ArticleThe American journal of tropical medicine and hygiene2010
Divergent roles of IRAK4-mediated innate immune responses in two experimental models of severe malaria.
Article in The American journal of tropical medicine and hygiene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 10 citations in OpenAlex.
- Genetic analysis of cerebral malaria in the mouse model infected with Plasmodium berghei.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- IRAK Inhibitor Protects the Intestinal Tract of Necrotizing Enterocolitis by Inhibiting the Toll-Like Receptor (TLR) Inflammatory Signaling Pathway in Rats.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Opsonization of malaria-infected erythrocytes activates the inflammasome and enhances inflammatory cytokine secretion by human macrophages.Malaria journal · 2012Article
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Severe malaria represents a clinical spectrum of disease. We propose that innate immune inflammatory responses to malaria play key roles in the pathogenesis and clinical outcomes of distinct severe malaria syndromes. To investigate this hypothesis, mice deficient in IRAK4, central to Toll-like receptor (TLR)-mediated signaling, were studied in two experimental models of malaria: Plasmodium berghei (PbA) and Plasmodium chabaudi (PccAS). Irak4(-/-)mice had decreased pro-inflammatory cytokine production during infection in both models. However, animals were relatively protected from PbA-associated symptoms compared with wild-type mice, whereas Irak4(-/-) animals were more susceptible to PccAS-associated disease. These results show that IRAK4-mediated innate immune inflammatory responses play critical roles in divergent clinical outcomes in murine malaria models. As such, integrated approaches, using more than one model, are required to fully understand the parasite/host interactions that characterize severe malaria, and more importantly, to fully assess the effect of adjunctive therapies targeting innate immune responses to malaria.
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