Journal
CIRCULATION RESEARCH
Volume 117, Issue 10, Pages 858-869Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCRESAHA.115.306539
Keywords
hypertension; inflammation; leukocytes; reactive oxygen species; T-lymphocytes
Funding
- National Institutes of Health (NIH): National Research Service Award [T32DK007770]
- American Heart Association [13BGIA14680069, 11SDG6770006]
- UCLA CTSI [UT1TR000124]
- NIH [HL110353, HL105294, HL039006, P01 HL58000]
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Rationale: Chronic inflammation is a major contributor to the progressive pathology of hypertension, and T-cell activation is required for the genesis of hypertension. However, the precise role of myeloid cells in this process is unclear. Objective: To characterize and understand the role of peripheral myeloid cells in the development of hypertension. Methods and Results: We examined myeloid cells in the periphery of hypertensive mice and found that increased numbers of CD11b(+)Gr1(+) myeloid cells in blood and the spleen are a characteristic of 3 murine models of experimental hypertension (angiotensin II, L-NG-nitroarginine methyl ester, and high salt). These cells express surface markers and transcription factors associated with immaturity and immunosuppression. Also, they produce hydrogen peroxide to suppress T-cell activation. These are characteristics of myeloid-derived suppressor cells (MDSCs). Depletion of hypertensive MDSCs increased blood pressure and renal inflammation. In contrast, adoptive transfer of wild-type MDSCs to hypertensive mice reduced blood pressure, whereas the transfer of nicotinamide adenine dinucleotide phosphate oxidase 2-deficient MDSCs did not. Conclusion: The accumulation of MDSCs is a characteristic of experimental models of hypertension. MDSCs limit inflammation and the increase of blood pressure through the production of hydrogen peroxide.
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