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Wu R, Lemne C, de Faire U, et al. Antibodies to Lysophosphatidylcholine Are Decreased in Borderline Hypertension. Hypertension. 2001;37(1):154-159doi: 10.1161/01.hyp.37.1.154.
Wu, R., Lemne, C., de Faire, U., & Frostegård, J. (2001). Antibodies to Lysophosphatidylcholine Are Decreased in Borderline Hypertension. Hypertension (Dallas, Tex. : 1979), 37(1), 154-159. https://doi.org/10.1161/01.hyp.37.1.154
Wu, Ruihua, et al. "Antibodies to Lysophosphatidylcholine Are Decreased in Borderline Hypertension." Hypertension (Dallas, Tex. : 1979) vol. 37,1 (2001): 154-159. doi: https://doi.org/10.1161/01.hyp.37.1.154
Wu R, Lemne C, de Faire U, Frostegård J. Antibodies to Lysophosphatidylcholine Are Decreased in Borderline Hypertension. Hypertension. 2001 Jan;37(1):154-159. doi: 10.1161/01.hyp.37.1.154. PMID: 11208771.
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Hypertension. 2001 Jan;37(1):154-159. doi: 10.1161/01.hyp.37.1.154.

Antibodies to Lysophosphatidylcholine Are Decreased in Borderline Hypertension.

Hypertension (Dallas, Tex. : 1979)

Ruihua Wu, Carola Lemne, Ulf de Faire, Johan Frostegård

Affiliations

  1. Department of Medicine (R.W., J.F.), Unit of Rheumatology, and CMM, Karolinska Hospital.

PMID: 11208771 DOI: 10.1161/01.hyp.37.1.154

Abstract

-Atherosclerosis is characterized by infiltration in the lesions of cytokine-producing T cells and macrophages, where oxidized LDL may play an important role. However, little is known about the role of the immune system in the development of hypertension. Lysophosphatidylcholine (LPC) is formed by phospholipase A(2)-induced hydrolysis and/or by oxidation of LDL and other phospholipid-containing membranes. The objective of the present study was to investigate the role of antibodies to LPC in borderline hypertension (BHT). Seventy-five men with BHT were compared with 75 age-matched normotensive (NT) men (diastolic blood pressure 85 to 94 and <80 mm Hg, respectively). Antibody levels to LPC of IgM and IgG isotypes and IgG subclasses were determined with ELISAs. BHT men had significantly lower anti-LPC antibody levels of both IgG class (P:=0.0002) and IgM class (P:=0.0003) than did NT controls. Subclass analysis indicated that IgG(1) (P:=0.0005), but not IgG(2), was decreased. Anti-LPC antibodies or immunoglobulin subclasses thereof were negatively associated with atherosclerosis on the basis of intima-media thickness (P:=0.02), metabolic factors (P:=0.02), smoking (P:=0.02), and endothelin (P:=0.03). LPC has proinflammatory properties and is toxic at higher concentrations and thus may play a role in atherogenesis. Furthermore, LPC functions as a vasoconstrictor in experimental systems by inhibiting NO-mediated vasorelaxation. An intriguing possibility is that anti-LPC antibodies counteract these effects. Taken together, our data indicate that anti-LPC antibodies may constitute a novel factor in the development of hypertension and atherosclerosis.

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