Hypertension and endothelial dysfunction in the pristane model of systemic lupus erythematosus

Daniel M McClung1, William J Kalusche1, Katie E Jones1

  • 1Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA.

Physiological Reports
|February 2, 2021
PubMed

Insights

Systemic lupus erythematosus (SLE) in mice induced hypertension and vascular dysfunction. Immune system changes in this lupus model contribute to these cardiovascular issues, highlighting a link between autoimmune disease and blood vessel health.

Area of Science:

  • Immunology
  • Cardiovascular Science
  • Autoimmune Disease Research

Background:

  • Systemic lupus erythematosus (SLE) is an autoimmune disorder affecting women of childbearing age.
  • SLE is characterized by loss of self-tolerance, autoreactive lymphocytes, and autoantibody production.
  • High rates of hypertension and cardiovascular disease are observed in patients with autoimmune diseases like SLE.

Purpose of the Study:

  • To investigate if the pristane-inducible model of SLE develops hypertension and vascular dysfunction.
  • To explore the relationship between immune system dysregulation and cardiovascular complications in SLE.

Main Methods:

  • Female C57BL/6 mice were administered either PBS or pristane to induce an SLE-like condition.
  • Autoantibody production, hypergammaglobulinemia, and immune cell populations were analyzed.
  • Mean arterial pressure (MAP) and mesenteric artery relaxation responses were measured.

Main Results:

  • Pristane-treated mice developed autoantibodies (anti-dsDNA, anti-ssDNA, anti-nRNP IgG) and hypergammaglobulinemia.
  • Elevated circulating neutrophils and CD4-CD8- thymocytes were observed in pristane-treated mice.
  • Pristane-treated mice exhibited elevated MAP and impaired vascular relaxation to acetylcholine.

Conclusions:

  • The pristane-inducible model of SLE successfully recapitulates key features of the disease, including hypertension and vascular dysfunction.
  • Immune system dysregulation in this lupus model is linked to the development of cardiovascular complications.
  • These findings suggest a significant role for immune dysfunction in driving hypertension and vascular disease in SLE.

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