Immune training in aged microglia [ChIP-seq]
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ABSTRACT:
PROVIDER: PRJNA957806 | ENA |
REPOSITORIES: ENA
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Project description:Acute cognitive impairment (i.e., delirium) is common in elderly emergency department patients and frequently results from infections that are unrelated to the central nervous system. Since activation of the peripheral innate immune system induces brain microglia to produce inflammatory cytokines that are responsible for behavioral deficits, we investigated if aging exacerbated neuroinflammation and sickness behavior after peripheral injection of lipopolysaccharide (LPS). Microarray analysis revealed a transcriptional profile indicating the presence of primed or activated microglia and increased inflammation in the aged brain. Furthermore, aged mice had a unique gene expression profile in the brain after an intraperitoneal injection of LPS, and the LPS-induced elevation in the brain inflammatory cytokines and oxidative stress was both exaggerated and prolonged compared with adults. Aged mice were anorectic longer and lost more weight than adults after peripheral LPS administration. Moreover, reductions in both locomotor and social behavior remained 24 h later in aged mice, when adults had fully recovered, and the exaggerated neuroinflammatory response in aged mice was not reliably paralleled by increased circulating cytokines in the periphery. Taken together these data establish that activation of the peripheral innate immune system leads to exacerbated neuroinflammation in the aged as compared with adult mice. This dysregulated link between the peripheral and central innate immune system is likely to be involved in the severe behavioral deficits that frequently occur in older adults with systemic infections. Experiment Overall Design: In this study, adult and aged mice were injected intraperitoneal with sterile saline or Escherichia coli LPS (0.33 mg/kg, ~10 µg/mouse; serotype 0127:B8, Sigma). This dosage of LPS was used because it induces a mild transient sickness behavior in young adults. Mice were killed 4 h after saline or LPS injection by CO2 asphyxiation. Blood samples were collected and brains were removed, separated in half at the longitudinal fissure, frozen in liquid nitrogen, and stored (-80°C) until assaying. Total RNA was later isolated from some brain samples for microarray analysis (n=3).
2007-09-07 | E-GEOD-3253 | biostudies-arrayexpress
Project description:Immune cells, the most core part of the immune system of the whole body, could rapidly response to the change of environment. Its roles in tissue homeostasis and disease were fairly clear except brain, an immune privilege site. Previous studies had revealed the contribution of microglia, a tissue-resident macrophage, for brain development and neuronal disease. But it was currently unknown whether the other subtypes of immune cells and which of the microglia populations program their function during different stages of development. Here, we analyzed the genes expression pattern of 26,456 immune cells from the whole zebrafish brain during adult and aged stage. Our analysis uncovered the present of lymphocyte in zebrafish brain, and gradually accumulated with aging. In addition, the number of microglia were reduced bute the diversity were increased in aged brain. Collectively, our data provide insights into zebrafish brain immune cells populations that explain the distinct composition of immune cells in adult and aged brain, which might contribute to understanding the roles of immune cells in aging-associated-disease.
2023-01-12 | GSE197673 | GEO
Project description:Age-dependent alterations in microglia behavior have been implicated in neurodegeneration and CNS injuries. Here, we compared the transcriptional profiles of young versus aged microglia during stroke recovery. CD45intermediateCD11b+ microglia were FACS-isolated from the brains of young (10-week-old) and aged (18-month-old) male mice 14 days after distal middle cerebral artery occlusion (dMCAO) or sham operation and subjected to RNA-sequencing analysis. Functional groups enriched in young microglia are indicative of upregulation in cell movement, cell interactions, inflammatory responses and angiogenesis, while aged microglia exhibited a reduction or no change in these features. We confirmed reduced chemoattractive capacities of aged microglia toward ischemic brain tissue in organotypic slide co-cultures, and delayed accumulation of aged microglia around dead neurons injected into the striatum in vivo. In addition, aging is associated with an overall failure to increase the expression of microglial genes involved in cell-cell interactions, such as CXCL10. Finally, impaired upregulation of pro-angiogenic genes in aged microglia was associated with a decline in neovascularization in aged mice compared to young mice after dMCAO. This study provides a new resource to understand the mechanisms underlying microglial alterations in the aged brain milieu and sheds light on new strategies to improve microglial functions in aged stroke victims.
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Project description:Microglia are important immune cells in the brain. Microglia undergo a series of alterations during aging and increase the susceptibility to brain dysfunctions. However, the characteristics of microglia during the aging process are not fully understood. In this study, we mapped transcriptional and epigenetic profiles of microglia from 3- to 24-month-old mice. We observed unexpected gender divergences and identified age-dependent microglia (ADEM) genes in the aging process. We then compared characteristics between microglial aging and activation. To dissect the function of aged microglia excluding the influence from other aged brain cells, we established an accelerated microglial turnover model without directly affecting other brain cells. By this model, we achieved aged microglia in non-aged brains and confirmed that aged microglia per se contribute to cognitive decline. Collectively, we provide a comprehensive resource to decode the aging process of microglia, shedding light on how microglia maintain brain functions.
2023-07-25 | GSE207948 | GEO
Project description:Microglia are important immune cells in the brain. Microglia undergo a series of alterations during aging and increase the susceptibility to brain dysfunctions. However, the characteristics of microglia during the aging process are not fully understood. In this study, we mapped transcriptional and epigenetic profiles of microglia from 3- to 24-month-old mice. We observed unexpected gender divergences and identified age-dependent microglia (ADEM) genes in the aging process. We then compared characteristics between microglial aging and activation. To dissect the function of aged microglia excluding the influence from other aged brain cells, we established an accelerated microglial turnover model without directly affecting other brain cells. By this model, we achieved aged microglia in non-aged brains and confirmed that aged microglia per se contribute to cognitive decline. Collectively, we provide a comprehensive resource to decode the aging process of microglia, shedding light on how microglia maintain brain functions.
2023-07-25 | GSE208386 | GEO
Project description:The role of IL-5 in brain neuroimmunity remains unknown. We investigated the role of IL-5 in cognitive function in aged mice. We examined the transcriptomes of sorted microglia and brain T cells from aged mice treated with PBS or IL-5.
2020-01-21 | GSE129999 | GEO
Project description:Background: Inhalation anesthetics may trigger the hypothalamic–pituitary–adrenal (HPA) axis. FK-506 binding protein (FKBP5) is a critical factor that regulates the HPA axis and is associated with perioperative neurocognitive impairment. However, it is unclear how inhalation anesthetics affects the expression of FKBP5 in different neural cells in the brain. Methods: We used single-nucleus RNA sequencing to characterize hippocampal transcriptome profiles in the brains of aged marmosets and mice after sevoflurane anesthesia. Results: Higher levels of FKBP5 were found in the hippocampi of aged mice after sevoflurane anesthesia. Single nuclear RNA sequencing results from aged mice and marmosets showed that the increased expression of FKBP5 mainly occurred in microglia. The expression of FKBP5 in the hippocampi of aged marmosets and mice increased following long-term exposure to sevoflurane anesthesia. Additionally, the brains of these animals displayed a marked increase in the expression of FKBP5 in microglia after sevoflurane anesthesia. Conclusion: Long-term exposure to sevoflurane augments FKBP5 expression in the hippocampi of aged marmosets and mice, specifically in the microglia.
2024-10-30 | GSE234493 | GEO
Project description:Senescence-associated alterations in microglia may have profound impact on cerebral homeostasis and stroke outcomes. However, the lack of a transcriptome-wide comparison between young and aged microglia in the context of ischemia limits our understanding of aging-related mechanisms. Herein, we performed bulk RNA sequencing analysis of microglia purified from cerebral hemispheres of young adult (10-week-old) and aged (18-month-old) mice 5 days after distal middle cerebral artery occlusion or sham operation. Considerable transcriptional differences were observed between young and aged microglia in healthy brains, indicating heightened chronic inflammation in aged microglia. Following stroke, the overall transcriptional activation was more robust in young microglia than in aged microglia. Gene clusters with functional implications in immune inflammatory responses, immune cell chemotaxis, tissue remodeling, and cell-cell interactions were markedly activated in microglia of young but not aged stroke mice. These alterations in microglial gene response may contribute to aging-driven vulnerability and poorer recovery after ischemic stroke.
2020-05-31 | GSE145265 | GEO