Lesions In Gut Research Articles

Parasitic anomalies observed in snow trout due to anthropogenic stress in water bodies

There is interrelationship of the environmental conditions and fish health. Decrease or increase of pollution in aquatic ecosystem have direct impact on presence or absence of parasites. Fish living under optimum environmental, well-nourished conditions are more resistant to diseases than fish weakened by malnutrition caused by parasite infestation or due to deterioration of environmental conditions because ofpollution. Fish encounters common parasites in wild and in culture systems. Parasites attach to the host through suckers and hooks and make their way inside the host through different means, which include skin, through mouth along with food, by means of gills. The hosts were collected during Jan 2019 to Jan 2020 from river Veshaw. During this study it was observed that presence of parasites causes some changes in fish which can serve as indicators of deterioration in aquatic habitat. Clinical signs were noticed in fish hosts collected from sites which received waste due to anthropogenic activities. Parasitic anomalies in the host collected from polluted site was observed to include body deformaties, gastric distention, lesions in gut, increased mucus production, damage in gill filaments etc.

Jejunal villus absorption and paracellular tight junction permeability are major routes for early intestinal uptake of food-grade TiO2 particles: an in vivo and ex vivo study in mice

BackgroundFood-grade TiO2 (E171 in the EU) is widely used as a coloring agent in foodstuffs, including sweets. Chronic dietary exposure raises concerns for human health due to proinflammatory properties and the ability to induce and promote preneoplastic lesions in the rodent gut. Characterization of intestinal TiO2 uptake is essential for assessing the health risk in humans. We studied in vivo the gut absorption kinetics of TiO2 in fasted mice orally given a single dose (40 mg/kg) to assess the ability of intestinal apical surfaces to absorb particles when available without entrapment in the bolus. The epithelial translocation pathways were also identified ex vivo using intestinal loops in anesthetized mice.ResultsThe absorption of TiO2 particles was analyzed in gut tissues by laser-reflective confocal microscopy and ICP-MS at 4 and 8 h following oral administration. A bimodal pattern was detected in the small intestine: TiO2 absorption peaked at 4 h in jejunal and ileal villi before returning to basal levels at 8 h, while being undetectable at 4 h but significantly present at 8 h in the jejunal Peyer’s patches (PP). Lower absorption occurred in the colon, while TiO2 particles were clearly detectable by confocal microscopy in the blood at 4 and 8 h after treatment. Ex vivo, jejunal loops were exposed to the food additive in the presence and absence of pharmacological inhibitors of paracellular tight junction (TJ) permeability or of transcellular (endocytic) passage. Thirty minutes after E171 addition, TiO2 absorption by the jejunal villi was decreased by 66% (p < 0.001 vs. control) in the presence of the paracellular permeability blocker triaminopyrimidine; the other inhibitors had no significant effect. Substantial absorption through a goblet cell (GC)-associated pathway, insensitive to TJ blockade, was also detected.ConclusionsAfter a single E171 dose in mice, early intestinal uptake of TiO2 particles mainly occurred through the villi of the small intestine, which, in contrast to the PP, represent the main absorption surface in the small intestine. A GC-associated passage and passive diffusion through paracellular TJ spaces between enterocytes appeared to be major absorption routes for transepithelial uptake of dietary TiO2.

The colon and terminal ileum in patients with ankylosing spondylitis and controls in Bangladesh: a macroscopic and microscopic study.

ObjectiveLittle is known about gut lesions in AS patients in a developing country, such as Bangladesh.MethodsFull colonoscopy, including the terminal ileum, was performed in 60 AS patients and 20 controls, without diarrhoea, to study macroscopic and microscopic lesions.ResultsIn the colon, in 60 AS patients 17 macroscopic lesions were found, of which 11 were in the rectum; only one lesion was found in 20 controls. The prevalence of microscopic lesions in the ascending colon, sigmoid colon and rectum was 51, 44 and 50 in patients, respectively, and 13, 9 and 8 in controls. In the terminal ileum, macroscopic and microscopic lesions were seen in 21/56 and 43/56 AS patients, respectively, and in 1/20 and 9/20 controls. In the AS group, macroscopic (38.5 vs 5%, P < 0.01) and microscopic (76.8 vs 45%, P = 0.009) lesions were more frequent than in controls; no IBD was diagnosed. Findings were comparable in the axial AS group (n = 25) and the mainly peripheral group (n = 35). In AS patients, marked eosinophilic infiltration was observed in the ascending colon and sigmoid colon but not in the rectum, and this infiltration was more than in controls. The colonic mucosa in controls was otherwise comparable with western studies. Anaemia was seen in 18/60 cases. No association was found between anaemia or HLA-B27 status and gut lesions.ConclusionThere was an equal percentage of microscopic lesions in the whole gut in AS cases and healthy controls. Previous helminth invasions might have played a role. Lesions differ significantly between AS and controls only in the ileum; therefore, the ileal lesions might be more disease related than the colonic ones.

Guillain Barré Syndrome is induced in Non-Obese Diabetic (NOD) mice following Campylobacter jejuni infection and is exacerbated by antibiotics

Campylobacter jejuni is a leading cause of bacterial gastroenteritis linked to several serious autoimmune sequelae such as the peripheral neuropathies Guillain Barré syndrome (GBS) and Miller Fisher syndrome (MFS). We hypothesized that GBS and MFS can result in NOD wild type (WT) mice or their congenic interleukin (IL)-10 or B7-2 knockouts secondary to C. jejuni infection. Mice were gavaged orally with C. jejuni strains HB93-13 and 260.94 from patients with GBS or CF93-6 from a patient with MFS and assessed for clinical neurological signs and phenotypes, anti-ganglioside antibodies, and cellular infiltrates and lesions in gut and peripheral nerve tissues. Significant increases in autoantibodies against single gangliosides (GM1, GQ1b, GD1a) occurred in infected NOD mice of all genotypes, although the isotypes varied (NOD WT had IgG1, IgG3; NOD B7-2−/− had IgG3; NOD IL-10−/− had IgG1, IgG3, IgG2a). Infected NOD WT and NOD IL-10−/− mice also produced anti-ganglioside antibodies of the IgG1 isotype directed against a mixture of GM1/GQ1b gangliosides. Phenotypic tests showed significant differences between treatment groups of all mouse genotypes. Peripheral nerve lesions with macrophage infiltrates were significantly increased in infected mice of NOD WT and IL-10−/− genotypes compared to sham-inoculated controls, while lesions with T cell infiltrates were significantly increased in infected mice of the NOD B7-2−/− genotype compared to sham-inoculated controls. In both infected and sham inoculated NOD IL-10−/− mice, antibiotic treatment exacerbated neurological signs, lesions and the amount and number of different isotypes of antiganglioside autoantibodies produced. Thus, inducible mouse models of post-C. jejuni GBS are feasible and can be characterized based on evaluation of three factors—onset of GBS clinical signs/phenotypes, anti-ganglioside autoantibodies and nerve lesions. Based on these factors we characterized 1) NOD B-7−/− mice as an acute inflammatory demyelinating polyneuropathy (AIDP)-like model, 2) NOD IL-10−/− mice as an acute motor axonal neuropathy (AMAN)-like model best employed over a limited time frame, and 3) NOD WT mice as an AMAN model with mild clinical signs and lesions. Taken together these data demonstrate that C. jejuni strain genotype, host genotype and antibiotic treatment affect GBS disease outcomes in mice and that many disease phenotypes are possible.

Exploring hazards of acute exposure of Acephate in Drosophila melanogaster and search for l-ascorbic acid mediated defense in it

This study reveals protective role of l-ascorbic acid (25, 50 and 100μg/mL) against toxic impacts of acute sub-lethal exposure of Acephate (5μg/mL) in a non-target organism Drosophila melanogaster. Organismal effect was evident from increased impairment in climbing activities (9 folds) of treated individuals who also manifested altered ocular architecture. These anomalies were reduced with l-ascorbic acid (l-AA) supplementation. Acephate induced apoptotic lesions in eye imaginal discs and gut confirmed tissue damage that also reduced with l-AA co-treatment. Reduction in viability of fat body cells (∼41%), neural cells (∼42%) and hemocytes (3 folds) indicates cytotoxic and immunotoxic potential of Acephate, which were significantly mitigated with l-AA co-administration. The sub-cellular toxic impacts of Acephate treatment became obvious from enhancement in activities of antioxidant enzymes (CAT by ∼1.63 folds, SOD by ∼1.32 folds), detoxifying enzymes (Cyp450 by ∼1.99 folds and GST by ∼1.34 folds), 2.1 times boost in HSP 70 expression, and inhibition of cholinesterase activity (by ∼0.66 folds). DNA breaks evident through comet assay confirmed Acephate triggered genotoxicity which could also be prevented through co-administration of. L-AA Furthermore, the study proposes the use of Drosophila as a model to screen chemicals for their protective potential against pesticide toxicity.