Senior Honors Projects, 2010-current

Date of Award

Spring 2016

Document Type

Dissertation/Thesis

Degree Name

Bachelor of Science (BS)

Department

Department of Biology

Advisor(s)

Chris Lantz

Abstract

Malaria is a mosquito-borne infection caused by the parasitic protozoan Plasmodium. This disease infects over 200-300 million people and causes nearly 400,000 deaths every year. Our laboratory previously examined malarial infection caused by Plasmodium berghei NK65, a lethal rodent strain that induces symptoms similar to those observed in humans. The results of this previous study indicated that the hematopoietic growth factor and immunoregulatory cytokine interleukin-3 (IL-3) suppressed protective immunity against infection with P. berghei NK65. However, the extent to which IL-3 contributes to host defense against blood-stage malaria infection caused by other Plasmodium species remains to be determined. In the present study, we have examined the roles of IL-3 in host defense against blood-stage malaria by using IL-3-deficient or “knockout” (KO) mice infected with either nonlethal P. yoelii 17XNL or lethal P. yoelii YM parasites. Survival and parasitemia were measured to monitor the course of infection in wild-type (WT) and IL-3 KO mice. We also characterized parameters indicative of a protective immunity, such as the development of splenomegaly and parasitized red blood cell (pRBC) levels. Surprisingly, we found that IL-3 did not significantly alter the normal clinical course of infection caused by these two Plasmodium strains. These studies indicate that the ability of IL-3 to influence blood-stage malaria infection is dependent on the particular Plasmodium species used to infect animals. These studies also suggest that Plasmodium species may differ in their ability to stimulate IL-3 production and/or differ in their ability to induce a type of host immune response that is IL-3 dependent.

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