Glia-mediated gut-brain cytokine signaling couples sleep to intestinal inflammation

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: June 30, 2024

Abstract Sickness-induced sleep is a behavior conserved across species that promotes recovery from illness, yet the underlying mechanisms are poorly understood. Here, we show interleukin-6-like cytokine signaling Drosophila gut to brain glial cells regulates sleep. Under healthy conditions, this pathway wakefulness. However, elevated in response oxidative stress – triggered by immune and inflammatory responses intestine induces The cytokines Unpaired 2 -3 upregulated enteroendocrine activate JAK-STAT cells, including those of blood-brain barrier (BBB). This activity maintains during oxidative-stress-induced intestinal disturbances, suggesting glia inhibits wake-promoting facilitate sleep-dependent restoration under these conditions. We find enteric peptide Allatostatin A (AstA) enhances wakefulness, stress, gut-derived 2/3 AstA receptor expression BBB glia, thereby sustaining an state inflammation or illness. Taken together, our work identifies gut-to-glial communication couples with homeostasis disease, enhancing sickness, contributes understanding how disturbances arise gastrointestinal disturbances.

Language: Английский

Glia-mediated gut-brain cytokine signaling couples sleep to intestinal inflammation

Published: Sept. 18, 2024

Sickness-induced sleep is a behavior conserved across species that promotes recovery from illness, yet the underlying mechanisms are poorly understood. Here, we show interleukin-6-like cytokine signaling Drosophila gut to brain glial cells regulates sleep. Under healthy conditions, this pathway wakefulness. However, elevated in response oxidative stress – triggered by immune and inflammatory responses intestine induces The cytokines Unpaired 2 -3 upregulated enteroendocrine activate JAK-STAT cells, including those of blood-brain barrier (BBB). This activity maintains during oxidative-stress-induced intestinal disturbances, suggesting glia inhibits wake-promoting facilitate sleep-dependent restoration under these conditions. We find enteric peptide Allatostatin A (AstA) enhances wakefulness, stress, gut-derived 2/3 AstA receptor expression BBB glia, thereby sustaining an state inflammation or illness. Taken together, our work identifies gut-to-glial communication couples with homeostasis disease, enhancing sickness, contributes understanding how disturbances arise gastrointestinal disturbances.

Language: Английский

Glia-mediated gut-brain cytokine signaling couples sleep to intestinal inflammation

Published: Sept. 18, 2024

Sickness-induced sleep is a behavior conserved across species that promotes recovery from illness, yet the underlying mechanisms are poorly understood. Here, we show interleukin-6-like cytokine signaling Drosophila gut to brain glial cells regulates sleep. Under healthy conditions, this pathway wakefulness. However, elevated in response oxidative stress – triggered by immune and inflammatory responses intestine induces The cytokines Unpaired 2 -3 upregulated enteroendocrine activate JAK-STAT cells, including those of blood-brain barrier (BBB). This activity maintains during oxidative-stress-induced intestinal disturbances, suggesting glia inhibits wake-promoting facilitate sleep-dependent restoration under these conditions. We find enteric peptide Allatostatin A (AstA) enhances wakefulness, stress, gut-derived 2/3 AstA receptor expression BBB glia, thereby sustaining an state inflammation or illness. Taken together, our work identifies gut-to-glial communication couples with homeostasis disease, enhancing sickness, contributes understanding how disturbances arise gastrointestinal disturbances.

Language: Английский