenditure, study, we investigated the effects of LPS administration, in order to trigger an inflammatory response in seabream tissues

Summary

Introduction

Fish living in their natural marine environment, as well as those confined in sea cages, are exposed to the potential detrimental effects of Gram-negative bacterial pathogens. That are highly sensitive to LPS by developing strong immune responses that can dangerously induce sepsis, fish are remarkably resistant to the toxic effects of LPS [2]. LPS can stimulate, on one hand, the production of inflammatory cytokines by activated immune cells and, on the other hand, antibody production that can lead to a protective response (reviewed in [1]). For this reason, LPS has received considerable attention as an immunostimulant in fish [4]. Molecules that in mammals are known to associate with LPS to allow it to interact with Toll-like receptor 4 (e.g., LPS-binding protein, CD14, LY96, etc.), or that act as intracellular mediators of LPS-activated toll-like receptor (TLR)

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