Moderate intestinal immunopathology after acute oral infection with Toxoplasma gondii oocysts is associated with expressive levels of serotonin.

Background: Invasion of the intestinal mucosa by T. gondii elicits a local immune response of variable intensity. These reactions can be lethal in C57BL/6 mice.

Acute infection with Toxoplasma gondii oocysts preferentially activates non-neuronal cells expressing serotonin in the jejunum of rats.

The interaction of Toxoplasma gondii with the gastrointestinal tract of its host is highly regulated. Once ingested, the parasite crosses the epithelium without altering the permeability of the intestinal barrier. Nevertheless, many studies report alterations ranging from structural to functional damage in cells and tissues that make up the wall of the small and large intestine.

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

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.

Immunocompetent host develops mild intestinal inflammation in acute infection with Toxoplasma gondii.

Toxoplasma gondii (T. gondii) is the causative agent of toxoplasmosis, common zoonosis among vertebrates and high incidence worldwide. During the infection, the parasite needs to transpose the intestinal barrier to spread throughout the body, which may be a trigger for an inflammatory reaction.

Toxoplasma gondii infection causes structural changes in the jejunum of rats infected with different inoculum doses.

Aim: To evaluate the mucosal tunic and submucosal plexus of the jejunum of rats infected with different inoculum doses of Toxoplasma gondii.

Main Methods: Rats were infected with different inoculum doses (50, 500, 1000 and 5000 oocysts) of the T. gondii for 30days, while a control group (CG) received saline solution.

Desired and side effects of the supplementation with l-glutamine and l-glutathione in enteric glia of diabetic rats.

Background/aims: Enteric neuropathy associated with Diabetes Mellitus causes dysfunction in the digestive system, such as: nausea, diarrhea, constipation, vomiting, among others. The aim of this study was to compare the effects of supplementation with 2% l-glutamine and 1% l-glutathione on neurons and enteric glial cells of ileum of diabetic rats.

Methods: Thirty male Wistar rats have been used according to these group distributions: Normoglycemic (N), Normoglycemic supplemented with l-glutamine (NG), Normoglycemic supplemented with l-glutathione (NGO), Diabetic (D), Diabetic supplemented with l-glutamine (DG) and Diabetic supplemented with l-glutathione (DGO).

Kinetics of acute infection with Toxoplasma gondii and histopathological changes in the duodenum of rats.

Toxoplasma gondii crosses the intestinal barrier to spread into the body. We investigate the intestinal wall and epithelial cells of the duodenum of rats infected with T. gondii during different time points of acute infection.

Is L-glutathione more effective than L-glutamine in preventing enteric diabetic neuropathy?

Background: Diabetes and its complications appear to be multifactorial. Substances with antioxidant potential have been used to protect enteric neurons in experimental diabetes.

Aim: This study evaluated the effects of supplementation with L-glutamine and L-glutathione on enteric neurons in the jejunum in diabetic rats.

Effect of l-glutamine on myenteric neuron and of the mucous of the ileum of diabetic rats.

The objective of this work was to investigate the effect of the L-glutamine supplementation to prevent - diabetes induced changes in myenteric neurons and also to verify the effect on the mucosa of the ileum of Wistar rats. The animals were divided in five groups (n = 5): untreated normoglycaemic (UN), normoglycaemic treated with L-glutamine (NG), untreated diabetics (UD), diabetics treated with L-glutamine, starting on the 4th (DG4) or 45th day following diabetes induction (DG45). The amino acid was added to the diet at 1%.

Histological evaluation of the periodontal ligament from aged Wistar rats supplemented with ascorbic acid.

Ascorbic acid (AA) is able to neutralize reactive oxygen species and is essential for collagen synthesis. In aging process oxidative stress is elevated. This study aims to investigate the effects of AA supplementation on the periodontal ligament (PL) of rats during aging.

Supplementation with 0.1% and 2% vitamin E in diabetic rats: analysis of myenteric neurons immunostained for myosin-V and nNOS in the jejunum.

Context: Diabetes mellitus is a disease characterized by hyperglycemia that, when allowed to progress long-term untreated, develops vascular and neurological complications, which are responsible for the development of alterations in the enteric nervous system in diabetic patients. In the gastrointestinal tract, diabetes mellitus promotes motor and sensory changes, and in the reflex function of this system, causing gastroparesis, diarrhea, constipation, megacolon, slow gastrointestinal transit, gastric stasis and dilation with decreased or increased peristaltic contractions. Several studies have shown that oxidative stress is the main responsible for the vascular and neurological complications affecting the enteric nervous system of diabetics.