| First Author | Seki T | Year | 2018 |
| Journal | Parasitol Int | Volume | 67 |
| Issue | 1 | Pages | 64-69 |
| PubMed ID | 28359899 | Mgi Jnum | J:271735 |
| Mgi Id | MGI:6282128 | Doi | 10.1016/j.parint.2017.03.008 |
| Citation | Seki T, et al. (2018) IL-33/ST2 contributes to severe symptoms in Plasmodium chabaudi-infected BALB/c mice. Parasitol Int 67(1):64-69 |
| abstractText | It has been reported that IL-33 contributes to potentiation of Th2 inflammatory diseases and protection against helminth infection. Increased plasma IL-33 levels have been observed in patients with severe falciparum malaria, however, the role of IL-33 in malaria remains unclear. Here we report that IL-33 enhances inflammatory responses in malaria infection. ST2-deficiency altered severity of inflammation in the liver and serum levels of pro-inflammatory cytokines such as TNF-alpha and IL-6, and IL-13 that is a Th2 cytokine during Plasmodium chabaudi infection. IL-13-deficient mice have similar phenotype with ST2-deficient mice during P. chabaudi infection. Furthermore, ST2- and IL-13-deficiency reduced mortality from P. chabaudi infection. These results indicate that IL-33/ST2 can induce production of proinflammatory cytokines, such as TNF-alpha and IL-6, through production of IL-13 in P. chabaudi-infected BALB/c mice, suggesting that IL-33/ST2 play a critical role in inflammatory responses to malaria infection. Thus, these findings may define a novel therapeutic target for patients with severe malaria. |
