Schizophrenia has been long thought to be a mainly neurodevelopmental disease, but current research increasingly highlights the involvement of autoimmunological and inflammatory processes. Recently, the gut-brain axis has become the focus of research as various components of this axis appear to be altered in psychiatric illnesses including schizophrenia. Schizophrenic patients not only show reduced diversity in their microbiome compared to healthy controls, but also several parameters of elevated peripheral and central inflammation. The Poly I:C mouse model is based on epidemiological findings suggesting that an infection during certain time frames of pregnancy increases the risk of the child to develop schizophrenia later in life. In this model for schizophrenia, we did not only find an increase in microglia cells during development but also disturbed microbiota composition. In a next step, the gut-brain axis will be further investigated. In particular, the activation status of microglia and astrocytes in the brain as well as the quantity of Th17 cells in the small intestines are analyzed and characterized in adolescent offspring of Poly I:C dams by flow cytometry. In addition, reduction of systemic inflammation and induction of dysbiosis, by pharmacological manipulation five days prior to sacrificing, using oral administration of aspirin or gentamicin, respectively, might provide further valuable information on treatment options and potential trigger during the prodromal phase of disease.