Chronic stress primes innate immune responses in mice and humans

Barrett, Tessa; Corr, Emma M.; Solingen, Coen van; Schlamp, Florencia; Brown, Emily J.; Koelwyn, Graeme J.; Lee, Angela H.; Shanley, Lianne C.; Spruill, Tanya M.; Bozal, Fazli K.; Jong, Annika de; Newman, Alexandra A C; Drenkova, Kamelia; Silvestro, Michele; Ramkhelawon, Bhama; Reynolds, Harmony R.; Hochman, Judith S.; Nahrendorf, Matthias; Świrski, Filip K.; Fisher, Edward A.; Moore, Kathryn J

doi:10.1016/j.celrep.2021.109595

Cited by 80 publications

(48 citation statements)

References 62 publications

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“…Psychological stress and depression have also been shown to induces remodeling of the chromatin landscape, which affects gene expression (62,63). Additionally, transgenerational epigenetic reprogramming has been associated with in utero and parental stress (reviewed in ( 64)) suggesting a repeating or even perpetual mechanism for maintaining health disparities in a variety of disease states in marginalized or oppressed communities.…”

Section: Discussionmentioning

confidence: 99%

Transcriptome and DNA methylome analyses reveal underlying mechanisms for the racial disparity in uterine fibroids

Paul¹,

Grey²,

Carpenter³

et al. 2022

JCI Insight

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Uterine fibroids (leiomyomas) affect Black women disproportionately in terms of prevalence, incidence, and severity of symptoms. The causes of this racial disparity are essentially unknown. We hypothesized that myometria of Black women are more susceptible to developing fibroids and examined the transcriptomic and DNA methylation profiles of myometria and fibroids from Black and White women for comparison.Myometrial samples cluster by race in both their transcriptome and DNA methylation profiles, whereas fibroid samples only cluster by race in the latter. More differentially expressed genes (DEGs) were detected in the Black and White myometrial sample comparison than in the fibroid comparison. Leiomyoma gene set expression analysis identified four clusters of DEGs, including a cluster of 24 genes with higher expression in myometrial samples from Black women. One of the DEGs in this group, VWF, was significantly hypomethylated at two CpG probes that are near a putative enhancer site in myometrial samples from Black women and in all fibroids and that correlate with VWF expression levels. These results suggest that the molecular basis for the disparity in fibroid disease between Black and White women could be found in the myometria before fibroid development and not in the fibroids themselves.

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Section: Discussionmentioning

confidence: 99%

Transcriptome and DNA methylome analyses reveal underlying mechanisms for the racial disparity in uterine fibroids

Paul¹,

Grey²,

Carpenter³

et al. 2022

JCI Insight

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“…And are there limits on the trigger or secondary stimulus? Some studies now suggest even non-immune stimuli can induce innate immune memory, including psychosocial stress, diet, and the gut microbiome [ 152 , 153 ]. In addition, not many stressors have been studied as a second hit, with most studies using LPS as the immune challenge to define immune memory, but some other potential secondary stressors include neurodegeneration [ 134 , 136 ] and pathogens [ 154 , 155 ].…”

Section: Microglia Innate Immune Memorymentioning

confidence: 99%

Developmental Stressors Induce Innate Immune Memory in Microglia and Contribute to Disease Risk

Carloni

Ramos

Hayes

2021

IJMS

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Many types of stressors have an impact on brain development, function, and disease susceptibility including immune stressors, psychosocial stressors, and exposure to drugs of abuse. We propose that these diverse developmental stressors may utilize a common mechanism that underlies impaired cognitive function and neurodevelopmental disorders such as schizophrenia, autism, and mood disorders that can develop in later life as a result of developmental stressors. While these stressors are directed at critical developmental windows, their impacts are long-lasting. Immune activation is a shared pathophysiology across several different developmental stressors and may thus be a targetable treatment to mitigate the later behavioral deficits. In this review, we explore different types of prenatal and perinatal stressors and their contribution to disease risk and underlying molecular mechanisms. We highlight the impact of developmental stressors on microglia biology because of their early infiltration into the brain, their critical role in brain development and function, and their long-lived status in the brain throughout life. Furthermore, we introduce innate immune memory as a potential underlying mechanism for developmental stressors’ impact on disease. Finally, we highlight the molecular and epigenetic reprogramming that is known to underlie innate immune memory and explain how similar molecular mechanisms may be at work for cells to retain a long-term perturbation after exposure to developmental stressors.

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“…However, it is still unclear whether it is possible to reduce the promoting effect of chronic stress on atherosclerosis by targeted inhibition of cellular inflammatory factors. For inflammatory cells, chronic stress can cause bone marrow cells to enter a highly reactive inflammatory state, cause leukocyte proliferation, and increase the number of circulating inflammatory monocytes [ 30 , 31 ]. In addition, inflammatory cells and inflammatory cytokines are not isolated from each other.…”

Section: Introductionmentioning

confidence: 99%

Recent Progress of Chronic Stress in the Development of Atherosclerosis

Gao

Wang

Meng

et al. 2022

Oxidative Medicine and Cellular Longevity

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With the development of the times, cardiovascular diseases have become the biggest cause of death in the global aging society, causing a serious social burden. Atherosclerosis is a chronic inflammatory disease, which can occur in large and medium-sized blood vessels in the whole body. It takes atherosclerotic plaque as the typical pathological change and endothelial injury as the core pathophysiological mechanism. It is the pathological basis of coronary heart disease, peripheral artery disease, cerebrovascular disease, and other diseases. Recent studies have shown that chronic stress plays an important role in the occurrence and development of atherosclerosis, endothelial injury, lipid metabolism, and chronic inflammation. This process involves a large number of molecular targets. It is usually the cause of atherosclerotic cardiovascular and cerebrovascular diseases. If chronic stress factors exist for a long time, patients have genetic susceptibility, and the combination of environmental factors triggers the pathogenesis, which may eventually lead to complete blockage of the blood vessels, unstable rupture of plaques, and serious adverse cardiovascular events. This paper reviews the role of chronic stress in the occurrence and development of atherosclerosis, focusing on the pathophysiological mechanism.

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Chronic stress primes innate immune responses in mice and humans

Cited by 80 publications

References 62 publications

Transcriptome and DNA methylome analyses reveal underlying mechanisms for the racial disparity in uterine fibroids

Transcriptome and DNA methylome analyses reveal underlying mechanisms for the racial disparity in uterine fibroids

Developmental Stressors Induce Innate Immune Memory in Microglia and Contribute to Disease Risk

Recent Progress of Chronic Stress in the Development of Atherosclerosis

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