With a seropositivity rate capable of reaching 60 % in adults, toxoplasmosis stands as one of the most prevalent zoonotic diseases worldwide (CDC, 2018). While infection with the obligate intracellular protozoan Toxoplasma gondii (T. gondii) typically remains asymptomatic, it can present as a mononucleosis-like illness and/or retinitis in immunocompetent individuals (Kochanowsky and Koshy, 2018). However, symptoms can escalate, especially in immunosuppressed individuals such as fetuses and AIDS patients, often linked to the parasite's tropism and its persistence in the brain, potentially leading to severe clinical outcomes.

In Brazil, the mortality rate is notably higher in the Southeast region, accounting for 54 % of deaths attributed to the disease between 2000 and 2019, followed by the Northeast (19 %), South (11 %), North (10 %), and Central-West (6 %) regions (Brasil. Ministério da Saúde, 2022).

Oral transmission stands as one of the primary routes of T. gondii transmission (Dubey, 1998), involving the invasion of the intestinal epithelial barrier. At this juncture, intestinal inflammation ensues (Dubey, 2010), marked by various transformations including inflammatory infiltrates, necrosis, and alterations in the intestinal wall, villi, crypts, and epithelium (Fux et al., 2003; Góis et al., 2016; Struck et al., 2012; Suzuki et al., 2000; Vicentino-Vieira et al., 2017).

The severity of the inflammatory cascade may be modulated by several factors, including parasite strain, duration of infection, host species, specific intestinal regions involved, and sex hormones (Kasper et al., 2004; Liesenfeld, 2002; Trevizan et al., 2016), as well as interleukin-22 levels and microbiota composition (Couturier-Maillard et al., 2018). Moreover, even within a single species, genetic background must be considered, as demonstrated in mice, where certain strains like BALB/c are resistant, while others like C57BL/6 are more vulnerable to T. gondii infection (Suzuki et al., 2000).

The C57BL/6 mouse strain is widely used in immunological research due to its well-characterized immune response and genetic homogeneity, providing a consistent and reliable model for studying host-pathogen interactions. Reports in literature show that the infection with cysts of ME49 strain of T. gondii cause intense damage in the ileum leading to the death of the animals in a few days (Dubey et al., 2012; Liesenfeld, 2002).

The modulation of intestinal inflammation hinges on the interaction between the immune system and the Enteric Nervous System (ENS), susceptible to abnormalities and intricately linked to inflammation severity (Margolis et al., 2011; Villanacci et al., 2008). In this context VIP is a neuropeptide known for its potent immunomodulatory properties, thus understanding the role of VIP can provide critical insights into how the body regulates inflammation and immune responses in the gut (Delgado et al., 2004).

The study of T. gondii infection in the intestine requires a protocol that addresses its complex pathological and immunological interactions. Although significant progress has been made, research targeting this organ still faces unresolved questions, particularly concerning sex-specific differences. Most studies have predominantly focused on male mice, leaving a critical gap in understanding the behavior of T. gondii in females. Given the biological differences that may influence immune responses and disease progression, further investigation into female models is essential to develop a more comprehensive understanding of the infection.

With this in mind, we propose evaluating morphoquantitative parameters in the colons of female C57BL/6 mice acutely infected with 1000 sporulated oocysts of T. gondii (ME-49 strain, genotype II).