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Adrenergic signaling in muscularis macrophages limits infection-induced neuronal loss

ABSTRACT: Adrenergic signaling in muscularis macrophages limits infection-induced neuronal loss

PROVIDER: PRJNA589300 | ENA |

REPOSITORIES: ENA

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Adrenergic signaling in muscularis macrophages limits infection-induced neuronal loss

Project description:Enteric–associated neurons (EAN) are closely associated with immune cells and continuously monitor and modulate homeostatic intestinal functions, including motility. Bidirectional interactions between immune and neuronal cells are altered during disease processes such as neurodegeneration or irritable bowel syndrome. We investigated how infection-induced inflammation affects intrinsic EAN (iEAN) and the role of intestinal muscularis macrophages (MM) in this process. Using murine models of enteric infections, we observed long-term gastrointestinal symptoms including reduced motility and loss of excitatory iEAN, which was mediated by an NLRP6 and caspase 11 mechanism, depended on infection history, and could be reversed by microbiota manipulation. MM responded to luminal infection by upregulating a neuroprotective program dependent on β2-adrenergic receptor (β2-AR) signaling, and mediated neuronal protection via an arginase 1-polyamine axis. Our results identify a mechanism of neuronal cell death post–infection and point to a role for tissue–resident MM in limiting neuronal damage.

2020-01-23 | GSE140309 | GEO

Adrenergic Signaling in Muscularis Macrophages Limits Infection-Induced Neuronal Loss.

Project description:Enteric-associated neurons (EANs) are closely associated with immune cells and continuously monitor and modulate homeostatic intestinal functions, including motility and nutrient sensing. Bidirectional interactions between neuronal and immune cells are altered during disease processes such as neurodegeneration or irritable bowel syndrome. We investigated the effects of infection-induced inflammation on intrinsic EANs (iEANs) and the role of intestinal muscularis macrophages (MMs) in this context. Using murine models of enteric infections, we observed long-term gastrointestinal symptoms, including reduced motility and loss of excitatory iEANs, which was mediated by a Nlrp6- and Casp11-dependent mechanism, depended on infection history, and could be reversed by manipulation of the microbiota. MMs responded to luminal infection by upregulating a neuroprotective program via β2-adrenergic receptor (β2-AR) signaling and mediated neuronal protection through an arginase 1-polyamine axis. Our results identify a mechanism of neuronal death post-infection and point to a role for tissue-resident MMs in limiting neuronal damage.

| S-EPMC7271821 | biostudies-literature

Enteric pathogens induce tissue tolerance and prevent neuronal loss from subsequent infections

Project description:The enteric nervous system (ENS) controls several intestinal functions including motility and nutrient handling, which can be disrupted by infection-induced neuropathies or neuronal cell death. We investigated possible tolerance mechanisms preventing neuronal loss and disruption in gut motility after pathogen exposure. We found that following enteric infections, muscularis macrophages (MMs) acquire a tissue-protective phenotype that prevents neuronal loss and dysmotility during subsequent challenge with unrelated pathogens. Bacteria-induced neuroprotection relied on activation of gut-projecting sympathetic neurons and signaling via b2-adrenergic receptors (b2AR) on MMs. In contrast, helminth-mediated neuroprotection was dependent on T cells and systemic production of interleukin (IL)-4 and -13 by eosinophils, which induced arginase-expressing MMs that prevented neuronal loss from an unrelated infection located in a different intestinal region. Collectively, these data suggest that distinct enteric pathogens trigger a state of disease- or tissue tolerance that preserves ENS number and functionality.

2021-08-17 | GSE182294 | GEO

Merkel Cells Activate Sensory Neural Pathways through Adrenergic Synapses

Project description:Epithelial-neuronal signaling is essential for sensory encoding in touch, itch and nociception; however, little is known about the release mechanisms and neurotransmitter receptors through which skin cells govern neuronal excitability. Merkel cells are mechanosensory epidermal cells that have long been proposed to activate neuronal afferents through chemical synaptic transmission. We employed a set of classical criteria for chemical neurotransmission as framework to directly test this hypothesis. RNA sequencing of adult Merkel cells demonstrated that they express presynaptic molecules and biosynthetic machinery for adrenergic transmission. Moreover, live-cell imaging directly demonstrated that Merkel cells mediate activity- and VMAT-dependent release of fluorescent catecholamine neurotransmitter analogues. Touch-evoked firing in Merkel-cell afferents was inhibited either by pre-synaptic silencing of SNARE-mediated vesicle release from Merkel cells or by neuronal deletion of b2-adrenergic receptors. Together, these results identify both pre- and postsynaptic mechanisms through which Merkel cells excite mechanosensory afferents to encode gentle touch.

2018-11-08 | GSE114336 | GEO

Comparison between lamina propria macrophages and muscularis macrophages

Project description:Lamina propria and muscularis macrophages, were sorted at steady steate and 2h after oral exposure to an attenuated form of Salmonella, comparison among these populations showed that the muscularis macrophages quckly respond to the presence of intestinal bacteria, upregulating some important tissue protective genes.

2016-01-29 | GSE74131 | GEO

Loss of adrenergic nerves in bone marrow drives hematopoietic stem cell niche aging

Project description:Loss of adrenergic nerves in bone marrow drives hematopoietic stem cell niche aging

| PRJNA431366 | ENA

Loss of UBE3A impacts both neuronal and non-neuronal cells in human cerebral organoids.

Project description:Loss of UBE3A impacts both neuronal and non-neuronal cells in human cerebral organoids.

| PRJNA1064612 | ENA

Loss of neuronal Tet2 enhances hippocampal-dependent cognitive function

Project description:Loss of neuronal Tet2 enhances hippocampal-dependent cognitive function

| PRJNA719090 | ENA

Neuronal VCP loss of function recapitulates FTLD-TDP pathology

Project description:Neuronal VCP loss of function recapitulates FTLD-TDP pathology

| PRJNA738150 | ENA

LOSS OF NEURONAL TET2 ENHANCES HIPPOCAMPAL-DEPENDENT COGNITIVE FUNCTION

Project description:LOSS OF NEURONAL TET2 ENHANCES HIPPOCAMPAL-DEPENDENT COGNITIVE FUNCTION

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