PATCH
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB19801 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1951450.fastq.gz | Fastqsanger.gz | |||
| ERR1951460.fastq.gz | Fastqsanger.gz | |||
| ERR1951470.fastq.gz | Fastqsanger.gz | |||
| ERR1951480.fastq.gz | Fastqsanger.gz | |||
| ERR1951490.fastq.gz | Fastqsanger.gz |
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Project description:Prenatal stress (PS) is a repeated exposure to aversive situations during pregnancy, including high emotional strain, and suspected to impact physiological systems in infants. Pediatric eczema develops quickly after birth at flexural sites subjected to continuous mechanical constraints. While epidemiological studies have suggested an association between PS and higher risk of eczema in children, no causative biological link has been identified to date. Here we show that early-onset eczema at birth originates from molecular dysregulations of neuroimmune circuits in utero triggered by fluctuations in the maternal hypothalamic-pituitary-adrenal axis. We found that offspring from stressed pregnant dams have dysregulated Mcpt5+ mast cells and skin-projecting neurons, and quickly develop eczema in response to harmless mechanical frictions. We demonstrate that PS transiently modulates maternal corticosterone levels, which profoundly alters the developmental program of skin mast cells expressing Nr3c1 and adjacent sensory neurons conveying mechanosensation. Therapeutic normalization of corticosterone levels or genetic depletion of Mcpt5+ mast cells during stressed gestation prevents dysregulation of neuroimmune pathways and fully protects from eczema development at birth. Our findings support a new model in which early-onset pediatric eczema originates from dysregulations in fetal immune and somatosensory systems caused by fluctuations in maternal glucocorticoids induced by stress.
2025-06-21 | GSE272169 | GEO
Project description:Prenatal stress (PS) is a repeated exposure to aversive situations during pregnancy, including high emotional strain, and suspected to impact physiological systems in infants. Pediatric eczema develops quickly after birth at flexural sites subjected to continuous mechanical constraints. While epidemiological studies have suggested an association between PS and higher risk of eczema in children, no causative biological link has been identified to date. Here we show that early-onset eczema at birth originates from molecular dysregulations of neuroimmune circuits in utero triggered by fluctuations in the maternal hypothalamic-pituitary-adrenal axis. We found that offspring from stressed pregnant dams have dysregulated Mcpt5+ mast cells and skin-projecting neurons, and quickly develop eczema in response to harmless mechanical frictions. We demonstrate that PS transiently modulates maternal corticosterone levels, which profoundly alters the developmental program of skin mast cells expressing Nr3c1 and adjacent sensory neurons conveying mechanosensation. Therapeutic normalization of corticosterone levels or genetic depletion of Mcpt5+ mast cells during stressed gestation prevents dysregulation of neuroimmune pathways and fully protects from eczema development at birth. Our findings support a new model in which early-onset pediatric eczema originates from dysregulations in fetal immune and somatosensory systems caused by fluctuations in maternal glucocorticoids induced by stress.
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Project description:Prenatal stress (PS) is a repeated exposure to aversive situations during pregnancy, including high emotional strain, and suspected to impact physiological systems in infants. Pediatric eczema develops quickly after birth at flexural sites subjected to continuous mechanical constraints. While epidemiological studies have suggested an association between PS and higher risk of eczema in children, no causative biological link has been identified to date. Here we show that early-onset eczema at birth originates from molecular dysregulations of neuroimmune circuits in utero triggered by fluctuations in the maternal hypothalamic-pituitary-adrenal axis. We found that offspring from stressed pregnant dams have dysregulated Mcpt5+ mast cells and skin-projecting neurons, and quickly develop eczema in response to harmless mechanical frictions. We demonstrate that PS transiently modulates maternal corticosterone levels, which profoundly alters the developmental program of skin mast cells expressing Nr3c1 and adjacent sensory neurons conveying mechanosensation. Therapeutic normalization of corticosterone levels or genetic depletion of Mcpt5+ mast cells during stressed gestation prevents dysregulation of neuroimmune pathways and fully protects from eczema development at birth. Our findings support a new model in which early-onset pediatric eczema originates from dysregulations in fetal immune and somatosensory systems caused by fluctuations in maternal glucocorticoids induced by stress.
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Project description:Prenatal stress (PS) is a repeated exposure to aversive situations during pregnancy, including high emotional strain, and suspected to impact physiological systems in infants. Pediatric eczema develops quickly after birth at flexural sites subjected to continuous mechanical constraints. While epidemiological studies have suggested an association between PS and higher risk of eczema in children, no causative biological link has been identified to date. Here we show that early-onset eczema at birth originates from molecular dysregulations of neuroimmune circuits in utero triggered by fluctuations in the maternal hypothalamic-pituitary-adrenal axis. We found that offspring from stressed pregnant dams have dysregulated Mcpt5+ mast cells and skin-projecting neurons, and quickly develop eczema in response to harmless mechanical frictions. We demonstrate that PS transiently modulates maternal corticosterone levels, which profoundly alters the developmental program of skin mast cells expressing Nr3c1 and adjacent sensory neurons conveying mechanosensation. Therapeutic normalization of corticosterone levels or genetic depletion of Mcpt5+ mast cells during stressed gestation prevents dysregulation of neuroimmune pathways and fully protects from eczema development at birth. Our findings support a new model in which early-onset pediatric eczema originates from dysregulations in fetal immune and somatosensory systems caused by fluctuations in maternal glucocorticoids induced by stress.
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Project description:Role of gut microbiota in eczema development
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Project description:Breastfeeding is thought to influence the immune system development of infants and may even affect various immunological responses later in life. Breast milk provides a rich source of early nutrition for the growth and developmental of infants. However, the presence of certain compounds in breast milk related to an unhealthy lifestyle or the diet of lactating mothers may negatively impact infants6. Based on a cohort study, we found that the composition of mother’s milk containing high amount of long-chain saturated fatty acids (LCSFAs) was related to a higher incidence of atopic dermatitis (AD) in children. Similarly, a mouse model in which breastfed offspring were fed milk high in LCSFAs also resulted in AD onset later in life. We showed that LCSFAs are damage-associated molecular patterns, which initiate a series of inflammatory events in the gut involving type 3 innate lymphoid cells (ILC3s). A remarkable increase in inflammatory ILC3s was observed in the gut, and the migration of these ILC3s to the skin contributed to the pathogenesis of AD. Gene expression analysis of ILC3s isolated from the gut revealed up-regulation of genes that increase ILC3s and chemokines, which may play a role in ILC migration to the skin. Even in the absence of adaptive immunity, Rag1 knockout mice fed a high-LCSFA milk diet developed eczema, accompanied by increased gut ILC3s. Here, we propose that early exposure to LCSFAs in infants may affect the balance of intestinal innate immunity, inducing a highly inflammatory environment with the proliferation of ILC3s and production of interleukin-17 and interleukin-22, which are attributed to the pathogenesis of AD.
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