Pathogenesis of Alcohol-Exacerbated Malaria in Plasmodium berghei-Infected Mice

Malaria is still a pressing global health challenge, especially in sub-Saharan Africa, where behavioural factors such as alcohol consumption may exacerbate its impact. The present study is aimed at investigating the pathogenesis of alcohol-exacerbated malaria in Plasmodium berghei-infected an animal model (mice). Mice were separated into four treatment groups: control, alcohol control, P. berghei and P. berghei plus acute alcohol treatment groups. Animals were infected with malaria through intraperitoneal injection of P. berghei and an acute dose of ethanol (20% v/v, oral) was introduced 48 h post-infection. Parasitaemia was monitored using the Giemsa-stained thin blood smears. Haematological parameters were assessed using an automated blood analyser. Liver function was evaluated by measuring serum levels of AST and ALT; oxidative stress biomarkers (MDA, SOD, CAT, GSH) were evaluated, and cytokine profiles (TNF-α, IFN-γ, IL-6, IL-1β) were quantified using ELISA kits. Results show that acute alcohol intake led to a significant increase in parasitaemia in the P. berghei group (p < 0.01). Haematological analysis revealed a significant (p < 0.001) reduction in RBC count, haemoglobin levels, haematocrit percentage, platelet count and others in the P. berghei plus acute alcohol treatment group. Liver enzyme assays revealed elevated AST and ALT levels (p < 0.001) in the P. berghei group, due to acute alcohol. Cytokine analysis revealed a significant (p < 0.01) upregulation of pro-inflammatory cytokines (TNF-α, IFN-γ, IL-1β and IL-6), due to acute alcohol. Oxidative stress was significantly (p < 0.001) increased, evidenced by significant elevation of MDA and significant depletions in GSH, SOD and CAT, due to acute alcohol. These results suggest that alcohol exacerbates malaria pathogenesis by increasing parasitaemia, promoting immune dysregulation, liver injury and oxidative stress, in a murine model.