Salt augments macrophage-driven host defense in the skin
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
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| ERR768113.fastq.gz | Fastqsanger.gz | |||
| ERR768114.fastq.gz | Fastqsanger.gz | |||
| ERR768115.fastq.gz | Fastqsanger.gz | |||
| ERR768116.fastq.gz | Fastqsanger.gz | |||
| ERR768117.fastq.gz | Fastqsanger.gz |
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Project description:Immune cells regulate a hypertonic microenvironment in the skin; however, possible functions of increased skin Na+ concentrations are unknown. We found that Na+ accumulated at the site of bacterial skin infections in humans and in mice. We used the protozoan parasite Leishmania (L.) major as a model of skin-prone macrophage infection to test the hypothesis that skin-Na+ storage facilitates antimicrobial host defense. Activation of macrophages in the presence of high NaCl concentrations modified epigenetic markers and enhanced p38 mitogen-activated protein kinase (p38/MAPK)-dependent nuclear factor of activated T cells 5 (NFAT5) activation. This high-salt response resulted in elevated type-2 nitric oxide synthase (Nos2)-dependent NO production and improved L. major elimination. Finally, we found that increasing Na+ content in the skin by a high-salt diet boosted activation of macrophages in an Nfat5-dependent manner and promoted cutaneous antimicrobial defense. We suggest that the hypertonic microenvironment could serve as a barrier to infection.
2015-02-26 | E-MTAB-3343 | biostudies-arrayexpress
Project description:Immune cells regulate a hypertonic microenvironment in the skin; however, the biological advantage of increased skin Na(+) concentrations is unknown. We found that Na(+) accumulated at the site of bacterial skin infections in humans and in mice. We used the protozoan parasite Leishmania major as a model of skin-prone macrophage infection to test the hypothesis that skin-Na(+) storage facilitates antimicrobial host defense. Activation of macrophages in the presence of high NaCl concentrations modified epigenetic markers and enhanced p38 mitogen-activated protein kinase (p38/MAPK)-dependent nuclear factor of activated T cells 5 (NFAT5) activation. This high-salt response resulted in elevated type-2 nitric oxide synthase (Nos2)-dependent NO production and improved Leishmania major control. Finally, we found that increasing Na(+) content in the skin by a high-salt diet boosted activation of macrophages in a Nfat5-dependent manner and promoted cutaneous antimicrobial defense. We suggest that the hypertonic microenvironment could serve as a barrier to infection.
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Project description:Enteric nervous system (ENS)-derived neuropeptides modulate immune cell function, yet our understanding of how inflammatory cues directly influence enteric neuron responses during infection is considerably lacking. Here, we characterize a primary enteric sensory neuron (PSN) subset that produces the neuropeptides neuromedin U (NMU) and calcitonin gene-related peptide beta (CGRPβ) and co-expresses receptors for the type 2 cytokines IL-4 and IL-13. Type 2 cytokines were sufficient to upregulate NMU and CGRPβ expression in PSNs, in vitro and in vivo, which was abrogated by PSN-specific Il13ra1 deletion. Importantly, PSN-specific Il13ra1 deletion impaired host defense to the gastrointestinal helminth H. polygyrus, diminished enteric sensory neuron populations, and blunted muscularis immune responses. Co-administration of NMU23 and CGRPβ rescued helminth clearance deficits and restored anti-helminth immunity. Mechanistically, we show that CGRPβ signaling synergizes with IL-4 in intestinal macrophages, inducing alternatively-activated macrophage defense responses, altogether illustrating the critical role of bi-directional neuro-immune crosstalk in regulating intestinal type 2 immunity.
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Project description:Enteric nervous system (ENS)-derived neuropeptides modulate immune cell function, yet our understanding of how inflammatory cues directly influence enteric neuron responses during infection is considerably lacking. Here, we characterize a primary enteric sensory neuron (PSN) subset that produces the neuropeptides neuromedin U (NMU) and calcitonin gene-related peptide beta (CGRPβ) and co-expresses receptors for the type 2 cytokines IL-4 and IL-13. Type 2 cytokines were sufficient to upregulate NMU and CGRPβ expression in PSNs, in vitro and in vivo, which was abrogated by PSN-specific Il13ra1 deletion. Importantly, PSN-specific Il13ra1 deletion impaired host defense to the gastrointestinal helminth H. polygyrus, diminished enteric sensory neuron populations, and blunted muscularis immune responses. Co-administration of NMU23 and CGRPβ rescued helminth clearance deficits and restored anti-helminth immunity. Mechanistically, we show that CGRPβ signaling synergizes with IL-4 in intestinal macrophages, inducing alternatively-activated macrophage defense responses, altogether illustrating the critical role of bi-directional neuro-immune crosstalk in regulating intestinal type 2 immunity.
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