olayers. The results showed strong antigenicity of the OVA in the super natant collected from the Transwell basal chambers. Our previous studies indicate that upon selleck chemicals the epithelial barrier dysfunction, a large quantity of macromolecular antigens can be transported into the deep region of the intestinal mucosa. Consequently, an intestinal allergy may be induced. It is suggested by previous studies that multiple factors are involved in the regula tion of the degradation of the endocytic proteins in epithe lial cells, such as ubiquitin editing enzyme A20 is required in the endosome lysosome fusion, which can be disturbed by inhibition of A20 resulting in incompletely degradation of the endocytic antigens. Inhibition of myosin by tumor necrosis factor also induces intestinal epithelial bar rier dysfunction.
Our data have added one more fac tor to the knowledge pool of epithelial barrier studies by showing evidence that Alix is required in maintaining epi thelial barrier function. It is noteworthy that exposure to SEB in the culture does not affect the TER as shown by the present data. The results implicate that the paracellular pathway is not influ enced by SEB. The results are in line with previous studies. Lu et al indicate that SEB can activate monocytes to re lease proinflammatory cytokines to increase epithelial bar rier permeability, but exposure to SEB alone does not affect TER, such an abnormality may be prevented by the addition of transforming growth factor B2. Our data indicate that the over expression of Alix also has the inhibitory effect on SEB induced epithelial barrier dys function.
Previous studies suggest that SEB facilitates the development of intestinal allergy via modulating dendritic cell properties or act as an adjuvant. The present data provide novel information that SEB also compro mises the transcellular antigen transport in the epithelial barrier. Conclusions The present data show that human intestinal epithelial cell line, T84 cells, expresses Alix, which can be inhib ited by SEB to induce epithelial barrier dysfunction. Over expression of Alix has the potential to attenuate the abnormally high epithelial barrier permeability. MicroRNAs are small non coding RNAs with the length Brefeldin_A of 21 to 25 nucleotides that posttranscrip tionally regulate the expression of target genes, and play important roles in various biological processes, including development, differentiation, proliferation, and apoptosis.
Several studies have suggested that alterations of their expression may paly a role in the regulation of the cellular response to hypoxia. Hypoxia availability affects cells and tissues during enough nor mal embryonic development and pathological conditions such as myocardial infarction, inflammation and tumori genesis. Hypoxia inducible factor 1 is recognized as the master transcription factor consisting of a constitu tively expressed HIF 1B subunit and an oxygen regulated HIF 1 subunit in response to hypoxia. In normoxia, HIF 1 is maintain