Cyclophosphamide treatment for hypertension and renal injury in an experimental model of systemic lupus erythematosus

Physiol Rep. 2019 May;7(10):e14059. doi: 10.14814/phy2.14059.

Abstract

Cardiovascular disease is the major cause of mortality among patients with the autoimmune disorder systemic lupus erythematosus (SLE). Our laboratory previously reported that immunosuppression with mycophenolate mofetil, a common therapy in patients with SLE, attenuates the development of hypertension in an experimental model of SLE. Cyclophosphamide (CYC) is another common therapy for patients with SLE that has contributed to improved disease management; however, its impact on the development of hypertension associated with SLE is not clear. We tested whether treatment with CYC (25 mg/kg, once/week, IP injection) for 4 weeks would attenuate hypertension in an established female mouse model of SLE with hypertension (30-week-old NZBWF1 females). Plasma anti-dsDNA IgG levels, pathogenic for the disease, were lower in CYC-treated SLE mice compared to vehicle-treated SLE mice, suggesting efficacy of the therapy to suppress aberrant immune system function. Mean arterial pressure (MAP) was assessed by carotid artery catheters in conscious mice. Treatment did not attenuate the development of hypertension when compared to vehicle-treated SLE mice; however, urinary albumin excretion was lower in CYC-treated animals. Corresponding with the reduction in autoantibodies, data suggest that CYC treatment lowered circulating CD45R+ B cells. Paradoxically, circulating CD11b+ Ly6G+ neutrophils were increased in CYC-treated SLE mice compared to vehicle treated. Estrus cycling data also suggest that CYC treatment had an impact on ovarian function that may be consistent with reduced circulating estrogen levels. Taken together, these data suggest that CYC treatment attenuates autoantibody production and renal disease during SLE, but that the potential to affect MAP may be blunted by the increase in circulating neutrophils and CYC's impact on ovarian function.

Keywords: Autoimmunity; hypertension; immunosuppression; sex hormones.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Antibodies, Antinuclear / blood
  • Antigens, Ly / blood
  • Arterial Pressure / drug effects*
  • Autoimmunity / drug effects*
  • B-Lymphocytes / drug effects
  • B-Lymphocytes / immunology
  • B-Lymphocytes / metabolism
  • Biomarkers / blood
  • CD11b Antigen / blood
  • Cyclophosphamide / pharmacology*
  • Disease Models, Animal
  • Estrogens / blood
  • Estrus / drug effects
  • Female
  • Hypertension / blood
  • Hypertension / immunology
  • Hypertension / physiopathology
  • Hypertension / prevention & control*
  • Immunosuppressive Agents / pharmacology*
  • Kidney / drug effects*
  • Kidney / immunology
  • Kidney / metabolism
  • Kidney / physiopathology
  • Leukocyte Common Antigens / blood
  • Lupus Erythematosus, Systemic / blood
  • Lupus Erythematosus, Systemic / drug therapy*
  • Lupus Erythematosus, Systemic / immunology
  • Lupus Erythematosus, Systemic / physiopathology
  • Lupus Nephritis / blood
  • Lupus Nephritis / immunology
  • Lupus Nephritis / physiopathology
  • Lupus Nephritis / prevention & control*
  • Mice, Inbred NZB
  • Neutrophils / drug effects
  • Neutrophils / immunology
  • Neutrophils / metabolism
  • Ovary / drug effects*
  • Ovary / immunology
  • Ovary / metabolism
  • Ovary / physiopathology

Substances

  • Antibodies, Antinuclear
  • Antigens, Ly
  • Biomarkers
  • CD11b Antigen
  • Estrogens
  • Immunosuppressive Agents
  • Ly6G antigen, mouse
  • Cyclophosphamide
  • Leukocyte Common Antigens