Transforming growth factor-β enhances secretory component and major histocompatibility complex class I antigen expression on rat IEC-6 intestinal epithelial cells

Cytokine ◽  
1991 ◽  
Vol 3 (6) ◽  
pp. 543-550 ◽  
Author(s):  
Dennis W. McGee ◽  
Wilhelm K. Aicher ◽  
John H. Eldridge ◽  
Jane V. Peppard ◽  
Jiri Mestecky ◽  
...  
2008 ◽  
Vol 99 (3) ◽  
pp. 449-454 ◽  
Author(s):  
Wai Ling Chow ◽  
Yuan Kun Lee

Fucose is present in foods, and it is a major component of human mucin glycoproteins and glycolipids.l-Fucose can also be found at the terminal position of many cell-surface oligosaccharide ligands that mediate cell-recognition and adhesion-signalling pathways. Mucin fucose can be released through the hydrolytic activity of pathogens and indigenous bacteria, leading to the release of free fucose into the intestinal lumen. The immunomodulating effects of free fucose on intestinal epithelial cells (enterocyte-like Caco-2) were investigated. It was found that the presence ofl-fucose up regulated genes and secretion of their encoded proteins that are involved in both the innate and adaptive immune responses, possibly via the toll-like receptor-2 signalling pathway. These include TNFSF5, TNFSF7, TNF-α, IL12, IL17 and IL18.Besides modulating immune reactions in differentiated Caco-2 cells, fucose induced a set of cytokine genes that are involved in the development and proliferation of immune cells. These include the bone morphogenetic proteins (BMP) BMP2, BMP4, IL5, thrombopoietin and erythropoietin. In addition, the up regulated gene expression of fibroblast growth factor-2 may help to promote epithelial cell restitution in conjunction with the enhanced expression of transforming growth factor-β mRNA. Since the exogenous fucose was not metabolised by the differentiated Caco-2 cells as a carbon source, the reactions elicited were suggested to be a result of the direct interaction of fucose and differentiated Caco-2 cells. The presence of free fucose may signal the invasion of mucin-hydrolysing microbial cells and breakage of the mucosal barrier. The intestinal epithelial cells respond by up regulation and secretion of cytokines, pre-empting the actual invasion of pathogens.


2001 ◽  
Vol 69 (4) ◽  
pp. 2589-2595 ◽  
Author(s):  
R. E. Lyons ◽  
J. P. Anthony ◽  
D. J. P. Ferguson ◽  
N. Byrne ◽  
J. Alexander ◽  
...  

ABSTRACT A murine model was used to characterize the local immune and inflammatory response during ocular toxoplasmosis. Major histocompatibility complex (MHC) class I, normally expressed at low levels in immune-privileged sites such as the eye, was up-regulated during infection as determined by competitive reverse transcriptase (RT)-PCR and immunocytochemistry for both β2-microglobulin and the MHC class I heavy chain. However, the eyes of chronically infected mice also had increased levels of mRNA transcripts for transforming growth factor β, a cytokine associated with immune privilege and constitutively expressed in normal eyes. Transcripts for a number of inflammatory mediators, including interleukin-6 (IL-6), were increased during chronic infection. The role of IL-6 was further investigated by comparing disease progression and the development of the local immune response in wild-type (WT) and IL-6-deficient mice (IL-6−/− mice). Following infection, IL-6−/− mice developed more severe inflammation in the retina and vitreous humor compared with WT mice. This increased severity of disease was associated with reduced ocular IL-1α and increased tumor necrosis factor α mRNA production compared with WT mice. Moreover, the increased severity of disease in IL-6−/− mice correlated with increased eye parasite burden as determined by RT-PCR for the Toxoplasma gondiibradyzoite-specific LDH2 gene. These results demonstrate alterations to components of immune privilege as a result of ocular toxoplasmosis and a role for IL-6 in controlling parasite numbers and inflammation in the eye.


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