Toxoplasma gondii infection remains a significant global health concern, promoting the urgent need
for effective therapeutic strategies. This study aimed to evaluate the therapeutic potential of chitosan
nanoparticles (CSNPs) and curcumin-loaded chitosan nanoparticles (Cur-CSNPs) against the chronic
Toxoplasma gondii (ME49 strain) in an experimental mouse model. This achieved by investigating
their ability to reduce parasitic load, oxidative stress, histopathological lesion, and to enhance the
host immune response. Sixty female BALB/c mice were divided into five groups: infected untreated
group, Spiramycin®-treated group, CSNPs-treated group, Cur-CSNPs-treated group, and negative
control group. The Cur-CSNPs-treated group exhibited the lowest brain cyst counts, along with
significant reductions in cyst size. Hematological indices revealed no significant reduction in total
white blood cell (WBC) counts or in the percentage of neutrophils, monocytes, and eosinophils in
both the CSNPs and Cur-CSNPs treated groups, compared to the infected untreated group and
Spiramycin-treated group. However, both nanoparticle-treated groups exhibited a significant decrease
in the percentage of lymphocytes compared to the infected untreated group. Significant differences
in total antioxidant capacity (TAC) and malondialdehyde (MDA) levels were observed, with the
Cur-CSNPs treated group displaying values comparable to the negative control. Histopathological
examination revealed substantial improvements in the brain, liver, and spleen tissues of Cur-CSNPstreated
animals, characterized by preserved tissue architecture and reduced inflammatory lesions.
Immunohistochemical analysis further revealed reduced expression of IL-6 and TNF-α, indicating a
mitigated inflammatory response. These findings highlight the promising therapeutic role of Cur-
CSNPs in controlling chronic T. gondii infection and suggest their potential as a novel strategy for
developing effective antiparasitic treatments.
Keywords Toxoplasma, Curcumin, Chitosan nanoparticles, Oxidative stress, TNF-α, Histopathological
lesions