Unmasking the intestinal impact: Acute Toxoplasma gondii infection induces severe morphological and immunological changes in female C57BL/6 mice

Toxoplasmosis, caused by the protozoan Toxoplasma gondii (T. gondii), is a common zoonotic disease with a seropositivity rate of up to 60 % in adults. While often asymptomatic, it can cause severe complications in immunocompromised individuals. Oral transmission is the primary route of infection, leading to intestinal inflammation. This study evaluated morphoquantitative changes in the colons of female C57BL/6 mice acutely infected with T. gondii. Mice were divided into control and infected groups and euthanized five days post-infection for colon collection. Histological analyses quantified intraepithelial lymphocytes, goblet cells, mast cells, and collagen fibres, while immunostaining assessed neurons and vasoactive intestinal peptide (VIP) expression. Infected mice exhibited increased intraepithelial lymphocytes and myeloperoxidase activity, alongside a significant reduction in AB-1.0-positive goblet cells, indicating impaired mucus secretion. Notably, the longitudinal muscle layer showed increased thickness, whereas the submucosal layer and crypt depth were reduced. Histopathological evaluation revealed epithelial hyperplasia, mucosal ulceration, and abscess formation. A decrease in myenteric neurons was also observed, although VIP expression remained unchanged. These findings demonstrate that acute T. gondii infection induces substantial alterations in intestinal structure, including immune cell infiltration, goblet cell depletion, and muscle layer remodelling. The reduction in myenteric neurons, despite stable VIP expression, suggests specific neuroimmune interactions in the infected gut. Collectively, this study highlights the profound impact of T. gondii on colonic morphology and function, underscoring the complexity of host–parasite interactions during acute infection.