Effect of acetylsalicylic acid on total myenteric neurons in mice experimentally infected with Trypanosoma cruzi.

We investigated the effects of acetylsalicylic acid (ASA) on the total myenteric neuronal population in the descending colon in Trypanosoma cruzi-infected mice. Thirty-five male Swiss mice, 60 days old, were divided into a control group (C group), control group treated with ASA (CA group), infected group (I group), and infected group treated with ASA (IA group). A total of 1300 trypomastigotes of the Y strain of T. cruzi were intraperitoneally inoculated in the IA and I groups. The CA and IA groups were treated with ASA intraperitoneally. At 75 days post-infection (dpi), all of the animals were sacrificed. Neurons in the colon were stained with Giemsa, quantified, and measured. No difference in the course of infection was observed between the IA and I groups, reflected by the parasitemia curve. Acetylsalicylic acid treatment in the CA and IA groups did not alter the total number of myenteric neurons compared with the C and I groups. The CA and IA groups exhibited an increase in the nuclear area, cytoplasmic area, and neuronal body area compared with the C and I groups. Future studies should elucidate the mechanism of action of ASA against Chagas' disease in the chronic phase.

Probiotics protect the intestinal wall of morphological changes caused by malnutrition.

This study sought to morphometrically analyze the jejunal wall of protein-malnourished rats administered a probiotic supplement. The sample consisted of recently weaned Wistar rats (Rattus norvegicus) distributed among four groups: animals given a commercial diet (G1, n = 4); animals given the same ration as G1 plus a probiotic supplement (G2, n = 4); animals given a 4% protein diet (G3, n = 4); and animals given the same ration as G3 plus a probiotic supplement (G4, n = 4). After 12 weeks, part of the jejunum was harvested and subjected to routine histological processing. Transverse sections with a thickness of 3 µm were stained with HE, and histochemical techniques were used to assay for glycoconjugates, including staining with periodic acid-Schiff (PAS) + diastase, Alcian Blue (AB) solution at pH 2.5, and Alcian Blue solution at pH 1.0. Morphometric analysis of the bowel wall showed that the probiotic culture used in this study induced hypertrophy of several layers of the jejunal wall in well-nourished animals and reduced the bowel wall atrophy usually observed in protein-malnourished animals. Neither malnutrition nor the use of probiotics altered the relationship between the number of goblet cells and the number of enterocytes.

Characterization of the myenteric neuronal population and subpopulation of the duodenum of adult wistar rat fed with hypoproteic chow.

The effects of severe protein malnutrition (4%) on myenteric neurons of Wistar rat duodenum, in relation to a standard 22%-protein diet for rodents, were assessed in this study. Segments of the duodenum from 10 rats from each nutritional group were submitted to the elaboration of whole mounts - 5 stained with Giemsa to determine the total population of myenteric neurons and the others stained by a histochemical method to detect nervous cells through the NADPH-diaphorase enzyme activity for studying the subpopulation of nitrergic neurons. The area of 100 neurons per animal, totalizing 2,000 neurons, were randomly measured by using the Image Pro-Plus(®)software. Malnourished rats presented 34.38% lower body weight and 10.60% duodenum length reduction when compared to the control group. Quantitative analysis demonstrated no significant differences between control and malnourished group by using Giemsa; however, as the organ reduction was not followed by an increase inversely proportional to the density of neurons, the condition imposed suggests the loss of neurons from the total population. Nevertheless, through NADPH-d histochemistry, there was a neuronal density increase for the malnourished group. There was no significant difference between the groups for both techniques with respect to the morphometric analysis of the body cell.

Myenteric neuronal plasticity induced by Toxoplasma gondii (genotype III) on the duodenum of rats.

The effects of acute and chronic infection caused by Toxoplasma gondii on duodenal myenteric neurons were analyzed. Eighteen rats were assigned into four groups: Acute Control Group (ACG, n=4); Acute Experimental Group (AEG, n=4); Chronic Control Group (CCG, n=5); and Chronic Experimental Group (CEG, n=5). Rats from the AEG and CEG were inoculated orally with 105 genotype III (BTU-II strain) tachyzoites of T. gondii isolated from a dog with neurological signs. Acute groups were killed after 24 hours after the inoculation and the chronic groups after 30 days. Whole-mount from the duodenum were stained with Giemsa. The population density of myenteric neurons, as well the body cell, nuclear and cytoplasmic area were analyzed. Both acute and chronic toxoplasmic infection did not provoke neuronal loss. On the other hand, plastic alterations were observed: decreasing of the nuclear and cytoplasmic area during the acute phase and neuronal hypertrophy during the chronic phase.

Probiotics prevent growth deficit of colon wall strata of malnourished rats post-lactation.

The objective of this study was to analyze morphometrically the colon wall strata of malnourished rats supplemented with probiotics. Sixteen recently weaned Wistar rats (Rattus norvegicus) were distributed into four groups: animals that received commercial chow (G1, n = 4); animals that received the same feed as G1 and were supplemented with probiotics (G2, n = 4); animals that received chow with 4% of proteins (G3, n = 4); animals that received the same feed as G3 and were supplemented with probiotics (G4, n = 4). After 12 weeks, the proximal colon was collected and submitted to histological processing. Three-µm cuts were stained with H.E., Periodic Acid Schifff (P.A.S.) + diasthasis solution and Alcian Blue (A.B.) pH 2.5 and pH 1.0. The morphometric analysis of the intestinal wall showed that the supplementation with ABT-4 probiotic culture prevents the growth deficit of colon wall strata that normally occurs in malnourished rats right after lactation. Besides, no alteration was observed in the proportion of the number of globet cells in relation to the number of enterocytes in malnourished rats, regardless of the supplementation with probiotics.

Intraepithelial lymphocytes, goblet cells and VIP-IR submucosal neurons of jejunum rats infected with Toxoplasma gondii.

Toxoplasma gondii (T. gondii) crosses the intestinal barrier in oral infections and can lead to changes in different cell types, including the neurons located there. In the gastrointestinal system, the autonomous nervous system component that regulate blood flow and mucous secretion is the submucosal plexus. The aim of this study was to examine the effects of T. gondii infection on intraepithelial lymphocytes (IELs), goblet cells and submucosal neurons that are immunoreactive to vasoactive intestinal peptide (VIP-IR) of rat jejunum. Twenty male rats distributed as a control group (CG) and an infected group (IG), which received a suspension with 500 parasite oocysts (strain ME-49, genotype II) orally, were assessed. Routine histological sections were used to quantify IELs and to detect mucins secreted by goblet cells. Whole mounts including the submucosal layer were examined using immunofluorescence to detect the VIP neurotransmitter. Quantitative alterations in IELs were not observed. However, the reduction (P < 0.05) in the number of goblet cells that produce neutral mucins (PAS+) and sulphomucins (AB pH 1.0) and the maintenance of sialomucin-secreting cells (AB pH 2.5) resulting in a more fluid mucous were observed. Concerning the VIP-IR submucosal neurons, an increase in fluorescence on IG animals was observed. There was a reduction (P < 0.05) in the number of VIP-IR submucosal neurons and atrophy of their cell bodies in IG rats. Infection with T. gondii caused alterations in the chemical composition of the intestinal mucous and reduction in the neuron number and atrophy of the remaining neurons in this cell subpopulation.

Neuronal changes caused by Trypanosoma cruzi: an experimental model.

Define an experimental model by evaluating quantitative and morphometric changes in myenteric neurons of the colon of mice infected with Trypanosoma cruzi. Twenty-eight Swiss male mice were distributed into groups: control (CG, n=9) and inoculated with 100 (IG(100), n=9) and 1000 (IG(1000), n=10) blood trypomastigotes, Y strain-T. cruzi II. Parasitemia was evaluated from 3-25 days post inoculation (dpi) with parasites peak of 7.7 × 10(6) and 8.4 × 10(6) trypomastigotes/mL at 8(th) dpi (p>0.05) in IG(100) and IG(1000), respectively. Chronic phase of the infection was obtained with two doses of 100mg/Kg/weight and one dose of 250mg/Kg/weight of Benznidazole on 11, 16 and 18 dpi. Three animals from each group were euthanized at 18, 30 and 75 dpi. The colon was stained with Giemsa. The quantitative and morphometric analysis of neurons revealed that the infection caused a decrease of neuronal density on 30(th) dpi (p<0.05) and 75 dpi (p<0.05) in IG(100) and IG(1000). Infection caused death and neuronal hypertrophy in the 75(th) dpi in IG(100) and IG(1000) (p<0.05, p<0.01). The changes observed in myenteric neurons were directly related to the inoculate and the time of infection.

Neuronal changes caused by Trypanosoma cruzi: an experimental model

Define an experimental model by evaluating quantitative and morphometric changes in myenteric neurons of the colon of mice infected with Trypanosoma cruzi. Twenty-eight Swiss male mice were distributed into groups: control (CG, n=9) and inoculated with 100 (IG100, n=9) and 1000 (IG1000, n=10) blood trypomastigotes, Y strain-T. cruzi II. Parasitemia was evaluated from 3-25 days post inoculation (dpi) with parasites peak of 7.7 × 10(6) and 8.4 × 10(6) trypomastigotes/mL at 8th dpi (p>0.05) in IG100 and IG1000, respectively. Chronic phase of the infection was obtained with two doses of 100mg/Kg/weight and one dose of 250mg/Kg/weight of Benznidazole on 11, 16 and 18 dpi. Three animals from each group were euthanized at 18, 30 and 75 dpi. The colon was stained with Giemsa. The quantitative and morphometric analysis of neurons revealed that the infection caused a decrease of neuronal density on 30th dpi (p<0.05) and 75 dpi (p<0.05) in IG100 and IG1000. Infection caused death and neuronal hypertrophy in the 75th dpi in IG100 and IG1000 (p<0.05, p<0.01). The changes observed in myenteric neurons were directly related to the inoculate and the time of infection.

Definir um modelo experimental de avaliação de alterações quantitativas e morfométricas nos neurônios mientéricos do cólon de camundongos infectados pelo Trypanosoma cruzi. Vinte e oito camundongos Swiss machos foram distribuídos nos grupos: controle (GC, n=9) e infectados com 100 (IG100, n=9) e 1000 (IG1000, n=10) tripomastigotas sanguíneos, cepa Y-T. cruzi II. A parasitemia foi avaliada 3-25 dias pós inoculação (dpi), com pico de parasitos de 7,7 × 10(6) e 8,4 × 10(6) tripomastigotas/mL no 8º dpi (p>0,05) em IG100 e IG1000, respectivamente. A fase crônica da infecção foi obtida com duas doses de 100mg/Kg/weight e uma dose de 250mg/Kg/ weight do benznidazol, em 11, 16 e 18 dpi. Três animais de cada grupo foram sacrificados aos 18, 30 e 75 dpi. O cólon foi corado com Giemsa. A análise quantitativa e morfométrica de neurônios revelou que a infecção causou uma diminuição da densidade neuronal no 30º dpi (p<0,05) e 75 dpi (p<0,05) em IG100 e IG1000. A infecção causou morte e hipertrofia neuronal no 75º dpi em IG100 e IG1000 (p<0,05, p<0,01). As alterações observadas nos neurônios mientéricos foram diretamente relacionadas ao inóculo e tempo de infecção.