[[[ Background: ]]] Inflammatory cytokines play a crucial role in the human immune response to infection by malaria. During the initial sporozoite infection of the liver the presence of Interleukin-6 (IL-6) can be determinant. IL-6 controls systemic iron homeostasis through hepcidin, which is produced mainly by hepatocytes. An elevated basal hepcidin level in the liver can be induced by chronic inflammatory disease. Hepcidin is also a peptide with antimicrobial properties. [[[ Presentation of the hypothesis: ]]] We hypothesize that elevated basal hepcidin levels in the liver inhibit the development of malaria infection. When hepcidin is abundant, hepatocytes sequester iron, and this inhibits sporozoite development in liver-stage malaria infection. [[[ Testing the hypothesis: ]]] The validity of our hypothesis can be proven by observing sporozoite growth in hepcidin-treated hepatocytes, or in hepatocytes, stimulated with IL-6 to increase hepcidin levels before incubation with malaria sporozoites and observing the effect the hepcidin knockout function has on the infection. [[[ Implications of the hypothesis: ]]] Confirmation of our hypothesis could help to understand the complexity of the malaria infection.
Elevated basal hepcidin levels in the liver may inhibit the development of malaria infection: Another piece towards solving the malaria puzzle?
간에서의 상승된 기초 헤프시딘 수치는 말라리아 감염의 발전을 억제할 수 있다: 말라리아 퍼즐을 푸는 또 다른 단서?
[Category] 말라리아,
[Article Type] journal-article
[Source] pubmed
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