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Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone [ATAC-seq]

ABSTRACT: Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone [ATAC-seq]

PROVIDER: PRJNA564138 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10075880_1.fastq.gz	Fastqsanger.gz
	SRR10075880_2.fastq.gz	Fastqsanger.gz
	SRR10075881_1.fastq.gz	Fastqsanger.gz
	SRR10075881_2.fastq.gz	Fastqsanger.gz
	SRR10075882_1.fastq.gz	Fastqsanger.gz

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Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone [ATAC-seq]

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 | GSE136972 | GEO

Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone [RNA-seq]

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Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone

Project description:Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone

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Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone [RNA-seq]

Project description:Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone [RNA-seq]

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Long-term programming of CD8 T cell immunity by perinatal exposure to stress hormone

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-01-01 | GSE136980 | GEO

Long-Term Programming of CD8 T Cell Immunity by Perinatal Exposure to Glucocorticoids.

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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Prenatal inflammation remodels lung immunity and function by programming ILC2 hyperactivation

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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Gestational diabetes augments group B Streptococcus perinatal infection through disruptions in maternal immunity and the vaginal microbiota

Project description:Group B Streptococcus (GBS) is a pervasive perinatal pathogen, yet factors driving GBS dissemination in utero are poorly defined. Gestational diabetes mellitus (GDM), a complication marked by dysregulated immunity and maternal microbial dysbiosis, increases risk for GBS perinatal disease. We interrogated host-pathogen dynamics in a novel murine GDM model of GBS colonization and perinatal transmission. GDM mice had greater GBS in utero dissemination and subsequently worse neonatal outcomes. Dual-RNA sequencing revealed differential GBS adaptation to the GDM reproductive tract, including a putative glycosyltransferase (yfhO), and altered host responses. GDM disruption of immunity included reduced uterine natural killer cell activation, impaired recruitment to placentae, and altered vaginal cytokines. Lastly, we observed distinct vaginal microbial taxa associated with GDM status and GBS invasive disease status. Our translational model of GBS perinatal transmission in GDM hosts recapitulates several clinical aspects and enables discovery of host and bacterial drivers of GBS perinatal disease.

2023-07-05 | GSE236335 | GEO

Intrahepatic microbes govern liver immunity by programming NKT cells

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Consequences of perinatal bisphenol A exposure in a mouse model of multiple sclerosis

Project description:Multiple sclerosis (MS) is a complex disease influenced by genetic and environmental contributing factors. Endocrine disrupting compounds (EDCs) such as bisphenol A (BPA) affect gene expression and hormone-regulated systems throughout the body. We investigated the effects of BPA on Theiler’s-virus induced demyelination (TVID), a mouse model of MS. Perinatal BPA exposure, combined with viral infection, resulted in a decreased level of viral antibodies, accelerated the onset of TVID symptoms, increased inflammation in both the spinal cord and digestive tract, and amplified immune-related gene expression changes induced by viral infection. These results demonstrate the effect of BPA on the trajectory of TVID, and illustrate how multiple factors collectively influence autoimmune disease. For microarray: 7 samples

2013-08-01 | E-GEOD-46551 | biostudies-arrayexpress

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