Abstract
BackgroundPlasmodium and Schistosoma are two of the most common parasites in sub-tropical areas. Deregulation of the immune response to Plasmodium falciparum, characterized by a Th1 response, leads to cerebral malaria (CM), while a Th2 response accompanies chronic schistosomiasis.MethodsThe development of CM was examined in mice with concomitant Schistosoma mansoni and Plasmodium berghei ANKA infections. The effect of S. mansoni egg antigen injection on disease development and survival was also determined. Cytokine serum levels were estimated using ELISA. Statistical analysis was performed using t-test.ResultsThe results demonstrate that concomitant S. mansoni and P. berghei ANKA infection leads to a reduction in CM. This effect is dependent on infection schedule and infecting cercariae number, and is correlated with a Th2 response. Schistosomal egg antigen injection delays the death of Plasmodium-infected mice, indicating immune involvement.ConclusionsThis research supports previous claims of a protective effect of helminth infection on CM development. The presence of multiple parasitic infections in patients from endemic areas should therefore be carefully noted in clinical trials, and in the development of standard treatment protocols for malaria. Defined helminth antigens may be considered for alleviation of immunopathological symptoms.
Highlights
Plasmodium and Schistosoma are two of the most common parasites in tropical areas
The results demonstrate that IPSE/alpha-1 has a role in changing the course of malaria infection, leading to increased survival, and that a shift in cytokine expression is associated with cerebral malaria (CM) reduction
Mice were divided into four groups, two of which were infected with P. berghei four or seven weeks after injection of 100 S. mansoni cercariae
Summary
Deregulation of the immune response to Plasmodium falciparum, characterized by a Th1 response, leads to cerebral malaria (CM), while a Th2 response accompanies chronic schistosomiasis. An infectious disease caused by the Plasmodium parasite, is a source of enormous morbidity and mortality. Cerebral malaria (CM), seen in about 7% of Plasmodium falciparum malaria cases, is characterized by the presence of neurological features, especially impaired consciousness [1]. Parasite-triggered cerebral inflammation is a possible cause of death from CM [2]. The immune response is critical in determining the outcome of infection [2]. CM is characterized by a Th1 response, with overproduction of some cytokines (e.g. interferon-g, IFNg), combined with underproduction of others (e.g. interleukin-10, IL-10) [3]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
