title: IL-33/ST2 contributes to severe symptoms in Plasmodium chabaudi-infected BALB/c mice.
abstract: 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-α 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-α 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.
authors.affiliation: Department of Environmental Parasitology, Tokyo Medical and Dental University, Tokyo, Japan.
authors.forename: Takenori
authors.initials: T
authors.lastname: Seki
authors.affiliation: Department of Environmental Parasitology, Tokyo Medical and Dental University, Tokyo, Japan; Department of Immune Regulation, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
authors.forename: Kazushige
authors.initials: K
authors.lastname: Obata-Ninomiya
authors.affiliation: Department of Environmental Parasitology, Tokyo Medical and Dental University, Tokyo, Japan.
authors.forename: Rieko
authors.initials: R
authors.lastname: Shimogawara-Furushima
authors.affiliation: Department of Environmental Parasitology, Tokyo Medical and Dental University, Tokyo, Japan.
authors.forename: Toshio
authors.initials: T
authors.lastname: Arai
authors.affiliation: Department of Environmental Parasitology, Tokyo Medical and Dental University, Tokyo, Japan.
authors.forename: Nobuaki
authors.initials: N
authors.lastname: Akao
authors.affiliation: Division of Respirology, Neurology, and Rheumatology, Department of Medicine 1, Kurume University School of Medicine, Fukuoka, Japan.
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Hoshino
authors.affiliation: Department of Environmental Parasitology, Tokyo Medical and Dental University, Tokyo, Japan. Electronic address: matata.vip@tmd.ac.jp.
authors.forename: Nobuo
authors.initials: N
authors.lastname: Ohta
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D000072179:Interleukin-1 Receptor-Like 1 Protein / Q000235:genetics* / Q000378:metabolism; D000067596:Interleukin-33 / Q000235:genetics* / Q000378:metabolism; D008288:Malaria / Q000235:genetics / Q000276:immunology* / Q000469:parasitology; D051379:Mice; D008807:Mice, Inbred BALB C; D016788:Plasmodium chabaudi / Q000502:physiology
chemical_list: C486189:Il1rl1 protein, mouse; C506535:Il33 protein, mouse; D000072179:Interleukin-1 Receptor-Like 1 Protein; D000067596:Interleukin-33
keywords: IL-33; Malaria; Parasitic disease; Proinflammatory cytokines