Monocyte Chemoattractant Protein-1 Production by Intestinal Epithelial Cells<i>In Vitro:</i>A Role for p38 in Epithelial Chemokine Expression

Waterhouse, Christopher C. M.; Joseph, Robbie R.; Winsor, Geoffrey L.; Lacombe, Tyler A.; Stadnyk, Andrew W.

doi:10.1089/107999001750169853

Cited by 19 publications

(6 citation statements)

References 28 publications

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“…Stimulation of IEC by LPS has been shown to activate MAP kinase and NF-κB [19,37]. Involvement of tyrosine kinase has been demonstrated by blockade of LPS-mediated MCP-1 release [38]. Blockade of G protein mediated p38 MAP kinase activation decreased LPS-stimulated IL-8 secretion in the present study, and abrogation of IL-8 release was obtained by inhibition of phosphatidylinositol-3′ kinase.…”

Section: Discussionsupporting

confidence: 59%

Responsiveness of intestinal epithelial cell lines to lipopolysaccharide is correlated with Toll-like receptor 4 but not Toll-like receptor 2 or CD14 expression

Böcker

Yezerskyy

Feick

et al. 2003

International Journal of Colorectal Disease

112

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Section: Discussionsupporting

confidence: 59%

Responsiveness of intestinal epithelial cell lines to lipopolysaccharide is correlated with Toll-like receptor 4 but not Toll-like receptor 2 or CD14 expression

Böcker

Yezerskyy

Feick

et al. 2003

International Journal of Colorectal Disease

112

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“…MCP-1 is a chemoattractant for lymphocytes, monocytes, and macrophages and can stimulate macrophages to undergo respiratory burst activ- (21) and Clostridium difficile A toxin (22). MCP-1 expression is regulated in part by the mitogen-activated protein kinase p38 (43). Ricin activates p38 mitogen-activated protein kinase in a variety of cell types, including human monocytes/ macrophages and intestinal epithelial cells (8,12,23).…”

Section: Resultsmentioning

confidence: 99%

Evidence for Widespread Epithelial Damage and Coincident Production of Monocyte Chemotactic Protein 1 in a Murine Model of Intestinal Ricin Intoxication

2007

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The development of small-animal models is necessary to understand host responses and immunity to emerging infectious diseases and potential bioterrorism agents. In this report we have characterized a murine model of intestinal ricin intoxication. Ricin administered intragastrically (i.g.) to BALB/c mice at doses ranging from 1 to 10 mg/kg of body weight induced dose-dependent morphological changes in the proximal small intestine (i.e., duodenum), including widespread villus atrophy and epithelial damage. Coincident with epithelial damage was a localized increase in monocyte chemotactic protein 1, a chemokine known to be associated with inflammation of the intestinal mucosa. Immunity to intestinal ricin intoxication was achieved by immunizing mice i.g. with ricin toxoid and correlated with elevated levels of antitoxin mucosal immunoglobulin A (IgA) and serum IgG antibodies. We expect that this model will serve as a valuable tool in identifying the inflammatory pathways and protective immune responses that are elicited in the intestinal mucosa following ricin exposure and will prove useful in the evaluation of antitoxin vaccines and therapeutics.The development and testing of effective vaccines and therapeutics against potential bioterrorism agents pose major challenges to the biomedical scientific community (2). Foremost is the fact that human exposure to these so-called select agents is rare and often is poorly documented in the clinic. Consequently, an understanding of the molecular basis of both pathophysiology of and protective immunity to this diverse collection of viruses, microbial pathogens, and toxins must rely on the use of well-established animal models. This is especially true in the case of ricin toxin, a potent ribosome-inactivating protein from the castor bean (Ricinus communis) that has already proven to be an effective murder weapon and bioterrorism agent (25).While ricin (ϳ64 kDa) is one of the simplest members of the A-B family of toxins, it is also one of the most promiscuous (32, 37). The toxin's single A subunit (RTA) is an N-glycosidase that selectively depurinates a conserved adenine residue within 28S rRNA and in this respect is indistinguishable from shiga toxin (11). The toxin's B subunit (RTB) is a bivalent lectin that mediates toxin attachment to terminal galactose residues on glycoproteins and glycolipids (4). The ubiquitous nature of ricin's receptors, combined with its universally conserved enzymatic substrate, enables ricin to intoxicate virtually all known cell types. Not surprisingly, ricin can be lethal to humans following injection, inhalation, or ingestion (3,6,26).Although a recent expert panel workshop sponsored by the National Institutes of Health deemed the adulteration of food and water supplies to be the most likely mechanism by which ricin would be disseminated as a bioterrorism agent, very little is known about the effects of ricin on the gastrointestinal mucosa (1). Ingestion of whole castor beans results in severe abdominal pain, vomiting, diarrhea, and (depending o...

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“…Therefore, we next determined the effect of culturing the IEC-18 cells with both TGF-[31 and IL-1[3. A dose of 1 ng/ml IL-113 was used because this level has been previously shown to induce maximal secretion of MCP-1 by IEC-18 cells (Waterhouse et al, 2001). Cuhure of the IEC-18 cells with 10 ng/ml TGF-[31 and 1 nghnl IL-I[3 resulted in a significant (P < 0.05) increase in MCP-1 secretion as compared with cells cultured with IL-I[3 alone (Fig.…”

Section: Effect Of Tgf-fll On Mcp-1 Secretion By Epithelial Cell Linesmentioning

confidence: 93%

Transforming growth factor-β1 enhances the secretion of monocyte chemoattractant protein-1 by the IEC-18 intestinal epithelial cell line

Magida

McGee

2003

In Vitro Cell.Dev.Biol.-Animal

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Intestinal epithelial cells (IEC) are known to produce monocyte chemoattractant protein-1 (MCP-1). However, MCP-1 production, as with many other cytokines, can be regulated by a network of cytokines present in the environment of the IEC. Both IEC and inflammatory cells have been shown to produce transforming growth factor-beta (TGF-beta), and the regulatory effect of this cytokine on MCP-1 secretion by IEC has not been determined. Using the IEC-18 cell line, we have found that TGF-beta1 alone induced the secretion of high levels of MCP-1. Treatment with TGF-beta1 also enhanced the levels of MCP-1 messenger ribonucleic acid. However, costimulation of the cells with TGF-beta1 and interleukin-1beta (IL-1beta) resulted in significant, but less than additive, increases in MCP-1 secretion. Finally, the enhancing effect of TGF-beta1 on MCP-1 secretion was not due to IL-6. These results suggest that TGF-beta1 from IEC or inflammatory cells may significantly enhance the secretion of MCP-1 by IEC and play an important role in inflamed mucosal tissues.

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Monocyte Chemoattractant Protein-1 Production by Intestinal Epithelial CellsIn Vitro:A Role for p38 in Epithelial Chemokine Expression

Cited by 19 publications

References 28 publications

Responsiveness of intestinal epithelial cell lines to lipopolysaccharide is correlated with Toll-like receptor 4 but not Toll-like receptor 2 or CD14 expression

Responsiveness of intestinal epithelial cell lines to lipopolysaccharide is correlated with Toll-like receptor 4 but not Toll-like receptor 2 or CD14 expression

Evidence for Widespread Epithelial Damage and Coincident Production of Monocyte Chemotactic Protein 1 in a Murine Model of Intestinal Ricin Intoxication

Transforming growth factor-β1 enhances the secretion of monocyte chemoattractant protein-1 by the IEC-18 intestinal epithelial cell line

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