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Published on: March 29, 2017
The parabrachial nucleus elicits a vigorous corticosterone feedback response to the pro-inflammatory cytokine IL-1β
Ferdinand Jagot1, Romane Gaston-Breton2, Ana Jeemin Choi3
1Institut Pasteur, Université de Paris Cité, Inserm U1224, Microenvironment and Immunity Unit, 75015 Paris, France; Institut Pasteur, Université de Paris Cité, CNRS UMR 3571, Perception and Memory Unit, 75015 Paris, France; PhD Program, Ecole Doctorale Bio Sorbonne Paris Cité (BioSpc), Université de Paris Cité, 75005 Paris, France.
Abstract:
The central nervous system regulates systemic immune responses by integrating the physiological and behavioral constraints faced by an individual. Corticosterone (CS), the release of which is controlled in the hypothalamus by the paraventricular nucleus (PVN), is a potent negative regulator of immune responses. Using the mouse model, we report that the parabrachial nucleus (PB), an important hub linking interoceptive afferent information to autonomic and behavioral responses, also integrates the pro-inflammatory cytokine IL-1β signal to induce the CS response. A subpopulation of PB neurons, directly projecting to the PVN and receiving inputs from the vagal complex (VC), responds to IL-1β to drive the CS response. Pharmacogenetic reactivation of these IL-1β-activated PB neurons is sufficient to induce CS-mediated systemic immunosuppression. Our findings demonstrate an efficient brainstem-encoded modality for the central sensing of cytokines and the regulation of systemic immune responses.
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