Atherosclerosis and the role of immune cells

Ilhan, Fulya; Kalkanlı, Sevgi

doi:10.12998/wjcc.v3.i4.345

Cited by 110 publications

(83 citation statements)

References 107 publications

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“…In conclusion, this is the first study, to our knowledge, demonstrating that night shift leads to the disruption of rhythmic circadian immune functions in humans. We already know that some medical conditions reported in shift workers (e.g., autoimmune diseases, obesity, atherosclerosis) are related to alterations in immune functions (64,65). The present study reveals the possibility that some of these alterations are associated with or result from a dysregulation of immune clocks and other clocks that are part of the circadian system.…”

Section: Discussionmentioning

confidence: 54%

Simulated Night Shift Disrupts Circadian Rhythms of Immune Functions in Humans

Cuesta

Boudreau

Dubeau-Laramée

et al. 2016

The Journal of Immunology

112

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Recent research unveiled a circadian regulation of the immune system in rodents, yet little is known about rhythms of immune functions in humans and how they are affected by circadian disruption. In this study, we assessed rhythms of cytokine secretion by immune cells and tested their response to simulated night shifts. PBMCs were collected from nine participants kept in constant posture over 24 h under a day-oriented schedule (baseline) and after 3 d under a night-oriented schedule. Monocytes and T lymphocytes were stimulated with LPS and PHA, respectively. At baseline, a bimodal rhythmic secretion was detected for IL-1β, IL-6, and TNF-α: a night peak was primarily due to a higher responsiveness of monocytes, and a day peak was partly due to a higher proportion of monocytes. A rhythmic release was also observed for IL-2 and IFN-γ, with a nighttime peak due to a higher cell count and responsiveness of T lymphocytes. Following night shifts, with the exception of IL-2, cytokine secretion was still rhythmic but with peak levels phase advanced by 4.5–6 h, whereas the rhythm in monocyte and T lymphocyte numbers was not shifted. This suggests distinct mechanisms of regulation between responsiveness to stimuli and cell numbers of the human immune system. Under a night-oriented schedule, only cytokine release was partly shifted in response to the change in the sleep–wake cycle. This led to a desynchronization of rhythmic immune parameters, which might contribute to the increased risk for infection, autoimmune diseases, cardiovascular and metabolic disorders, and cancer reported in shift workers.

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Section: Discussionmentioning

confidence: 54%

Simulated Night Shift Disrupts Circadian Rhythms of Immune Functions in Humans

Cuesta

Boudreau

Dubeau-Laramée

et al. 2016

The Journal of Immunology

112

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“…Atherosclerosis is a disease of major arteries in which high levels of low-density lipoprotein bearing oxidative modifications accumulate in vessel walls, attracting phagocytic immune cells to form plaques 110,111 . Cardiovascular disease as a result of atherosclerosis is the primary cause of mortality in the Western world and is on the rise globally 112 .…”

Section: Senescence In Age-related Diseasementioning

confidence: 99%

Cellular senescence in aging and age-related disease: from mechanisms to therapy

Childs

Durik

Baker

et al. 2015

Nat Med

1,750

1,489

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Cellular senescence, a process that imposes permanent proliferative arrest on cells in response to various stressors, has emerged as a potentially important contributor to aging and age-related disease, and it is an attractive target for therapeutic exploitation. A wealth of information about senescence in cultured cells has been acquired over the past half century; however, senescence in living organisms is poorly understood, largely because of technical limitations relating to the identification and characterization of senescent cells in tissues and organs. Furthermore, newly recognized beneficial signaling functions of senescence suggest that indiscriminately targeting senescent cells or modulating their secretome for anti-aging therapy may have negative consequences. Here we discuss current progress and challenges in understanding the stressors that induce senescence in vivo, the cell types that are prone to senesce, and the autocrine and paracrine properties of senescent cells in the contexts of aging and age-related diseases as well as disease therapy.

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“…The combined up‐regulation of ICAM‐1 and CCL2 help initiate the formation of atherosclerotic plaques by inducing the migration and adhesion of monocytes to the subendothelial space. There in the intima, the monocytes scavenge oxidized lipid particles, transform into foam cells, and secrete inflammatory cytokines and proteases, such as matrix metalloprotease, contributing to the activation of endothelial cells and the progression of atherosclerosis (10). Once activated, endothelial cells can also secrete proinflammatory cytokines, such as IL‐1β and −6, further fueling the atherosclerotic process (11, 12).…”

mentioning

confidence: 99%

Monocyte exosomes induce adhesion molecules and cytokinesviaactivation of NF‐κB in endothelial cells

Tang¹,

Sun²,

et al. 2016

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HIV-infected individuals have activated monocytes with an IFNα phenotype and elevated levels of circulating LPS. These individuals also have a risk of premature cardiovascular disease. The effect of activated monocyte exosomes (Exos) on endothelial cells is unknown. To determine whether Exos from immune-activated monocytes could alter endothelial cell expression and contribute to monocyte/macrophage transmigration and adhesion, we isolated Exos from monocytes stimulated with IFNα, LPS, or both (I/L). We show that monocyte Exos contain different inflammatory microRNA cargo depending on stimulation. When LPS Exos or I/L Exos were added to HUVECs, we found a significant increase in adhesion molecule ICAM-1, chemokine ligand (CCL)-2, and cytokine IL-6 mRNAs and proteins compared with cells treated with IFNα Exos or Exos derived from unstimulated monocytes. Inhibition of transcription factor NF-κB, a common inflammatory cytokine pathway, prevented induction of CCL2, IL6, and ICAM1 Inhibition of TLR4 resulted in differential blockage of the targets. Our results demonstrate for the first time that primary human monocyte Exos enter endothelial cells and cause dysfunction via the TLR4 and NF-κB pathways, which may contribute to heart disease in HIV infection and other diseases involving chronic immune activation.-Tang, N., Sun, B., Gupta, A., Rempel, H., Pulliam, L. Monocyte exosomes induce adhesion molecules and cytokines via activation of NF-κB in endothelial cells.

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Atherosclerosis and the role of immune cells

Cited by 110 publications

References 107 publications

Simulated Night Shift Disrupts Circadian Rhythms of Immune Functions in Humans

Simulated Night Shift Disrupts Circadian Rhythms of Immune Functions in Humans

Cellular senescence in aging and age-related disease: from mechanisms to therapy

Monocyte exosomes induce adhesion molecules and cytokinesviaactivation of NF‐κB in endothelial cells

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