Acute Toxoplasma gondii infection alters the number of neurons and the proportion of enteric glial cells in the duodenum in Wistar rats

Abstract

Background Toxoplasma gondii infection can occur through the ingestion of raw meat that contains tissue cysts or food that contains oocysts. Through the ingestion of oocysts, the parasite crosses the intestinal barrier, where the enteric nervous system is located. The objective was to investigate the kinetics of neuronal and glial responses during acute T. gondii infection. Methods We used 45 Wistar rats that were divided into a control group and infected groups that were evaluated at 6, 12, 24, 48, 72 hours, 7 days, 10 days, and 15 days after infection. The rats received 5000 sporulated oocysts of the parasite orally. To detect neurons and enteric glia cells, the myenteric and submucosal plexuses of the duodenum underwent double‐labeling immunohistochemical techniques to evaluate HuC/HuD and S100, HuC/HuD and ChAT, and HuC/HuD and nNOS. Key Results We observed a reduction of the total neuron population in the submucosal plexus 72 hours after infection. Cholinergic neurons decreased in the submucosal plexus 15 days after infection, and nitrergic neurons decreased in the myenteric plexus 72 hours after infection. A decrease in the number of glial cells was observed 7 days after infection in the submucosal plexus, and an increase in the enteric glial cell (EGC)/neuron ratio was found in both plexuses 48 hours after infection. Conclusions and Inferences We found decrease of neurons and increase in the EGC/neuron ratio in both plexuses caused by acute T. gondii infection, with major alterations 72 hours after oral infection. The number of cholinergic neurons decreased in the submucosal plexus, and the number of nitrergic neurons decreased in the myenteric plexus. A decrease in the number of enteric glial cells was observed in the submucosal plexus, and an increase in the enteric glial cell/neuron ratio was observed in both ganglionate plexuses of the duodenum.

Small intestine remodeling in male Goto–Kakizaki rats

“…It is important to point out that attenuated GI transit time and diarrhea were correlated with a decreased nNOS enteric inhibitory subpopulations in diabetic animals (Ferreira et al, 2018). Previous studies demonstrated that hyperglycemia‐related oxidative stress and inflammation are primary inducers of enteric nervous system dysfunction, resulting in marked changes in intestinal motility and intestinal secretion activity (Chandrasekharan et al, 2011; Trevizan et al, 2019; Voukali et al, 2011). Herein, we identified some changes in intestinal morphology and evidence of enteric nervous system remodeling in GK rats; however, the underlying mechanisms responsible for these alterations are still unclear.…”

“…The myenteric plexus was obtained by removing the submucosal tissue and mucous layer. The submucosal plexus was obtained by removing the mucosal and muscular layer (Trevizan et al, 2019). A total of 10 animals (five per group) were used for this set of experiments.…”

A New Target Organ of Leishmania (Viannia) braziliensis Chronic Infection: The Intestine

“…However, the neuroplastic response to inflammation enables intestinal homeostasis (Mawe et al, 2009). Hypertrophy of neuron bodies in the myenteric plexus at 90 days of infection suggests an increase in their metabolic activity; this acts as a mechanism of adaptation to adverse conditions suffered by these cells (Araujo, 2015;Trevizan et al, 2019). Such alterations can interfere with intestinal motility and consequently lead to an increase in muscle layers, as this plexus is responsible for the coordinating movements of intestinal relaxation and contraction (Nezami and Srinivasan, 2010;Machado et al, 2021).…”

Biomarkers and Their Possible Functions in the Intestinal Microenvironment of Chagasic Megacolon: An Overview of the (Neuro)inflammatory Process

“…In fact, enteric glial cells and their products participate in intestinal homeostasis, especially in neuronal survival. Thus, the reduction of these cells has already been suggested to be associated with infectious [115,116] and noninfectious intestinal diseases [117][118][119], which are characterized by 4 Journal of Immunology Research neurodegeneration, like in CD. Evidence shows a glial cell and neuron network owing to the production of NTs such as NGF, NT-3/4/5, and glial cell line-derived neurotrophic factor (GDNF).…”