scholarly journals Successful engraftment of epithelial cells derived from autologous rabbit buccal mucosal tissue, encapsulated in a polymer scaffold in a rabbit model of a urethral stricture, transplanted using the transurethral approach

2021 ◽  
Vol 18 ◽  
pp. 127-132
Author(s):  
Akio Horiguchi ◽  
Kenichiro Ojima ◽  
Masayuki Shinchi ◽  
Toshihiro Kushibiki ◽  
Yoshine Mayumi ◽  
...  
2019 ◽  
Vol 20 (6) ◽  
pp. 1504 ◽  
Author(s):  
Subha Arthur ◽  
Palanikumar Manoharan ◽  
Shanmuga Sundaram ◽  
M Rahman ◽  
Balasubramanian Palaniappan ◽  
...  

Na-amino acid co-transporters (NaAAcT) are uniquely affected in rabbit intestinal villus cell brush border membrane (BBM) during chronic intestinal inflammation. Specifically, Na-alanine co-transport (ASCT1) is inhibited secondary to a reduction in the affinity of the co-transporter for alanine, whereas Na-glutamine co-transport (B0AT1) is inhibited secondary to a reduction in BBM co-transporter numbers. During chronic intestinal inflammation, there is abundant production of the potent oxidant peroxynitrite (OONO). However, whether OONO mediates the unique alteration in NaAAcT in intestinal epithelial cells during chronic intestinal inflammation is unknown. In this study, ASCT1 and B0AT1 were inhibited by OONO in vitro. The mechanism of inhibition of ASCT1 by OONO was secondary to a reduction in the affinity of the co-transporter for alanine, and secondary to a reduction in the number of co-transporters for B0AT1, which were further confirmed by Western blot analyses. In conclusion, peroxynitrite inhibited both BBM ASCT1 and B0AT1 in intestinal epithelial cells but by different mechanisms. These alterations in the villus cells are similar to those seen in the rabbit model of chronic enteritis. Therefore, this study indicates that peroxynitrite may mediate the inhibition of ASCT1 and B0AT1 during inflammation, when OONO levels are known to be elevated in the mucosa.


2021 ◽  
Vol 17 (2) ◽  
pp. e1009290
Author(s):  
Alyson R. Warr ◽  
Carole J. Kuehl ◽  
Matthew K. Waldor

Enterohemorrhagic Escherichia coli (EHEC) is a food-borne pathogen that causes diarrheal disease and the potentially lethal hemolytic uremic syndrome. We used an infant rabbit model of EHEC infection that recapitulates many aspects of human intestinal disease to comprehensively assess colonic transcriptional responses to this pathogen. Cellular compartment-specific RNA-sequencing of intestinal tissue from animals infected with EHEC strains containing or lacking Shiga toxins (Stx) revealed that EHEC infection elicits a robust response that is dramatically shaped by Stx, particularly in epithelial cells. Many of the differences in the transcriptional responses elicited by these strains were in genes involved in immune signaling pathways, such as IL23A, and coagulation, including F3, the gene encoding Tissue Factor. RNA FISH confirmed that these elevated transcripts were found almost exclusively in epithelial cells. Collectively, these findings suggest that Stx potently remodels the host innate immune response to EHEC.


Molecules ◽  
2020 ◽  
Vol 25 (21) ◽  
pp. 4897
Author(s):  
Jiaxin Liu ◽  
Lifu Luo ◽  
Fei Xu ◽  
Ge Li ◽  
Jicong Chen ◽  
...  

Vascular endothelial growth factor (VEGF) expression increased significantly in the pathogenesis of age-related macular degeneration, which induced the formation of pathological blood vessels. Dexamethasone is an exogenous anti-angiogenic drug while bevacizumab is an endogenous anti-angiogenic drug. They both have been widely used in ophthalmology. However, independent administration is not enough to completely block the development of choroidal neovascularization (CNV), and the number of eyes vitreous injections is limited. Reasonable combination of drugs may produce significantly better therapeutic effect than single drug treatment. The cyclic RGD (cRGD) peptide has a particularly high affinity with retinal pigment epithelial cells, where VEGF secretes from. In this study, we prepared nanoparticles of bevacizumab and dexamethasone with cRGD peptide as the target (aBev/cRGD-DPPNs). The particle size of the aBev/cRGD-DPPNs was 213.8 ± 1.5 nm, SEM results showed that the nano-carriers were well dispersed and spherical. The cell uptake study demonstrated the selectivity of the aBev/cRGD-DPPN to ARPE-19 with αVβ3 over expressed. The aBev/cRGD-DPPNs had a better apoptosis induction effect and an obvious inhibitory effect on migration, invasion, and capillary-like structures formation of human umbilical vein epithelial cells. The fluorescein fundus angiography study, immunohistochemistry and histopathological evaluation showed the aBev/cRGD-DPPNs greatly reduced the development of CNV on a rabbit model.


1969 ◽  
Vol 43 (1-2) ◽  
pp. 69-78 ◽  
Author(s):  
R. K. Kaushik ◽  
V. P. Sharma Deorani

1. In primary infections of chicks with 300 or 600 H. gallinae infective eggs, no clinical signs were apparent. Nodules were absent in all the experimental chicks as well as controls. Microscopically, few juveniles were observed in the caecal mucosa and the usual changes were mild congestion, few haemorrhages, and desquamation of superficial lining epithelial cells. Sections through a few thickened areas revealed a breached muscularis mucosa through which proliferated mucosal tissue had just invaginated into submucosa. The liver showed no changes.2. With primary infection of chicks with 300 or 600 infective H. gallinae eggs, and their subsequent infection after 25 days with 1,000 infective eggs, there were no clinical signs after either primary or secondary infections. Nodules of varying sizes were present on the caecal wall of infected birds only, their size and number varying with age of infection. Histopathologically, the types of nodules observed were, one associated with juveniles and the other with their absence; and nodules were present both in the invaginated mucosa and in the submucosa. It was confirmed that these caecal nodules were due to irritation by H. gallinae juveniles and their metabbolites, and that these nodules were more a reaction of already sensitised caeca to subsequent infections, a fact hitherto unreported. The liver showed nothing abnormal, and there was not much difference between the haematological values of experimental and control chicks.3. The actual process of formation of caecal nodules is demonstrated for the first time. The feasible explanation seems to be that on irritation of the already sensitised caeca by H. gallinae juveniles and their metabolites, hyperplasia of lymphoid tissue and epithelial cells results, which leads to a breach of the muscularis mucosa through which proliferated tissue of the mucosa invaginates. Later the muscularis mucosa constricts off and closes the nodule, the mucosa over it regenerates and becomes continuous. The present observations also indicate that the sterile nodular lesions usually found in natural infections may be the result of frequent infections, thus sensitising the chicks to subsequent infections.


2020 ◽  
Author(s):  
Alyson R. Warr ◽  
Carole J. Kuehl ◽  
Matthew K. Waldor

AbstractEnterohemorrhagic Escherichia coli (EHEC) is a food-borne pathogen that causes diarrheal disease and the potentially lethal hemolytic uremic syndrome. We used an infant rabbit model of EHEC infection that recapitulates many aspects of human intestinal disease to comprehensively assess colonic transcriptional responses to this pathogen. Cellular compartment-specific RNA-sequencing of intestinal tissue from animals infected with EHEC strains containing or lacking Shiga toxins (Stx) revealed that EHEC infection elicits a robust response that is dramatically shaped by Stx, particularly in epithelial cells. Many of the differences in the transcriptional responses elicited by these strains were in genes involved in immune signaling pathways, such as IL23A, and coagulation, including F3, the gene encoding Tissue Factor. RNA FISH confirmed that these elevated transcripts were found almost exclusively in epithelial cells. Collectively, these findings suggest that within the intestine, Stx primarily targets epithelial cells, and that the potent Stx-mediated modulation of innate immune signaling skews the host response to EHEC towards type 3 immunity.Significance StatementEnterohemorrhagic Escherichia coli (EHEC) is a potentially lethal foodborne pathogen. During infection, EHEC releases a potent toxin, Shiga toxin (Stx), into the intestine, but there is limited knowledge of how this toxin shapes the host response to infection. We used an infant rabbit model of infection that closely mimics human disease to profile intestinal transcriptomic responses to EHEC infection. Comparisons of the transcriptional responses to infection by strains containing or lacking Stx revealed that this toxin markedly remodels how the epithelial cell compartment responds to infection. Our findings suggest that Stx biases the intestinal innate immune response to EHEC and provide insight into the complex host-pathogen dialogue that underlies disease.


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