Chronic variable stress activates hematopoietic stem cells
Open accessAbstract
Exposure to psychosocial stress is a risk factor for many diseases, including atherosclerosis. Although incompletely understood, interaction between the psyche and the immune system provides one potential mechanism linking stress and disease inception and progression. Known cross-talk between the brain and immune system includes the hypothalamic-pituitary-adrenal axis, which centrally drives glucocorticoid production in the adrenal cortex, and the sympathetic-adrenal-medullary axis, which controls stress-induced catecholamine release in support of the fight-or-flight reflex. It remains unknown, however, whether chronic stress changes hematopoietic stem cell activity. Here we show that stress increases proliferation of these most primitive hematopoietic progenitors, giving rise to higher levels of disease-promoting inflammatory leukocytes. We found that chronic stress induced monocytosis and neutrophilia in humans. While investigating the source of leukocytosis in mice, we discovered that stress activates upstream hematopoietic stem cells. Under conditions of chronic variable stress in mice, sympathetic nerve fibers released surplus noradrenaline, which signaled bone marrow niche cells to decrease CXCL12 levels through the β3-adrenergic receptor. Consequently, hematopoietic stem cell proliferation was elevated, leading to an increased output of neutrophils and inflammatory monocytes. When atherosclerosis-prone Apoe(-/-) mice were subjected to chronic stress, accelerated hematopoiesis promoted plaque features associated with vulnerable lesions that cause myocardial infarction and stroke in humans.
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Mice exposed to CVS or CSDS show expansion of myeloid progenitor cells and reduced lymphoid progenitors.
“Specifically, mice exposed to either CVS or CSDS exhibit an expansion of myeloid progenitor cells, along with a downregulation of lymphoid progenitors33,59.”
From Central regulation of stress-evoked peripheral immune responses (2023) · cites this paper as [33]
The passage labeled Abstract (page unavailable) reports higher bone-marrow numbers of both myeloid progenitors and common lymphoid progenitors after chronic variable stress, contrary to the claimed reduction in lymphoid progenitors. This paper’s reported mouse experiment used chronic variable stressors; the cited passages do not establish the CSDS portion of the claim. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredStress changes blood cell formation so that monocytes and neutrophils increase, lymphocytes decrease, and pro-inflammatory activity rises in peripheral immune tissues.
“Recent studies have reported stress-induced alterations in hematopoiesis that result in monocytosis, neutrophilia and lymphocytopenia and, consequently, upregulation of pro-inflammatory processes in immunologically-relevant peripheral tissues.”
From Central regulation of stress-evoked peripheral immune responses (2023) · cites this paper as [33]
The paper reports stress-induced increases in monocytes and neutrophils and, in stressed mice, increased inflammation in atherosclerotic plaques (sections labeled Abstract; page unavailable). It does not support lymphocytopenia: the ICU residents had higher, not lower, blood lymphocyte counts during the stressful rotation. The peripheral-tissue finding is specifically from plaques in atherosclerosis-prone mice, not peripheral immune tissues generally. (LLM, conf=0.90)
Experimental — accuracy not yet measuredMDD in humans and chronic stress in rodents are linked to monocytosis, neutrophilia and lymphocytopenia, which may result from altered HSC subpopulation proliferation or leukocyte mobilization from bone marrow.
“MDD in humans and chronic stress in rodents are associated with monocytosis, neutrophilia and lymphocytopenia, which can be attributed to altered proliferation of hematopoietic stem cell (HSC) subpopulations or mobilization of leukocytes from the bone marrow33,56–58.”
From Central regulation of stress-evoked peripheral immune responses (2023) · cites this paper as [33]
The paper reports monocytosis and neutrophilia in stressed ICU residents and mice, and increased HSC proliferation in stressed mice (Abstract; page not provided). It does not study humans with MDD or establish HSC activity in humans. The lymphocytopenia claim conflicts with its report of increased lymphocytes in the stressed residents; the authors also favor increased leukocyte production over short-term mobilization as the explanation for their human observations. (LLM, conf=0.88)
Experimental — accuracy not yet measuredAnimals exposed to chronic stress are more prone to develop inflammatory conditions such as experimental autoimmune encephalitis, colitis, atherosclerosis and diabetes.
“Moreover, animals that are exposed to chronic stress are predisposed to the development of inflammatory conditions, such as experimental autoimmune encephalitis, colitis, atherosclerosis and diabetes31–34.”
From Central regulation of stress-evoked peripheral immune responses (2023) · cites this paper as [33]
The paper reports that chronic stress increased plaque inflammation in atherosclerosis-prone mice (Abstract; page not provided), supporting the atherosclerosis example. Its discussion of broader implications does not report that stressed animals are more prone to experimental autoimmune encephalitis, colitis, or diabetes. (LLM, conf=0.88)
Experimental — accuracy not yet measuredNoradrenaline released by sympathetic fibres in the bone marrow niche suppresses CXCL12 expression.
“Mechanistically, it has been shown that signaling by noradrenaline released by these sympathetic fibres within the bone marrow niche suppresses expression of CXCL1233”
From Central regulation of stress-evoked peripheral immune responses (2023) · cites this paper as [33]
Chronic variable stress activates hematopoietic stem cells (HSCs), driving sustained myelopoiesis and enhanced release of inflammatory monocytes into circulation.
“Heidt et al. demonstrated that chronic variable stress activates hematopoietic stem cells (HSCs), driving sustained myelopoiesis and enhanced release of inflammatory monocytes into circulation [80].”
From Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation (2025) · cites this paper as [80]
Chronic stress mobilizes the innate immune system and stimulates enhanced proliferation and release of inflammatory monocytes and neutrophils into the bloodstream.
“Chronic stress mobilizes the innate immune system and stimulates enhanced proliferation and release of inflammatory monocytes and neutrophils into the bloodstream12, 13.”
From Social stress induces neurovascular pathology promoting depression (2017) · cites this paper as [13]
NE decreases the inhibitory chemokine CXCL12, and stress-induced hematopoietic stem cell differentiation is associated with decreased CXCL12 expression in the BM.
“One such way that leukocytes are stimulated by NE is by decreasing the inhibitory chemokine CXCL12 (Katayama et al, 2006;Heidt et al, 2014).”
From Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal (2017) · cites this paper as Heidt et al, 2014
The myelopoietic response of RSD is mediated by NE.
“Further investigation revealed that the myelopoietic response of RSD is mediated by NE (Wohleb et al, 2011;Hanke et al, 2012;Heidt et al, 2014).”
From Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal (2017) · cites this paper as Heidt et al, 2014
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- Authors
- Heidt, T., Sager, H. B., Courties, G., Dutta, P., Iwamoto, Y., Zaltsman, A., von zur Muhlen, C., Bode, C., Fricchione, G. L., Denninger, J., Lin, C. P., Vinegoni, C., Libby, P., Swirski, F. K., Weissleder, R., & Nahrendorf, M.
- Affiliations
- Harvard University (US)
- University of Freiburg (DE)
- Massachusetts General Hospital (US)
- Brigham and Women's Hospital (US)
- Corresponding author
- Nahrendorf, Matthias
- ORCID
- Venue
- Nature Medicine
- Published
- 2014-06-22
- Volume
- 20
- Issue
- 7
- Pages
- 754-758
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC4087061
- OpenAlex
- W2152934881
- Cited by
- 803
- References
- 52
- Citations by year
- 2026: 72 · 2025: 84 · 2024: 74 · 2023: 67 · 2022: 68 · 2021: 72 · 2020: 82 · 2019: 59 · 2018: 59 · 2017: 52 · 2016: 48 · 2015: 55 · 2014: 10
- FWCI
- 38.99
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- National Heart, Lung, and Blood Institute (R01HL117829, HHSN268201000044C, R01HL114477, R01HL096576, K99HL121076)
- Topics
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
- Keywords
- chronic variable stress, hematopoietic stem cells, psychosocial stress, atherosclerosis, leukocytosis, neutrophilia, monocytosis, sympathetic nervous system, norepinephrine, beta3-adrenergic receptor, CXCL12, bone marrow microenvironment, inflammatory monocytes, ApoE-deficient mice, stress-immune interaction
- MeSH terms
- Animals, Disease Susceptibility, Hematopoietic Stem Cells, Humans, Stress, Psychological, Cell Proliferation, Mice, Chemokine CXCL12
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