Experimental erythrocytic malaria infection induces elevated serum amyloid P production in mice.

Experimental blood-stage malaria infection of NIH mice was observed to induce an acute phase response (APR). Infection of mice with either P. chabaudi, P. vinckei (both non-lethal) or P. berghei (lethal infection) resulted in elevated serum amyloid P (SAP) production, the major acute phase protein in mice. Peak production occurred at the peak of the parasitaemia (approximately day 10 post infection). SAP isolated from the serum of P. chabaudi infected mice was shown to inhibit the growth of intra-erythrocytic malaria parasites in vitro. Furthermore, isolated SAP suppressed the proliferative response of splenocytes taken from a naïve mouse to concanavalin A. To assess if SAP had a protective role in vivo during experimental blood-stage infection, IL-6 deficient mice, which have a significantly reduced APR, were infected with P. chabaudi. A significant extension to the primary parasitaemia was observed in IL-6 deficient mice compared to infected wild type mice. These observations demonstrate that blood-stage malaria infection induces a systemic APR and that this may contribute to the immune response to infection in an anti-parasitic or immunomodulatory manner.