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Neuro-mesenchyme units control ILC2 and obesity via a brain-adipose circuit [GAT ILC2s]

ABSTRACT: Signals from sympathetic neurons and immune cells regulate adipocytes contributing to fat tissue biology. Interactions between the nervous and immune systems have recently emerged as major regulators of host defence and inflammation1-4. Nevertheless, whether neuronal and immune cells cooperate in brain-body axes to orchestrate metabolism and obesity remains elusive. Here we report a novel neuro-mesenchyme unit that controls group 2 innate lymphoid cells (ILC2), adipose tissue physiology, metabolism and obesity via a brain-adipose circuit. We found that sympathetic nerve terminals act on neighbouring adipose mesenchymal cells via the beta-2 adrenergic receptor to control the expression of the glial-derived neurotrophic factor (GDNF) and the activity of ILC2 in gonadal fat. Accordingly, ILC2-autonomous manipulation of the GDNF receptor machinery led to altered ILC2 function, energy expenditure, insulin resistance and propensity to obesity. Retrograde tracing, chemical, surgical and chemogenetic manipulations identified a sympathetic aorticorenal circuit that modulates gonadal fat ILC2 and connects to high-order brain areas, including the paraventricular nucleus of the hypothalamus (PVH). Our work decodes a neuro-mesenchymal unit that translates long-range neuronal circuitry cues into adipose-resident ILC2 function, shaping the host metabolism and obesity.

ORGANISM(S): Mus musculus

PROVIDER: GSE179551 | GEO | 2021/07/07

REPOSITORIES: GEO

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Neuro-mesenchyme units control ILC2 and obesity via a brain-adipose circuit [GAT MSCs]

Project description:Signals from sympathetic neurons and immune cells regulate adipocytes contributing to fat tissue biology. Interactions between the nervous and immune systems have recently emerged as major regulators of host defence and inflammation1-4. Nevertheless, whether neuronal and immune cells cooperate in brain-body axes to orchestrate metabolism and obesity remains elusive. Here we report a novel neuro-mesenchyme unit that controls group 2 innate lymphoid cells (ILC2), adipose tissue physiology, metabolism and obesity via a brain-adipose circuit. We found that sympathetic nerve terminals act on neighbouring adipose mesenchymal cells via the beta-2 adrenergic receptor to control the expression of the glial-derived neurotrophic factor (GDNF) and the activity of ILC2 in gonadal fat. Accordingly, ILC2-autonomous manipulation of the GDNF receptor machinery led to altered ILC2 function, energy expenditure, insulin resistance and propensity to obesity. Retrograde tracing, chemical, surgical and chemogenetic manipulations identified a sympathetic aorticorenal circuit that modulates gonadal fat ILC2 and connects to high-order brain areas, including the paraventricular nucleus of the hypothalamus (PVH). Our work decodes a neuro-mesenchymal unit that translates long-range neuronal circuitry cues into adipose-resident ILC2 function, shaping the host metabolism and obesity.

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A Brain-Melanocortin-Vagus axis mediates adipose tissue expansion independently of energy intake.

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