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IL-1? promotes liver inflammation and necrosis during blood-stage Plasmodium chabaudi malaria.


ABSTRACT: Malaria causes hepatic inflammation and damage, which contribute to disease severity. The pro-inflammatory cytokine interleukin (IL)-1? is released by non-hematopoietic or hematopoietic cells during liver injury. This study established the role of IL-1? in the liver pathology caused by blood-stage P. chabaudi malaria. During acute infection, hepatic inflammation and necrosis were accompanied by NLRP3 inflammasome-independent IL-1? production. Systemically, IL-1? deficiency attenuated weight loss and hypothermia but had minor effects on parasitemia control. In the liver, the absence of IL-1? reduced the number of TUNEL+ cells and necrotic lesions. This finding was associated with a lower inflammatory response, including TNF-? production. The main source of IL-1? in the liver of infected mice was inflammatory cells, particularly neutrophils. The implication of IL-1? in liver inflammation and necrosis caused by P. chabaudi infection, as well as in weight loss and hypothermia, opens up new perspectives for improving malaria outcomes by inhibiting IL-1 signaling.

SUBMITTER: de Menezes MN 

PROVIDER: S-EPMC6527574 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature

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