Toxoplasmosis and Risk of Endothelial Dysfunction: Role of Oxidative Stress and Pro-Inflammatory Mediators

Infection with Toxoplasma gondii (T. gondii) leads to activation of T-helper cells (Th-1 and Th-2) which are involved in the synthesis and release of different cytokines which may lead to endothelial dysfunction.

To evaluate the endothelial function in patients with acute toxoplasmosis.

This case-control study involved 31 patients with toxoplasmosis aged 19 - 47 years matched with 20 healthy subjects. Anti-T. gondii antibody (IgG, IgM, IgA) was determined by direct antigen-antibody reaction. Interleukin-6(IL-6), endothelin-1 (ET-1) and human malondialdehyde (MDA) serum levels were measured.

IgM, IgG and IgA levels were high in the infected patients compared with controls (P < 0.01). Furthermore, IL-6 serum level was high in the infected patients compared with controls (P < 0.01). In addition, ET-1 level was high in acute toxoplasmosis (7.29 ± 4.59 pg/mL) compared with controls (3.11 ± 1.69 pg/mL) (P < 0.01). In addition, MDA serum level was high (9.34 ± 4.17 nmol/mL) compared with controls (2.87 ± 1.13 nmol/mL), (P < 0.01). In acute toxoplasmosis IgM serum level was significantly correlated with IgG (r = 0.55, P = 0.001), IgA (r = 0.57, P = 0.0008), IL-6 (r = 0.45, P = 0.01), ET-1 (r = 0.51, P = 0.003) and MDA (r = 0.85, P = 0.0001).

Acute toxoplasmosis is associated with significant oxidative stress and pro-inflammatory changes which contribute to development of endothelial dysfunction.