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Lifestyle effects on hematopoiesis and atherosclerosis

Matthias Nahrendorf1, Filip K Swirski1

  • 1From the Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston. mnahrendorf@mgh.harvard.edu fswirski@mgh.harvard.edu.

Circulation Research
|February 28, 2015
PubMed

Insights

Lifestyle factors like diet and stress impact chronic inflammatory diseases by altering immune cell production. This study explores how these factors influence hematopoietic processes, potentially affecting atherosclerosis risk.

Area of Science:

  • Cardiovascular Science
  • Immunology
  • Hematology

Background:

  • Chronic inflammatory diseases, such as atherosclerosis, are influenced by lifestyle factors including diet, exercise, stress, and sleep.
  • Psychosocial stress and poor diet exacerbate cardiovascular disease, while exercise and good sleep habits are protective.
  • The role of inflammation-associated leukocyte production in mediating lifestyle effects on atherosclerosis is under investigation.

Purpose of the Study:

  • To investigate how lifestyle factors influence the molecular and cellular mechanisms of hematopoiesis.
  • To explore the hypothesis that lifestyle can alter hematopoietic topography, shifting immune cell production.
  • To understand the impact of these changes on the macrophage supply chain and atherosclerosis progression.

Main Methods:

  • The study focuses on exploring the mechanistic links between lifestyle modifiers and hematopoiesis.
  • It examines how external factors influence progenitor-extrinsic and intrinsic communication nodes.
  • The research investigates neuroimmune and immunometabolic axes in relation to immune cell production.

Main Results:

  • Lifestyle factors may rearrange hematopoietic topography, diverting immune cell production from bone marrow to periphery.
  • This shift can lead to quantitative and qualitative changes in the macrophage supply chain.
  • Altered macrophage number and phenotype in lesions are potential consequences.

Conclusions:

  • Inflammation-associated leukocyte production is proposed as a key mediator of lifestyle effects on atherosclerosis.
  • Future therapeutics could target the hematopoietic tree's output and location to mitigate atherosclerosis risk.
  • Public health policies should consider these lifestyle-hematopoiesis interactions.

Keywords:
atherosclerosisbone marrowcell proliferationdiethematopoiesismacrophagesmonocytespsychosocial, stresssleepspleen

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