CETP deficiency slows parasite egg development, a possible reason it persists at high frequency across East Asia (Biochem Biophys Res Commun 2001)

Original title: Cholesteryl ester transfer protein deficiency causes slow egg embryonation of Schistosoma japonicum

Biochem Biophys Res Commun · 17 August 2001 · 6

Okumura-Noji K, Sasai K, Zhan R, Kawaguchi H, Maruyama H, Tada T, Takahashi H, Okazaki M, Miida T, Sakuma N, Kimura G, Ohta N et al.

Investigating a potential cause for the geographic accumulation of CETP deficiency in Eastern Asia, this study examined its association with Schistosoma japonicum, a regionally endemic parasite. Eggs of S. japonicum showed slow embryonation when cultured in CETP-deficient human plasma; restoring CETP to deficient plasma rescued normal embryonation, while inhibiting CETP in normal plasma did not slow embryonation. Egg embryonation was also retarded in the liver, but not the intestine, of wild-type mice compared to CETP-transgenic mice, and liver granulomatous lesions around parasite eggs were less severe in wild-type than CETP-transgenic mice. The authors conclude CETP deficiency may protect against Schistosomiasis japonica by retarding egg embryonation and consequent liver granulomatosis, an effect not directly attributable to the lack of plasma CETP activity itself but to abnormal lipoproteins arising from chronic CETP deficiency.

Original abstract

In our attempt to discover a potential cause for accumulation of cholesteryl ester transfer protein (CETP) deficiency in Eastern Asia, we studied the association of CETP deficiency with pathogenesis of Schistosoma japonicum, a life-threatening parasite peculiar to this region. The eggs of S. japonicum showed slow embryonation when cultured in CETP-deficient human plasma. Restoration of CETP to the deficient plasma rescued it, while inhibition of CETP in normal plasma did not cause slow embryonation of the cultured eggs. The egg embryonation was also retarded in the liver but not in the intestine of wild-type mice in comparison to the CETP-transgenic mice. The granulomatous lesion around the parasite eggs in the liver was less in the wild-type than in the CETP-transgenic mice. Thus, CETP deficiency may act against Schistosomiasis japonica by retarding egg embryonation, a potential cause of liver granulomatosis. It does not seem directly due to the lack of CETP activity in plasma but to abnormal lipoprotein generated by chronic CETP deficiency.

Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.