Main Article Content

Voon Kin Chin Wing Chui Chong Norshariza Nordin Tze Yan Lee Zakaria Zainul Amiruddin Haniza Hassan rusliza basir


The balance between Th1 and Th2 cytokines during malaria infection strongly influences the consequences of the infection. Excessive release of Th1 cytokines have been linked to severe immunopathological conditions in human while Th2 cytokines were associated with parasitic clearance. The involvement of cytokine cascade in the immunopathogenesis of malaria infection has been widely studied, however, their specific association in terms of survival and severe infection remains obscure. Therefore, in this study, we investigated the cytokine profiles and histopathological features of malaria in the survival and severe model of the infection as an attempt to further understand the disease pathogenesis in these stages. The survival model showed mild parasitaemia development with full recovery by day 14 of infection, whereas the severe model exhibited high parasitaemia with 100% mortality after peak parasitaemia. Both severe and survival models showed almost similar levels of histopathological severity during peak parasitaemia. Meanwhile, the severe model produced highly elevated levels of pro-inflammatory cytokines, TNF-α and IL-1α, but low level of the anti-inflammatory cytokine, IL-4 as compared to the survival model which showed low levels of TNF-α and IL-1α IL-1, but high level of IL-4. We postulate that the survival model survived malaria infection by producing a predominant Th2-type immune response during peak parasitaemia despite the severe pathological conditions during the infection. Furthermore, the severe pathological condition during malaria may not be directly associated with the high levels of pro-inflammatory cytokines like TNF-α and IL-1α.


Download data is not yet available.

Article Details

How to Cite
CHIN, Voon Kin et al. COMPARISON OF PATHOGENESIS OF P. BERGHEI INFECTION IN MOUSE AND RAT MODELS. Journal of Health and Translational Medicine, [S.l.], v. 22, n. 2, p. 4-12, nov. 2019. ISSN 2289-392X. Available at: <>. Date accessed: 14 dec. 2019.

Most read articles by the same author(s)