Malaria Immunopathology

Plasmodium is the causative agent of malaria, the
most deadly parasitic infection worldwide.
Pathogenesis of the disease involves an exacerbated
immunological response; however, the role of
parasite components remains largely unexplored. The
current study was designed to assess the
contribution of hemozoin (HZ), a metabolic product
of Plasmodium, to the inflammatory events
associated to malaria. HZ was found to induce
various macrophage functions (e.g. chemokine and
nitric oxide production) through specific signaling
pathways. Importantly, the proinflammatory activity
of HZ was demonstrated in vivo (e.g. leukocytosis,
chemokine and cytokine release) using a murine
model. These findings support the idea that HZ
participates in inflammatory mediator overproduction
during malaria and therefore, it could be a key
component in the development of the disease. HZ
might emerge as an attractive target to design new
therapeutic approaches against malaria to prevent
millions of deaths. This book should be especially
useful to graduate students and researchers
interested in understanding the molecular and
cellular basis of malaria pathogenesis.

Autorentext

She obtained her MSc and PhD degrees in Microbiology and Immunology from Université Laval. Her main interest is to unravel the molecular mechanisms that regulate the immune response to parasitic infections, more specifically malaria and leishmaniasis. Currently, she conducts her postdoctoral research at McGill University.

Klappentext

Plasmodium is the causative agent of malaria, the most deadly parasitic infection worldwide. Pathogenesis of the disease involves an exacerbated immunological response; however, the role of parasite components remains largely unexplored. The current study was designed to assess the contribution of hemozoin (HZ), a metabolic product of Plasmodium, to the inflammatory events associated to malaria. HZ was found to induce various macrophage functions (e.g. chemokine and nitric oxide production) through specific signaling pathways. Importantly, the proinflammatory activity of HZ was demonstrated in vivo (e.g. leukocytosis,chemokine and cytokine release) using a murine model. These findings support the idea that HZ participates in inflammatory mediator overproduction during malaria and therefore, it could be a key component in the development of the disease. HZ might emerge as an attractive target to design new therapeutic approaches against malaria to prevent millions of deaths. This book should be especially useful to graduate students and researchers interested in understanding the molecular and cellular basis of malaria pathogenesis.