Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone [RNA-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA564147 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10075964_1.fastq.gz | Fastqsanger.gz | |||
| SRR10075964_2.fastq.gz | Fastqsanger.gz | |||
| SRR10075965_1.fastq.gz | Fastqsanger.gz | |||
| SRR10075965_2.fastq.gz | Fastqsanger.gz | |||
| SRR10075966_1.fastq.gz | Fastqsanger.gz |
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Project description:Early life environmental exposure, particularly during perinatal period, can have a lifelong impact on organismal development and physiology. The biological rationale for this phenomenon is to promote physiological adaptation to the anticipated environment based on early life experience. However, perinatal exposure to adverse environments can also be associated with adult-onset disorders. Multiple environmental stressors induce glucocorticoids, which prompted us to investigate their role in developmental programming. Here, we report that perinatal glucocorticoid exposure had long-term consequences and resulted in diminished CD8 T cell response in adulthood and impaired control of tumor growth and bacterial infection. We found that perinatal glucocorticoid exposure resulted in persistent alteration of the hypothalamic-pituitaryadrenal (HPA) axis. Consequently, the level of the hormone in adults was significantly reduced, resulting in decreased CD8 T cell function. Our study thus demonstrates that perinatal stress can have long-term consequences on CD8 T cell immunity by altering HPA axis activity.
2020-01-01 | GSE136978 | GEO
Project description:Early life environmental exposure, particularly during perinatal period, can have a lifelong impact on organismal development and physiology. The biological rationale for this phenomenon is to promote physiological adaptation to the anticipated environment based on early life experience. However, perinatal exposure to adverse environments can also be associated with adult-onset disorders. Multiple environmental stressors induce glucocorticoids, which prompted us to investigate their role in developmental programming. Here, we report that perinatal glucocorticoid exposure had long-term consequences and resulted in diminished CD8 T cell response in adulthood and impaired control of tumor growth and bacterial infection. We found that perinatal glucocorticoid exposure resulted in persistent alteration of the hypothalamic-pituitaryadrenal (HPA) axis. Consequently, the level of the hormone in adults was significantly reduced, resulting in decreased CD8 T cell function. Our study thus demonstrates that perinatal stress can have long-term consequences on CD8 T cell immunity by altering HPA axis activity.
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Project description:Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone
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Project description:Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone [ATAC-seq]
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Project description:This SuperSeries is composed of the SubSeries listed below.
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Project description:Early life environmental exposure, particularly during perinatal period, can have a life-long impact on organismal development and physiology. The biological rationale for this phenomenon is to promote physiological adaptations to the anticipated environment based on early life experience. However, perinatal exposure to adverse environments can also be associated with adult-onset disorders. Multiple environmental stressors induce glucocorticoids, which prompted us to investigate their role in developmental programming. Here, we report that perinatal glucocorticoid exposure had long-term consequences and resulted in diminished CD8 T cell response in adulthood and impaired control of tumor growth and bacterial infection. We found that perinatal glucocorticoid exposure resulted in persistent alteration of the hypothalamic-pituitary-adrenal (HPA) axis. Consequently, the level of the hormone in adults was significantly reduced, resulting in decreased CD8 T cell function. Our study thus demonstrates that perinatal stress can have long-term consequences on CD8 T cell immunity by altering HPA axis activity.
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Project description:We examined how prenatal inflammation shapes tissue function and immunity in the lung by reprogramming tissue-resident immune cells from early development. Maternal, but not fetal, type I interferon-mediated inflammation provoked expansion and hyperactivation of group 2 innate lymphoid cells (ILC2s) seeding the developing lung. Hyperactivated ILC2s produced increased IL-5 and IL-13, were associated with acute Th2 bias, decreased Tregs, and persistent lung eosinophilia into adulthood. ILC2 hyperactivation was recapitulated by adoptive transfer of a fetal liver precursor following prenatal inflammation, indicative of developmental programming at the fetal progenitor level. Reprogrammed ILC2 hyperactivation and subsequent lung immune remodeling, including persistent eosinophilia, was associated with worsened histopathology and increased airway dysfunction equivalent to papain exposure, indicating increased asthma susceptibility in offspring. Our data elucidate a potential mechanism by which early-life inflammation results in increased asthma susceptibility, driven by hyperactivated ILC2s that drive persistent changes to lung immunity during perinatal development.
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Project description:Perinatal asphyxia remains a leading cause of neonatal mortality, and a major contributor to permanent neurological deficits. Even mild cases can result in long-term neurodevelopmental, cognitive, behavioural, and psychiatric disorders. However, the mechanisms underlying asphyxia-induced hypoxic-ischaemic brain injury remain poorly understood, limiting the development of targeted interventions during the critical early plastic period. To investigate how perinatal asphyxia-induced changes lead to neuropsychiatric deficits and associated histological and molecular alterations that progress into adulthood, we utilised a translationally relevant, non-invasive oxygen deprivation model of asphyxia in postnatal day 7 rats. 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The development of an acute inflammatory response after perinatal asphyxia marked by phenotypic transformation of microglia paralleled brain perfusion and stress hormone changes. Notably, microglial changes were mitigated by the blockade of proinflammatory interleukin-1 signalling via systemic IL-1 receptor antagonist (IL-1RA) administration in a therapeutically relevant time window. Importantly, early blockade of proinflammatory responses was able to prevent cognitive deficits in adulthood, and normalised inhibitory bouton densities. RNA sequencing analysis revealed asphyxia-induced dysregulation of molecular pathways targeting GABAergic signalling, potentially contributing to subsequent morphological and neuropsychiatric alterations. IL-1RA treatment appeared to engage distinct regulatory mechanisms, rather than merely reversing these disruptions in the acute post-asphyxia period. Collectively, these findings demonstrate that perinatal asphyxia induces marked behavioural deficits in attention and inhibitory control, paralleled by lasting inhibitory dysregulation, preceded by acute induction of microglia-driven inflammatory processes in the medial prefrontal cortex. Systemic IL-1RA administration may represent a promising therapeutic opportunity to prevent long-term cognitive impairments caused by perinatal asphyxia. Perinatal asphyxia remains a leading cause of neonatal mortality, and a major contributor to permanent neurological deficits. Even mild cases can result in long-term neurodevelopmental, cognitive, behavioural, and psychiatric disorders. However, the mechanisms underlying asphyxia-induced hypoxic-ischaemic brain injury remain poorly understood, limiting the development of targeted interventions during the critical early plastic period. To investigate how perinatal asphyxia-induced changes lead to neuropsychiatric deficits and associated histological and molecular alterations that progress into adulthood, we utilised a translationally relevant, non-invasive oxygen deprivation model of asphyxia in postnatal day 7 rats. We conducted comprehensive assessment of asphyxia-induced changes, integrating neurobehavioural profiling (evaluating cognitive, emotional, social, and neuromotor functions), microglial morphology analysis, neuroimaging, stress hormone measurement and whole-transcriptome sequencing techniques to elucidate the acute and long-term functional consequences. Consistent with clinical observations, the extensive functional assessment revealed distinct sex-dependent effects, including increased anxiety and impulsivity, attention deficits, and impaired inhibitory control, which were observed exclusively in males, with no apparent sensorimotor deficits. This phenotype resembling attention deficit hyperactivity disorder in adult rats was associated with a lasting increase in inhibitory bouton densities in the medial prefrontal cortex. The development of an acute inflammatory response after perinatal asphyxia marked by phenotypic transformation of microglia paralleled brain perfusion and stress hormone changes. Notably, microglial changes were mitigated by the blockade of proinflammatory interleukin-1 signalling via systemic IL-1 receptor antagonist (IL-1RA) administration in a therapeutically relevant time window. Importantly, early blockade of proinflammatory responses was able to prevent cognitive deficits in adulthood, and normalised inhibitory bouton densities. RNA sequencing analysis revealed asphyxia-induced dysregulation of molecular pathways targeting GABAergic signalling, potentially contributing to subsequent morphological and neuropsychiatric alterations. IL-1RA treatment appeared to engage distinct regulatory mechanisms, rather than merely reversing these disruptions in the acute post-asphyxia period. Collectively, these findings demonstrate that perinatal asphyxia induces marked behavioural deficits in attention and inhibitory control, paralleled by lasting inhibitory dysregulation, preceded by acute induction of microglia-driven inflammatory processes in the medial prefrontal cortex. Systemic IL-1RA administration may represent a promising therapeutic opportunity to prevent long-term cognitive impairments caused by perinatal asphyxia.
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