title: Modulation of interleukin-18 release produced positive outcomes on parasitaemia development and cytokines production during malaria in mice.
abstract: The involvement of interleukin-18 (IL-18) and the effects of modulating its release   on the course of malaria infection were investigated using Plasmodium berghei ANKA infection   in ICR mice as a model. Results demonstrated that plasma IL-18 concentrations in malarial   mice were significantly elevated and positively correlated with the percentage parasitaemia   development. Significant expressions of IL-18 were also observed in the brain, spleen and   liver tissues. Slower development of parasitaemia was observed significantly upon inhibition   and neutralization of IL-18, whereas faster development of parasitaemia was recorded when   the circulating levels of IL-18 were further augmented during the infection. Inhibition and   neutralization of IL-18 production also resulted in a significant decrease of plasma   concentrations of pro-inflammatory cytokines (TNFα, IFNγ, IL-1α and IL-6), whereas the   anti-inflammatory cytokine, IL-10, was significantly increased. Augmenting the release of IL-   18 during the infection on the other hand resulted in the opposite. Early mortality in malarial   mice was also observed when the circulating levels of IL-18 were further augmented. Results   proved the important role of IL-18 in immune response against malaria and suggest that IL-8   is pro-inflammatory in nature and may involve in mediating the severity of the infection   through a pathway of elevating the pro-inflammatory cytokine and limiting the release of   anti-inflammatory cytokine.
authors.affiliation: Department of Human Anatomy, Faculty of Medicine & Health Sciences, Universiti Putra Malaysia, 43400 Serdang, Selangor, Malaysia. rusliza@medic.upm.edu.my
authors.forename: R
authors.initials: R
authors.lastname: Basir
authors.forename: K
authors.initials: K
authors.lastname: Hasballah
authors.forename: M
authors.initials: M
authors.lastname: Jabbarzare
authors.forename: L H
authors.initials: LH
authors.lastname: Gam
authors.forename: A M
authors.initials: AM
authors.lastname: Abdul Majid
authors.forename: M F
authors.initials: MF
authors.lastname: Yam
authors.forename: M A M
authors.initials: MA
authors.lastname: Moklas
authors.forename: F
authors.initials: F
authors.lastname: Othman
authors.forename: M T
authors.initials: MT
authors.lastname: Che Norma
authors.forename: A
authors.initials: A
authors.lastname: Zalinah
authors.forename: R
authors.initials: R
authors.lastname: Mahmud
authors.forename: W O
authors.initials: WO
authors.lastname: Abdullah
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D001921:Brain / Q000276:immunology; D016207:Cytokines / Q000032:analysis / Q000097:blood / Q000378:metabolism*; D005786:Gene Expression Regulation; D020382:Interleukin-18 / Q000032:analysis / Q000378:metabolism* / Q000627:therapeutic use; D008099:Liver / Q000276:immunology; D008288:Malaria / Q000188:drug therapy / Q000276:immunology* / Q000401:mortality; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D018512:Parasitemia / Q000188:drug therapy / Q000276:immunology / Q000401:mortality; D010962:Plasmodium berghei / Q000187:drug effects / Q000254:growth & development / Q000276:immunology*; D011994:Recombinant Proteins; D013154:Spleen / Q000276:immunology
chemical_list: D000911:Antibodies, Monoclonal; D016207:Cytokines; D020382:Interleukin-18; D011994:Recombinant Proteins