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Intestinal epithelial suppressor of cytokine signaling 3 enhances microbial-induced inflammatory tumor necrosis factor-α, contributing to epithelial barrier dysfunction.

Thagia I, Shaw EJ, Smith E, Else KJ, Rigby RJ - Am. J. Physiol. Gastrointest. Liver Physiol. (2014)

Bottom Line: Activation of TLR5 signaling pathways, compared with other TLR, increases TNF-α mRNA in a dose-dependent manner and SOCS3 enhances TLR5-induced TNF-α.We also show that flagellin promotes transcription of TNFR2 and that SOCS3 limits this expression, presenting a mechanism of SOCS3 action.Our data also support the role of microbial ligands in epithelial wound healing and suggest that a functional consequence of increased TNF-α is reduced wound healing.

View Article: PubMed Central - PubMed

Affiliation: Division of Biomedical and Life Sciences, Faculty of Health and Medicine, Lancaster University, Lancaster, UK; and.

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TNFR2 was rapidly downregulated following flagellin treatment. Protein expression levels returned to baseline by 12 h posttreatment. A: representative photomicrographs of TNFR2 following flagellin treatment. Immunocytochemistry of IEC, untreated and following 1, 2, 4, 6, or 12 h flagellin treatment (0.1 μg/ml). Green, TNFR2; red, propidium iodide. B: Western blot, confirming TNFR2 immunochemistry staining and depicting TNFR1 expression following varying time points of flagellin treatment.
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Figure 4: TNFR2 was rapidly downregulated following flagellin treatment. Protein expression levels returned to baseline by 12 h posttreatment. A: representative photomicrographs of TNFR2 following flagellin treatment. Immunocytochemistry of IEC, untreated and following 1, 2, 4, 6, or 12 h flagellin treatment (0.1 μg/ml). Green, TNFR2; red, propidium iodide. B: Western blot, confirming TNFR2 immunochemistry staining and depicting TNFR1 expression following varying time points of flagellin treatment.

Mentions: We performed immunocytochemistry and Western blots to assess how TLR5 stimulation impacted on IEC TNFR2 protein expression. TNFR2 expression appeared reduced within 1 h at the cell surface receptor level and was regained to baseline by 6 h after flagellin treatment (Fig. 4A). SOCS3 overexpression may delay TNFR2 return to baseline levels, but expression appeared equivalent to that of control cells 12 h following treatment. Flagellin did not appear to impact of TNFR1 expression (Fig. 4B).


Intestinal epithelial suppressor of cytokine signaling 3 enhances microbial-induced inflammatory tumor necrosis factor-α, contributing to epithelial barrier dysfunction.

Thagia I, Shaw EJ, Smith E, Else KJ, Rigby RJ - Am. J. Physiol. Gastrointest. Liver Physiol. (2014)

TNFR2 was rapidly downregulated following flagellin treatment. Protein expression levels returned to baseline by 12 h posttreatment. A: representative photomicrographs of TNFR2 following flagellin treatment. Immunocytochemistry of IEC, untreated and following 1, 2, 4, 6, or 12 h flagellin treatment (0.1 μg/ml). Green, TNFR2; red, propidium iodide. B: Western blot, confirming TNFR2 immunochemistry staining and depicting TNFR1 expression following varying time points of flagellin treatment.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4281689&req=5

Figure 4: TNFR2 was rapidly downregulated following flagellin treatment. Protein expression levels returned to baseline by 12 h posttreatment. A: representative photomicrographs of TNFR2 following flagellin treatment. Immunocytochemistry of IEC, untreated and following 1, 2, 4, 6, or 12 h flagellin treatment (0.1 μg/ml). Green, TNFR2; red, propidium iodide. B: Western blot, confirming TNFR2 immunochemistry staining and depicting TNFR1 expression following varying time points of flagellin treatment.
Mentions: We performed immunocytochemistry and Western blots to assess how TLR5 stimulation impacted on IEC TNFR2 protein expression. TNFR2 expression appeared reduced within 1 h at the cell surface receptor level and was regained to baseline by 6 h after flagellin treatment (Fig. 4A). SOCS3 overexpression may delay TNFR2 return to baseline levels, but expression appeared equivalent to that of control cells 12 h following treatment. Flagellin did not appear to impact of TNFR1 expression (Fig. 4B).

Bottom Line: Activation of TLR5 signaling pathways, compared with other TLR, increases TNF-α mRNA in a dose-dependent manner and SOCS3 enhances TLR5-induced TNF-α.We also show that flagellin promotes transcription of TNFR2 and that SOCS3 limits this expression, presenting a mechanism of SOCS3 action.Our data also support the role of microbial ligands in epithelial wound healing and suggest that a functional consequence of increased TNF-α is reduced wound healing.

View Article: PubMed Central - PubMed

Affiliation: Division of Biomedical and Life Sciences, Faculty of Health and Medicine, Lancaster University, Lancaster, UK; and.

Show MeSH
Related in: MedlinePlus