Regulation of interleukin-8 production in a human colon epithelial cell line (HT-29)

Groß, Volker; Andus, Tilo; Daig, R; Aschenbrenner, E; Schölmerich, Jürgen; Falk, Werner

doi:10.1016/0016-5085(95)90436-0

Cited by 68 publications

(54 citation statements)

References 48 publications

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“…While the inflammatory cytokines TNF-␣, IL-1␤, IL-6 and IL-8 are mainly macrophage products, epithelial cells in the large intestine have also been reported to produce IL-1␤, IL-6 and IL-8 [25][26][27]. Our study showed that cytokine reductions associated with lesion inhibition involved IL-1␤ and IL-8, but not TNF-␣.…”

Section: Discussionmentioning

confidence: 47%

Prostaglandin E₂ Inhibits Lesion Formation in Dextran Sodium Sulphate‐Induced Colitis in Rats and Reduces the Levels of Mucosal Inflammatory Cytokines

et al. 2000

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Effects of rectally injected prostaglandin E2 (PGE2) in rats with dextran sodium sulphate (DSS)‐induced colitis were investigated in terms of histopathology, local myeloperoxidase (MPO) activity, local mRNA expression of interleukin‐1β (IL‐1β), tumour necrosis factor‐α (TNF‐α) and growth‐regulated gene produced/cytokine‐induced neutrophil chemoattractant (GRO/CINC)‐1, and secretion of TNF‐α and GRO/CINC‐1. In animals with no PGE2 treatment, DSS‐induced erosion and ulceration were particularly severe in the rectum and extended to the proximal colon. Neutrophil infiltration was characteristically present in the lesions and surrounding mucosa. MPO activity at lesion sites was increased. IL‐1β and GRO/CINC‐1 mRNA expression was increased, while TNF‐α mRNA expression was significantly decreased. GRO/CINC‐1 secretion was increased but a similar elevation of TNF‐α was not detected. In the PGE2‐treated group, lesion formation was inhibited grossly and microscopically. Neutrophil infiltration and MPO activity in and around lesions were lessened. The reduction in TNF‐α mRNA expression and secretion was not affected by PGE2. The expression of mRNA for IL‐1β and GRO/CINC‐1 was reduced, as was the secretion of GRO/CINC‐1. As mRNA expression and secretion of cytokines in lesions of non‐PGE2‐treated animals was similar to that reported in human ulcerative colitis, rectal injection of PGE2 may prove to be an effective therapy.

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Section: Discussionmentioning

confidence: 47%

Prostaglandin E₂ Inhibits Lesion Formation in Dextran Sodium Sulphate‐Induced Colitis in Rats and Reduces the Levels of Mucosal Inflammatory Cytokines

et al. 2000

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“…Previous studies have examined the signaling cascades triggered by proinflammatory stimuli (e.g., IL-1␤, TNF-␣) in intestinal epithelial cells (3,15,24). A common effector of these pathways is the transcription factor NF-B, a pleiotropic transcription factor that controls the expression of multiple genes involved in the inflammatory response, including IL-8 (24), ICAM-1 (23), and inducible nitric oxide synthase (37).…”

Section: Discussionmentioning

confidence: 99%

“…We selected IL-8 as a marker of NF-B activation and enterocyte proinflammatory secretion because of its important role in neutrophil recruitment and inflammation (41). Intestinal epithelial cells have been shown to secrete IL-8 in response to bacterial (13) and viral invasion (48), lipopolysaccharide (12), cytokines (12), and phorbol esters (15). Furthermore, IL-8 is elevated in the context of various intestinal pathologies including Crohn's disease, ulcerative colitis, and possibly intestinal neoplasia (12,41).…”

Section: Discussionmentioning

confidence: 99%

MAP kinases contribute to IL-8 secretion by intestinal epithelial cells via a posttranscriptional mechanism

Jijon

Panenka

Madsen

et al. 2002

American Journal of Physiology-Cell Physiology

122

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The intracellular pathways that regulate intestinal epithelial gene expression are poorly understood. In this study we examined the roles of extracellular signal-regulated kinase (ERK) and p38 in the expression of interleukin-8 (IL-8) and intercellular adhesion molecule-1 (ICAM-1) using the human intestinal cell line HT-29. HT-29 cells were treated with tumor necrosis factor-α (TNF-α) in the presence or absence of ERK and p38 pathway inhibitors. TNF-α treatment resulted in increased IL-8 and ICAM-1 protein and mRNA synthesis, increased ERK and p38 activity, and activation of the transcription factors activator protein-1 (AP-1) and nuclear factor-κB (NF-κB). Inhibition of the ERK and p38 pathways attenuated IL-8 secretion but did not alter ICAM-1 expression. Furthermore, AP-1 and NF-κB DNA binding was not affected by ERK and p38 inhibition. In contrast, ERK and p38 inhibition resulted in the accelerated degradation of the IL-8 mRNA, suggesting that in HT-29 cells, p38 and ERK contribute to TNF-α-stimulated IL-8 secretion by intestinal epithelial cells via a posttranscriptional mechanism that involves stabilization of the IL-8 transcript.

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“…It has recently been shown that some TNFx-mediated responses in endothelial cells and colonic epithelial cells involve tyrosine phosphorylation (van Hinsbergh et al, 1994;Gross et al, 1995;Weber et al, 1995). Although phosphorylation of proteins on tyrosine constitutes less than 0.01% of total intracellular phosphorylation this process may be the primary or exclusive indicator of signal transduction in multicellular orBridsh Joumal of Pharmacology (1996Pharmacology ( ) 119, 1149Pharmacology ( -1158 A. Burke-Gaffney & P.G.…”

Section: Introductionmentioning

confidence: 99%

Tumour necrosis factor‐α‐induced ICAM‐1 expression in human vascular endothelial and lung epithelial cells: modulation by tyrosine kinase inhibitors

Burke‐Gaffney

Hellewell

1996

British J Pharmacology

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Tumour necrosis factor‐α (TNFα) increases the expression of the adhesion molecule intercellular adhesion molecule‐1 (ICAM‐1) on cultured endothelial and epithelial cells and modulation of this may be important in controlling inflammation. Activation of tyrosine kinase(s) is known to be involved in the signal transduction pathways of many cytokines. In this study we have investigated the effects of the tyrosine kinase inhibitors, ST638, tyrphostin AG 1288 and genistein, on TNFα‐induced ICAM‐1 expression in human alveolar epithelial (A549) and vascular endothelial (EAhy926) cell lines and also normal human lung microvascular endothelial cells (HLMVEC). ICAM‐1 expression on cultured cells was determined by a sensitive enzyme‐linked immunosorbant assay (ELISA). Endothelial or epithelial monolayers were exposed to increasing doses of TNF‐α (0.01–10 ng ml−1), in the presence or absence of either ST638 (3–100 μm), AG 1288 (3–100 μm) or genistein (100 μm) and ICAM‐1 expression was measured at 4 and 24 h. Control experiments examined the effect of ST638 on phorbol 12‐myristate 13‐acetate (PMA, 20 ng ml−1, 4 h)‐stimulated ICAM‐1 and compared it to that of a specific protein kinase C inhibitor, Ro31‐8220 (10 μm). Also, functional consequences of changes in ICAM‐1 expression were assessed by measuring adhesion of 111In‐labelled human neutrophils to EAhy926 endothelial and A549 epithelial monolayers treated with TNFα, in the presence or absence of ST638. ST638 caused a concentration‐dependent reduction in TNFα‐ (0.1–10 ng ml−1‐induced ICAM‐1 on EAhy926 endothelial (at 4 h) and A549 epithelial monolayers (at 4 and 24 h). In contrast, ST638 caused a concentration‐dependent increase in TNFα‐ (0.1–10 ng ml−1‐induced ICAM‐1 on EAhy926 endothelial cells at 24 h. Similar effects were seen with AG 1288 or genistein. ST638 (100 μm) significantly (P < 0.01) inhibited ICAM‐1 expression on HLMVEC endothelial cells induced by 0.01 ng ml−1 TNFα at 4 or 24 h or 0.1 ng ml−1 at 4 h, but increased ICAM‐1 expression induced by 0.1 ng ml−1 TNFα at 24 h. ST638 did not significantly change the expression of PMA‐stimulated ICAM‐1 on either A549 epithelial, EAhy926 or HLMVEC endothelial cells. However, PMA‐induced ICAM‐1 expression was inhibited by Ro31‐8220. Also, treatment of epithelial or endothelial monolayers with TNFα and ST638 altered adhesion of human neutrophils to A549 epithelial or EAhy926 endothelial cells in a manner that corresponded to the alteration in ICAM‐1 expression. These results show that tyrosine kinase inhibitors alter TNFα‐induced ICAM‐1 expression, but that the cell type, concentration of TNFα and time of exposure to this cytokine determine whether expression is decreased or increased by the inhibitor. An increased understanding of the signal transduction pathway(s) involved in TNFα‐induced ICAM‐1 expression on lung epithelial and vascular endothelial cells may be of potential therapeutic value in the treatment of inflammatory disease.

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Regulation of interleukin-8 production in a human colon epithelial cell line (HT-29)

Cited by 68 publications

References 48 publications

Prostaglandin E₂ Inhibits Lesion Formation in Dextran Sodium Sulphate‐Induced Colitis in Rats and Reduces the Levels of Mucosal Inflammatory Cytokines

Prostaglandin E₂ Inhibits Lesion Formation in Dextran Sodium Sulphate‐Induced Colitis in Rats and Reduces the Levels of Mucosal Inflammatory Cytokines

MAP kinases contribute to IL-8 secretion by intestinal epithelial cells via a posttranscriptional mechanism

Tumour necrosis factor‐α‐induced ICAM‐1 expression in human vascular endothelial and lung epithelial cells: modulation by tyrosine kinase inhibitors

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Regulation of interleukin-8 production in a human colon epithelial cell line (HT-29)

Cited by 68 publications

References 48 publications

Prostaglandin E2 Inhibits Lesion Formation in Dextran Sodium Sulphate‐Induced Colitis in Rats and Reduces the Levels of Mucosal Inflammatory Cytokines

Prostaglandin E2 Inhibits Lesion Formation in Dextran Sodium Sulphate‐Induced Colitis in Rats and Reduces the Levels of Mucosal Inflammatory Cytokines

MAP kinases contribute to IL-8 secretion by intestinal epithelial cells via a posttranscriptional mechanism

Tumour necrosis factor‐α‐induced ICAM‐1 expression in human vascular endothelial and lung epithelial cells: modulation by tyrosine kinase inhibitors

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Prostaglandin E₂ Inhibits Lesion Formation in Dextran Sodium Sulphate‐Induced Colitis in Rats and Reduces the Levels of Mucosal Inflammatory Cytokines

Prostaglandin E₂ Inhibits Lesion Formation in Dextran Sodium Sulphate‐Induced Colitis in Rats and Reduces the Levels of Mucosal Inflammatory Cytokines