| First Author | de Menezes MN | Year | 2019 |
| Journal | Sci Rep | Volume | 9 |
| Issue | 1 | Pages | 7575 |
| PubMed ID | 31110285 | Mgi Jnum | J:281288 |
| Mgi Id | MGI:6357300 | Doi | 10.1038/s41598-019-44125-2 |
| Citation | de Menezes MN, et al. (2019) IL-1alpha promotes liver inflammation and necrosis during blood-stage Plasmodium chabaudi malaria. Sci Rep 9(1):7575 |
| abstractText | Malaria causes hepatic inflammation and damage, which contribute to disease severity. The pro-inflammatory cytokine interleukin (IL)-1alpha is released by non-hematopoietic or hematopoietic cells during liver injury. This study established the role of IL-1alpha 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-1alpha production. Systemically, IL-1alpha deficiency attenuated weight loss and hypothermia but had minor effects on parasitemia control. In the liver, the absence of IL-1alpha reduced the number of TUNEL(+) cells and necrotic lesions. This finding was associated with a lower inflammatory response, including TNF-alpha production. The main source of IL-1alpha in the liver of infected mice was inflammatory cells, particularly neutrophils. The implication of IL-1alpha 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. |
