Human and mouse leukocytes: different clockwork

Méndez-Ferrer, Simón

doi:10.1182/blood-2017-09-805374

Cited by 3 publications

(4 citation statements)

References 10 publications

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“…A converse result was found in humans, with an overexpression in men [35] . This contradiction is due to an inversion of circadian rhythm between mice and humans in relation with the timing of activity [36] . Fourthly, for safety reasons, most clinical trials exclude women who may become pregnant.…”

Section: Challenge Of Translating Animal Models Into Clinical Findingmentioning

confidence: 99%

Sex and bacterial infectious diseases

Mège

Bretelle

Léone

2018

New Microbes and New Infections

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Most infectious diseases are unequally distributed between male and female subjects. This sex dimorphism is confirmed by epidemiologic studies which suggest an increased number of male septic patients, while, due to the class age of septic patients, an overrepresentation of female patients would be expected. Lifestyle, recreational activities, professional exposition and access to care are plausible reasons for this dimorphism. However, biological differences should be carefully considered, particularly the weight of X-linked variability and the role of sex hormones. Animal models clearly show that clinical response to infection is more exuberant in males than in females. This is partly explained by an attenuation of the inflammatory response by female sex hormones. However, the translation from experimental studies to the bedside remains challenging as a result of confounding factors like age, hormone changes and response to treatment.

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Section: Challenge Of Translating Animal Models Into Clinical Findingmentioning

confidence: 99%

Sex and bacterial infectious diseases

Mège

Bretelle

Léone

2018

New Microbes and New Infections

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“…The Lapidot group confirmed these initial findings in humans using immature CD34+ cells (51). It is important to note that human and mouse hematopoietic cells appear to have a different clockwork, since inverted oscillations of circulating leukocytes have been described in immunodeficient mice carrying human and mouse leukocytes (52). Interspecies differences of stress-kinase regulation of reactive oxygen species (ROS), hypoxia-inducible factor 1α (HIF-1α) and clock genedependent regulation of the CXCL12 receptor CXCR4 appear to explain the opposite migratory patterns for human and mouse leukocytes (23).…”

Section: Neural Regulation Of Circadian Hsc Proliferationmentioning

confidence: 81%

“…Since neural signals are subjected to circadian fluctuations in the healthy/homeostatic BM, the disruption of neural circadian regulation might also contribute to disease/aging development, and thus represent a niche-related target for chronotherapies. In general, chronotherapy approaches in cancer have proven much more difficult than expected probably due to the interplay of different clocks and multiple entrainment signals in humans as a cause of notorious heterogeneity (52). It is important to note that the clock genes comprise only one of several cellular clocks.…”

Section: A Biological Meaning For Circadian Hsc Regulationmentioning

confidence: 99%

The Autonomic Nervous System Pulls the Strings to Coordinate Circadian HSC Functions

García‐García

Méndez-Ferrer

2020

Front. Immunol.

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As for many other adult stem cells, the behavior of hematopoietic stem and progenitor cells (HSPCs) is subjected to circadian regulatory patterns. Multiple HSPC functions, such as proliferation, differentiation or trafficking exhibit time-dependent patterns that require a tight coordination to ensure daily blood cell production. The autonomic nervous system, together with circulating hormones, relay circadian signals from the central clock-the suprachiasmatic nucleus in the brain-to synchronize HSC niche physiology according to light/darkness cycles. Research over the last 20 years has revealed how specific neural signals modulate certain aspects of circadian HSC biology. However, only recently some studies have started to decipher the cellular and molecular mechanisms that orchestrate this complex regulation in a time-dependent fashion. Here we firstly review some of the recent key findings illustrating how different neural signals (catecholaminergic or cholinergic) regulate circadian HSC egress, homing, maintenance, proliferation, and differentiation. In particular, we highlight the critical role of different neurotransmitter receptors in the bone marrow microenvironment to channel these neural signals and regulate antagonistic processes according to circadian cues and organismal demands. Then, we discuss the potential biological meaning of HSC circadian regulation and its possible utility for clinical purposes. Finally, we offer our perspective on emerging concepts in HSC chronobiology.

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“…As mice are nocturnal and humans are active during the day, release of mature human leukocytes from the BM of immune deficient chimeric mice occurred at a different time compared with mouse leukocyte release, because of interspecies differences in ROS and CXCR4 regulation [91,92]. Importantly, melatonin injection in the morning to immune deficient chimeric mice preengrafted with human stem and progenitor cells induced elevation of human LT-HSC surface markers similar to mouse HSPCs.…”

mentioning

confidence: 99%

Daily light and darkness onset and circadian rhythms metabolically synchronize hematopoietic stem cell differentiation and maintenance: The role of bone marrow norepinephrine, tumor necrosis factor, and melatonin cycles

Golan

Markus

Lapidot

2019

Experimental Hematology

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Hematopoietic stem and progenitor cells (HSPCs) are essential for daily mature blood cell production, host immunity, and osteoclast-mediated bone turnover. The timing at which stem cells give rise to mature blood and immune cells while maintaining the bone marrow (BM) reservoir of undifferentiated HSPCs and how these opposite tasks are synchronized are poorly understood. Previous studies revealed that daily light onset activates norepinephrine (NE)-induced BM CXCL12 downregulation, followed by CXCR4 + HSPC release to the circulation. Recently, we reported that daily light onset induces transient elevations of BM NE and tumor necrosis factor (TNF), which metabolically program BM HSPC differentiation and recruitment to replenish the blood. In contrast, darkness onset induces lower elevations of BM NE and TNF, activating melatonin production, which metabolically reprograms HSPCs, increasing their short-and long-term repopulation potential, and BM maintenance. How the functions of BMretained HSPCs are influenced by daily light and darkness cycles and their clinical potential are further discussed.

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Human and mouse leukocytes: different clockwork

Cited by 3 publications

References 10 publications

Sex and bacterial infectious diseases

Sex and bacterial infectious diseases

The Autonomic Nervous System Pulls the Strings to Coordinate Circadian HSC Functions

Daily light and darkness onset and circadian rhythms metabolically synchronize hematopoietic stem cell differentiation and maintenance: The role of bone marrow norepinephrine, tumor necrosis factor, and melatonin cycles

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