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. The tissue damage caused by inflammation and the functional effects depend on the host immunity, strain, and developmental form of the parasite. We investigated the effects of acute oral infection with T. gondii on histoarchitecture, enteric nervous system (ENS), and inflammatory markers in the jejunum and ileum of mice. METHODS: Female C57BL/6 mice were divided into a control group and a group orally infected with 1000 sporulated T. gondii oocysts (ME-49 strain). After 5 days, jejunum and ileum were collected and processed for analyzes (e.g., histological and histopathological examinations, ENS, cytokine dosage, myeloperoxidase, nitric oxide activity). MAIN RESULTS: In infected mice, we observed a significant increase in serotonin-immunoreactive cells (5-HT IR) in the intestinal mucosa, as well as cellular infiltrates in the lamina propria, periganglionitis, and ganglionitis in the myenteric plexus. We also noted decreased neuron density in the jejunum, increased population of enteric glial cells in the ileum, histomorphometric changes in the intestinal wall, villi, and epithelial cells, remodeling of collagen fibers, and increased myeloperoxidase activity, cytokines, and nitric oxide in the intestine. CONCLUSIONS AND INFERENCES: Acute infection of female mice with T. gondii oocysts resulted in changes in ENS and a marked increase in 5-HT. These changes are consistent with its modulatory role in the development of moderate acute inflammation. The use of this experimental model may lend itself to studies aimed at understanding the pathophysiological mechanisms of intestinal inflammation in humans involving ENS.

Toxoplasma gondii causes increased ICAM-1 and serotonin expression in the jejunum of rats 12 h after infection.

OBJECTIVE: To analyze the remodeling dynamics of total collagen, type I and III, the expression of ICAM-1 and 5-HT in the jejunum of rats. METHODS: Twenty-eight Wistar rats were randomly assigned to two experimental groups: the control group (CG, n = 7) and the infected group (receiving 5,000 sporulated T. gondii oocysts - ME49 strain, genotype II, n = 21). Seven infected rats each at 6 (G6), 12 (G12), and 24 (G24) hours post infection were sacrificed and segments of jejunum were collected for standard histological, histochemical, and immunohistochemistry processing techniques. RESULTS: The infection promoted ICAM-1 and 5-HT expression, type III collagen, and total mast cell increases. However, it also caused a reduction in the area occupied by type I collagen fibers, and in submucosa thickness, and caused ganglion and peri-ganglion alterations. CONCLUSION: The structural damage caused by toxoplasmic infection is intense during the first 24 h post inoculation. At peak dissemination, from 12 to 24 h, there is an increase in ICAM-1 and 5-HT expression, with intense migration of mast cells to the site of infection. There was also a reduction in submucosa thickness, and an effective loss of extracellular matrix (ECM) organization, which included changes in the dynamics of type I and III total collagen deposition.

Assemblages A and B of Giardia duodenalis reduce enteric glial cells in the small intestine in mice.

Infection of Giardia duodenalis is one of the most common human parasitic disease worldwide. This infection may be related to important changes in the enteric nervous system. The objective of this study was to evaluate the myenteric and submucosal plexuses, the intestinal muscle layer, and gastrointestinal transit in mice infected with assemblages A and B of G. duodenalis. Swiss albino mice (Mus musculus) were infected with assemblages A and B of G. duodenalis for 15 days. Gastrointestinal transit time was evaluated before euthanasia. Duodenum and jejunum were removed for histological and immunohistochemical analyses. It was observed a reduction in the enteric glial cell count and a decrease in the ratio of enteric glial cells to neurons. The number of neurons did not change, but morphological changes were observed in the duodenum and jejunum in both plexuses, including an increase in the nuclear area and a reduction of cell bodies in the myenteric plexus and a decrease in the nuclear area in the submucosal plexus. A reduction of the thickness of the muscle layer was observed in the duodenum, with no significant differences in the gastrointestinal transit times. Assemblages A and B of G. duodenalis decrease the number of enteric glial cells in the myenteric and submucosal plexuses, decrease the thickness of the muscle layer, and change the morphology of neurons. Graphical abstract ᅟ.

Comparative study of effects of assemblages AII and BIV of Giardia duodenalis on mucosa and microbiota of the small intestine in mice.

AIMS: Giardiasis is one of the major causes of diarrhea worldwide and its symptoms vary in intensity, which can be attributed to different parasite assemblages. The goal of the present study was to compare the effects of infection caused by assemblages AII and BIV ofGiardia duodenalis on the response of the small intestine, microbiota, and behavioral parameters in mice. MAIN METHODS: Swiss mice were infected with assemblages AII and BIV of G. duodenalis for 15 days. Leucometry, pain, intestinal microbiota and histological parameters of the duodenum and jejunum were evaluated in the experimental groups. KEY FINDINGS: Both assemblages modified the composition of the intestinal microbiota. Infection with assemblage AII promoted leukocytosis, reflected by increasing number of polymorphonuclear cells, intraepithelial lymphocytes and pain-related behavior, indicating that this was the more aggressive assemblage with regard to its effects on the intestinal mucosa and duodenum. SIGNIFICANCE: The specific assemblage of the parasite is an important parameter that affects symptomatology in the host.

Coronary disease risk assessment in men: Comparison between ASCVD Risk versus Framingham.

INTRODUCTION: This study evaluated the risk of men developing coronary heart disease and its determinant variables, comparing these results through two validated coronary risk scales. METHODS: A cross sectional epidemiological analytical study in which data were collected by spontaneous demand, through a semi-structured questionnaire, clinical examination, and blood collection. The Chi-square test, logistic regression and Kappa for statistical analysis were performed. RESULTS: The study included 637 men. Age was a determining factor (p<0.05) in blood pressure (BP) changes, central obesity, BMI, glycemia, total cholesterol, LDL and triglycerides. From this group of 637, 252 presented BP above the recommended values. It was found that 34.54% of men had high total cholesterol, 19.94% had high LDL, 46.78% presented HDL below normal values and 36.42% had elevated triglycerides. Metabolic syndrome was found in 24.96% of the men. With the Framingham scale, 637 men were evaluated, 12.56% were at intermediate-risk and 5.49% elevated risk, while on the ASCVD Risk scale 553 men were evaluated, and 7.05% had moderate risk and none had high coronary risk. In this study, 50.43% of men still had no previous diagnosis for any disease that increases the risk factors. CONCLUSIONS: The determinant clinical variables were age, blood pressure, smoking, central obesity, race and education. The Framingham scale allowed the assessment of cardiac risk of all men in the study, with no age restriction or cholesterol value, so in population studies it shows advantages over the ASCVD Risk due to its comprehensive feature of including all individuals.

Treatment with low doses of aspirin during chronic phase of experimental Chagas' disease increases oesophageal nitrergic neuronal subpopulation in mice.

Patients with Chagas' disease may develop dysfunctions of oesophageal and colonic motility resulting from the degeneration or loss of the myenteric neurons of the enteric nervous system. Studies have shown that the use of aspirin, also known as acetylsalicylic acid (ASA), influences the pathogenesis of the disease. However, this remains controversial. The aim of this study was to evaluate the consequences of treatment with low doses of aspirin during the chronic phase of Chagas' disease on oesophageal function. Twenty male Swiss mice, 60 days of age, were used. The animals were infected with Y strain of Trypanosoma cruzi, injected intraperitoneally. Aspirin was given at a dose of 50 mg/kg to some of the infected animals, from the 55th to 63rd day after inoculation on consecutive days, and from the 65th to 75th day on alternate days. We investigated food passage of time, wall structure and nitrergic neuronal population of the distal oesophagus. Our data revealed that the use of low doses of aspirin in chronic Chagas' disease caused an increase in the number of nitrergic neurons and partially prevented hypertrophy of the oesophagus. In addition, the aspirin administration impeded Chagas' diseases associated changes in intestinal transit time. Thus treatment with aspirin in the chronic phase of Chagas' disease changes the natural history of the disease and raises the possibility of using it as a new therapeutic approach to the treatment of this aspect of Chagas' disease pathology.

Oral dependent-dose toxoplasmic infection model induced by oocysts in rats: Myenteric plexus and jejunal wall changes.

Toxoplasmosis is a widely distributed disease caused by the protozoan Toxoplasma gondii that is mainly transmitted orally. Once ingested, the parasite crosses the intestinal barrier to reach the blood and lymph systems to migrate to other regions of the host. The objective of this study was to evaluate the changes in the myenteric plexus and the jejunal wall of Wistar rats caused by oral infection with T. gondii oocysts (ME-49 strain). Inocula of 10, 100, 500 and 5000 oocysts were used. The total population of myenteric neurons and the most metabolically active subpopulation (NADH-diaphorase positive - NADH-dp) exhibited a decrease proportional to the dose of T. gondii. There was also a quantitative increase in the subpopulation of NADPH-diaphorase-positive (NADPH-dp) myenteric neurons, indicating greater expression of the NOS enzyme. Neuronal atrophy was observed, and morphological and morphometric alterations such as jejunal atrophy were found in the infected groups. Hypertrophy of the external muscle with the presence of inflammatory foci was observed in the group infected with 5000 oocysts. The changes observed in the infected groups were proportional to the number of oocysts inoculated.

Atrophy of myenteric neurons in the ileum of rats submitted to severe protein deficiency - doi: 10.4025/actascibiolsci.v34i2.6793 / Atrofia de neurônios do plexo mientérico do íleo de ratos submetidos à intensa carência de proteínas - doi: 10.4025/actascibiolsci.v34i2.6793

The effects of a 4%-protein diet in adult rats with respect to the morphometric aspects of the myenteric plexus in the ileum were assessed. Twenty animals were randomly divided into two groups: Control Group (n = 10), which received 26%-protein chow, and Experimental Group (n = 10), which received 4%-protein chow for 90 days. Neurons in the myenteric plexus in the ileum in whole mount were evidenced through Giemsa and NADH-diaphorase techniques. The overall neuronal population as well as the subpopulation positive for NADH diaphorase presented atrophy, with a reduction of the perikaryon, nucleus and cytoplasm.

Objetivou-se avaliar os efeitos da oferta de uma dieta contendo 4% de proteínas para ratos adultos, quanto aos aspectos morfométricos do plexo mientérico do íleo. Vinte animais foram distribuídos aleatoriamente em dois grupos: Controle (n = 10) que receberam ração comercial com 26% de proteína e Experimental (n = 10) alimentados com ração com teor proteico reduzido para 4%, durante 90 dias. Neurônios do plexo mientérico do íleo presentes em preparados totais foram evidenciados por intermédio da técnica de Giemsa e da NADH-diaforase. Tanto a população neuronal total, assim como a subpopulação NADH-diaforase positiva sofreram atrofia com redução da área do pericário, do núcleo e do citoplasma.

Hypertrophy of the neurons in the ileum of rats infected with cysts of Toxoplasma gondii (genotype II) - DOI: 10.4025/actascibiolsci.v31i2.796 / Hypertrophy of the neurons in the ileum of rats infected with cysts of Toxoplasma gondii (genotype II) - DOI: 10.4025/actascibiolsci.v31i2.796

This paper verified possible alterations caused by a genotype II Toxoplasma gondii strain with respect to the total number and morphometry of the myenteric neurons in the terminal ileum and descending colon of rats. Eight rats were divided into two groups: control (n = 4) and experimental (n = 4). This group was inoculated orally with 20 tissue cysts of T. gondii from a genotype II strain (ME-49). Whole mounted from the terminal ileum and the descending colon were stained with Giemsa. There was not any neuronal loss on both organs. The neurons became hypertrophied in the terminal ileum, whereas morphometric alterations were not observed for the neurons in the descending colon.

This paper verified possible alterations caused by a genotype II Toxoplasma gondii strain with respect to the total number and morphometry of the myenteric neurons in the terminal ileum and descending colon of rats. Eight rats were divided into two groups: control (n = 4) and experimental (n = 4). This group was inoculated orally with 20 tissue cysts of T. gondii from a genotype II strain (ME-49). Whole mounted from the terminal ileum and the descending colon were stained with Giemsa. There was not any neuronal loss on both organs. The neurons became hypertrophied in the terminal ileum, whereas morphometric alterations were not observed for the neurons in the descending colon.