The expression of TRPV channels, prostaglandin E2 and pro-inflammatory cytokines during behavioural fever in fish

Citation

Boltana S, Sanhueza N, Donoso A, Aguilar A, Crespo D, Vergara D, Arriagada G, Morales-Lange B, Mercado L, Rey S, Tort L & MacKenzie S (2018) The expression of TRPV channels, prostaglandin E2 and pro-inflammatory cytokines during behavioural fever in fish. Brain, Behavior, and Immunity, 71, pp. 169-181. https://doi.org/10.1016/j.bbi.2018.03.023

Abstract
A fever, or increased body temperature, is a symptom of inflammation, which is a complex defence reaction of the organism to pathogenic infections. After pathogens enter the body, immune cells secrete a number of agents, the functions of which stimulate the body to develop a functional immune and fever response. In mammals it is known that \{PGE2\} is the principal mediator of fever. The extent to which \{PGE2\} and other pro-inflammatory cytokines such as TNF-α, IL-6, or IL-1β could be involved in the induction of behavioural fever in fish remains to be clarified. Several members of the transient receptor potential (TRP) family of ion channels have been implicated as transducers of thermal stimuli, including \{TRPV1\} and TRPV2, which are activated by heat. Here we show that members of the \{TRP\} family, \{TRPV1\} and TRPV4, may participate in the coordination of temperature sensing during the behavioural fever. To examine the behavioral fever mechanism in Salmo salar an infection with IPNV, infectious pancreatic necrosis virus, was carried out by an immersion challenge with 10 ×105 PFU/mL-1 of IPNV. Behavioural fever impacted upon the expression levels of both \{TRPV1\} and \{TRPV4\} mRNAs after the viral challenge and revealed a juxtaposed regulation of \{TRPV\} channels. Our results suggest that an increase in the mRNA abundance of \{TRPV1\} is tightly correlated with a significant elevation in the expression of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α and PGE2) in the Pre-Optic Area (POA) and cytokine release in plasma. Together, these data indicate that the reduction of \{TRPV4\} expression during behavioural fever may contribute to the onset of behavioural fever influencing movement toward higher water temperatures. Our data also suggest an effect of \{TRPV\} channels in the regulation of behavioural fever through activation of \{EP3\} receptors in the central nervous system by \{PGE2\} induced by plasma-borne cytokines. These results highlight for first time in mobile ectotherms the key role of pro-inflammatory cytokines and \{TRPV\} channels in behavioural fever that likely involves a complex integration of prostaglandin induction, cytokine recognition and temperature sensing.

Keywords
Ectotherm; behavioural fever; cytokine; TRP channels; virus

Journal
Brain, Behavior, and Immunity: Volume 71

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