Dietary betaine accumulates in the liver and intestinal tissue and stabilizes the intestinal epithelial structure in healthy and coccidia-infected broiler chicks

Author(s):  
H Kettunen ◽  
K Tiihonen ◽  
S Peuranen ◽  
M.T Saarinen ◽  
J.C Remus
2019 ◽  
Vol 13 (3) ◽  
pp. 33-38
Author(s):  
Shila Omidzahir ◽  
◽  
Maliheh Alijantabar Bayi ◽  
Fatemeh Kardel ◽  
Mohammad Mazandarani ◽  
...  

Background: The application of nano-particles (NPs) in various industries is growing. Since their toxicity is not clearly understood, they can cause adverse effects on the environment. The aim of this study was to evaluate the histopathological effects of iron oxide nano-particles on the small intestine of common carp, Cyprinus carpio. Methods: Four experimental treatments were designed (15 fish/treatment). Treatment 1 was the controls while Treatments 2, 3 and 4 were experimental. The experimental groups were exposed to 50, 75 and the 100 mg/L of iron oxide NPs, respectively. On days 14, 21 and 28, the fish were randomly picked from each tank, samples of the small intestine were dissected, and were examined for both the accumulation of the iron NPs and the tissue histopathologies. Results: The highest concentration of iron accumulation was detected for Treatment 3 on day 21, compared to all other treatment groups (p<0.05). However, iron accumulation in the tissue declined unexpectedly after day 21 despite the continued treatments at 100 mg/L of the iron NPs. The histopathological examinations revealed that the treatment beyond 21 days caused damages to the intestinal epithelial cells, including enterocytes, villi and the goblet cells. Conclusion: This study demonstrated that the effect of iron oxide NPs on the small intestinal tissue was dependant on the dose and duration of exposure. We conclude that the iron accumulation in the small intestine declined despite increasing the iron oxide NPs concentration and the exposure duration secondary to damages caused to the intestinal epithelial cell layer.


2005 ◽  
Vol 7 (12) ◽  
pp. 1782-1797 ◽  
Author(s):  
Mehri Zareie ◽  
Jason Riff ◽  
Kevin Donato ◽  
Derek M. McKay ◽  
Mary H. Perdue ◽  
...  

2015 ◽  
Vol 212 (11) ◽  
pp. 1783-1791 ◽  
Author(s):  
Patricia Aparicio-Domingo ◽  
Monica Romera-Hernandez ◽  
Julien J. Karrich ◽  
Ferry Cornelissen ◽  
Natalie Papazian ◽  
...  

Disruption of the intestinal epithelial barrier allows bacterial translocation and predisposes to destructive inflammation. To ensure proper barrier composition, crypt-residing stem cells continuously proliferate and replenish all intestinal epithelial cells within days. As a consequence of this high mitotic activity, mucosal surfaces are frequently targeted by anticancer therapies, leading to dose-limiting side effects. The cellular mechanisms that control tissue protection and mucosal healing in response to intestinal damage remain poorly understood. Type 3 innate lymphoid cells (ILC3s) are regulators of homeostasis and tissue responses to infection at mucosal surfaces. We now demonstrate that ILC3s are required for epithelial activation and proliferation in response to small intestinal tissue damage induced by the chemotherapeutic agent methotrexate. Multiple subsets of ILC3s are activated after intestinal tissue damage, and in the absence of ILC3s, epithelial activation is lost, correlating with increased pathology and severe damage to the intestinal crypts. Using ILC3-deficient Lgr5 reporter mice, we show that maintenance of intestinal stem cells after damage is severely impaired in the absence of ILC3s or the ILC3 signature cytokine IL-22. These data unveil a novel function of ILC3s in limiting tissue damage by preserving tissue-specific stem cells.


2020 ◽  
Vol 21 (3) ◽  
pp. 113-117
Author(s):  
S. T. Naphade

The present investigation includes the study of protein concentration in intestinal tissue of coccidiosis infected broiler chicks orally inoculated by the infection of Eimeria tenella sporulated oocysts and treated with Mercurius corrosivus by using the methods of histochemical techniques. The treatment of homoeopathic medicine Mercurius corrosivus was administered to the coccidiosis infected group of broiler chicks.For the study of protein concentration in intestinal tissue of the coccidiosis infected and non-infected broiler chicks, the histochemical technique was used. Histochemical study indicates that the presence of different concentration of protein content found in the intestinal tissue of the broiler chicks.Intestinal tissue of all the chicks of different groups have presence of protein content in variable concentrations. It is also observed that the presence of protein concentration was variable in different region and shows different traces like minimum, medium and maximum amount of protein content found in different region of the intestinal tissue.The amount of protein concentration was observed high in group B(INC) in comparison to the other group of chicks observed during the experimental period. The concluded results of the study by using histochemical techniques shows that the protein concentration in the intestinal tissue is demonstrated by the variable staining reaction. The concentration of protein content is maximum in the parasitic stages showing the utilization of the protein from the host tissue. Whereas the infected and treated group with homoeopathic medicine Mercurius corrosivus also showed variable staining reaction according to the presence of protein in the intestinal tissue.


2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S171-S171
Author(s):  
M Poletti ◽  
I Hautefort ◽  
A Treveil ◽  
A Demeter ◽  
E Rodriguez ◽  
...  

Abstract Background Intestinal homeostasis depends on complex interactions between the microbiota, the intestinal epithelium and the host immune system. Paneth cells play an important role thanks to their release of antimicrobial peptides and their dysfunction has been shown to contribute to Crohn’s disease. The human gut commensal Bifidobacteria has been highlighted as a protective agent in IBD. Whilst the specific modulating factors are largely unidentified, evidence suggests that Bifidobacteria can interact with host intestinal cells. Such interactions can alter host molecular pathways, resulting in a modified intestinal cell function. Understanding these effects is crucial to unravel the potential benefits of bifidobacteria for IBD. In this study, we developed a workflow to investigate the beneficial effects of the probiotic bifidobacteria in modulating gene regulation and function of different intestinal epithelial cells in the gut. Methods We gavaged either conventionally raised (SPF) or germ-free mice (n = 5) with Bifidobacterium breve UCC2003 (1–5 × 108 CFU), and sorted intestinal epithelial cell types (Lgr5+ stem cells, Paneth cells and transit-amplifying cells) from the mouse intestinal tissue by flow cytometry using a panel of known antibodies. Each isolated cell population (n = 200) was subsequently profiled by low input RNA sequencing and DNA methylation. Results Intracellular lysozyme staining for Paneth cells and initial gene expression data exploration suggests successful separation of the different populations from the mouse intestinal tissue using flow cytometry. Gene expression data were further analysed using network biology approaches to generate cell-type-specific molecular regulatory networks indicating genes regulation by bifidobacteria in each cell types. Overlaying the methylation data will elucidate the role of epigenetics played during this regulation. Together, these networks will improve our understanding of how Bifidobacteria affects these different cells types through communication with precursor stem cells and/or with direct effects on the fully differentiated cells, ultimately impacting their function. Conclusion In the future, we aim to use a similar workflow using two-dimensional human-derived organoids monolayers co-cultured with bifidobacteria to investigate the effects on host intestinal epithelial cell function in a high-throughput and patient-specific manner. This will increase our understanding of the complex role played by host genetics and microbial factors in the pathogenesis of gastrointestinal diseases such as IBD, and hopefully pave the way for translational developments in the prevention these pathologies.


Sign in / Sign up

Export Citation Format

Share Document