Interleukin 4 acts as an inducer of decay-accelerating factor gene expression in human intestinal epithelial cells

Andoh, Akira; Fujiyama, Yoshihide; Sumiyoshi, Kenichi; Sakumoto, Hitoshi; Bamba, Tadao

doi:10.1016/s0016-5085(96)70058-6

Cited by 49 publications

(45 citation statements)

References 4 publications

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“…As shown in Fig. 2A, DAF transcripts were detected as 2.2 and 1.6 kb in HT-29 cells, as reported previously (29,33). ITF induced a concentration-dependent increase in DAF mRNA abundance, and these effects reached a maximum at 10 M of ITF.…”

Section: Itf Stimulation Increases Daf Mrna Abundance In Ht-29 Cellssupporting

confidence: 87%

“…Northern blotting for human DAF gene was performed according to a method described previously (29). A probe specific for the human DAF gene also was prepared as described previously (29).…”

Section: Northern Blottingmentioning

confidence: 99%

“…Northern blotting for human DAF gene was performed according to a method described previously (29). A probe specific for the human DAF gene also was prepared as described previously (29). A probe for rat DAF gene was generated by RT-PCR with the following primers: 5Ј-AATGGTCACATCAACATACCAACT (511-534); and 3Ј-CGTTGG ATGACGTACCGTTGTCTT (1086 -1063) (14).…”

Section: Northern Blottingmentioning

confidence: 99%

“…Several factors have been reported to induce DAF expression in IECs; IL-4 and TNF-␣ strongly enhance DAF expression by HT-29 cells (29,33). However, the mechanisms regulating DAF expression by these factors vary.…”

Section: Itf Requires De Novo Protein Synthesis To Enhance Daf Expresmentioning

confidence: 99%

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Intestinal Trefoil Factor Induces Decay-Accelerating Factor Expression and Enhances the Protective Activities Against Complement Activation in Intestinal Epithelial Cells

Andoh

Kinoshita

Rosenberg

et al. 2001

The Journal of Immunology

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Mucosal damage induces a massive influx of serum complement components into the lumen. The epithelium produces a number of factors that can potentially ameliorate injury including intestinal trefoil factor (ITF), a small protease-resistant peptide produced and secreted onto the mucosal surface by goblet cells, and decay-accelerating factor (DAF), a protein produced by columnar epithelium which protects the host tissue from autologous complement injury. However, coordination of these intrinsic defensive products has not been delineated. DAF protein and mRNA expression were evaluated by immunoblotting and Northern blotting, respectively. NF-κB-DNA binding activity and DAF promoter activity were assessed by an electrophoretic gel mobility shift assay and a reporter gene luciferase assay, respectively. ITF induced a dose- and time-dependent increase in DAF protein and mRNA expression in human (HT-29 and T84) and rat (IEC-6) intestinal epithelial cells. In differentiated T84 cells grown on cell culture inserts, basolateral stimulation with ITF strongly enhanced DAF expression, but apical stimulation had no effects. The C3 deposition induced by complement activation was significantly blocked by the treatment with ITF. In HT-29 cells, ITF increased the stability of DAF mRNA. ITF also enhanced the promoter activity of the DAF gene via NF-κB motif and induced activation of NF-κB-DNA binding activity. ITF promotes protection of epithelial cells from complement activation via up-regulation of DAF expression, contributing to a robust mucosal defense.

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Section: Itf Stimulation Increases Daf Mrna Abundance In Ht-29 Cellssupporting

confidence: 87%

“…Northern blotting for human DAF gene was performed according to a method described previously (29). A probe specific for the human DAF gene also was prepared as described previously (29).…”

Section: Northern Blottingmentioning

confidence: 99%

Section: Northern Blottingmentioning

confidence: 99%

Section: Itf Requires De Novo Protein Synthesis To Enhance Daf Expresmentioning

confidence: 99%

See 2 more Smart Citations

Intestinal Trefoil Factor Induces Decay-Accelerating Factor Expression and Enhances the Protective Activities Against Complement Activation in Intestinal Epithelial Cells

Andoh

Kinoshita

Rosenberg

et al. 2001

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…Total cellular RNA was isolated by the acid guanidinium thiocyanate-phenol-chloroform method (8). Northern blots were performed according to a previously described method (2). Hybridizations were performed with 32 P-labeled human probes, generated by a random primed DNA labeling kit (Amersham, Arlington Heights, IL), and evaluated by autoradiography.…”

Section: Methodsmentioning

confidence: 99%

Phosphatidylinositol 3-kinase/Akt signaling mediates interleukin-32α induction in human pancreatic periacinar myofibroblasts

Nishida¹,

Andoh²,

Shioya³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Intestinal Lymphoepithelial Communication

Shanahan

1999

Mechanisms in the Pathogenesis of Enteric Diseases 2

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Interleukin 4 acts as an inducer of decay-accelerating factor gene expression in human intestinal epithelial cells

Cited by 49 publications

References 4 publications

Intestinal Trefoil Factor Induces Decay-Accelerating Factor Expression and Enhances the Protective Activities Against Complement Activation in Intestinal Epithelial Cells

Intestinal Trefoil Factor Induces Decay-Accelerating Factor Expression and Enhances the Protective Activities Against Complement Activation in Intestinal Epithelial Cells

Phosphatidylinositol 3-kinase/Akt signaling mediates interleukin-32α induction in human pancreatic periacinar myofibroblasts

Intestinal Lymphoepithelial Communication

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