Intestinal Production of Interleukin-1α during Endotoxemia in the Mouse

Mester, Marcelo; Tompkins, Ronald G.; Gelfand, Jeffrey A.; Dinarello, Charles A.; Burke, John F.; Clark, Burton D.

doi:10.1006/jsre.1993.1089

Cited by 64 publications

(31 citation statements)

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“…In this model, mice were challenged with endotoxin. Endotoxemia induces inflammatory processes in the intestine, including intestinal production of cytokines (8,9). Intraperitoneal administration of endotoxin to mice resulted in a significantly increased serum concentration of LBP (20.9 Ϯ 7.3 g/ml, p Ͻ 0.05) as compared with the controls (5.4 Ϯ 2.6 g/ml).…”

Section: The Lbp Content Of Mucus Is Enhanced During Endotoxemiamentioning

confidence: 98%

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Lipopolysaccharide-Binding Protein Is Vectorially Secreted and Transported by Cultured Intestinal Epithelial Cells and Is Present in the Intestinal Mucus of Mice

Vreugdenhil

Snoek

Greve

et al. 2000

The Journal of Immunology

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Lipopolysaccharide-binding protein (LBP) is an important modulator of the host’s response to endotoxin. In a previous study, we found evidence for the synthesis of LBP by intestinal epithelial cells. In this study, we explored the polarity of LBP secretion by these cells. Polarized monolayers of Caco-2 cells were used as intestinal mucosa model. Cells were stimulated apically or basally with cytokines, and LBP secretion was analyzed. Furthermore, the presence of LBP in intestinal mucus of healthy and endotoxemic mice was studied using a mucus-sampling technique. The constitutive unipolar LBP secretion from the apical cell surface was markedly enhanced when cells were exposed to cytokines at their apical surface. However, bioactive LBP was secreted from both cell surfaces after basolateral stimulation of cells. Cytokines also influenced the secretion of the acute phase proteins serum amyloid A, apoA-I, and apoB from both surfaces of Caco-2 cells. Furthermore, transport of exogenous LBP from the basolateral to the apical cell surface was demonstrated. In line with these in vitro data, the presence of LBP in intestinal mucus was strongly enhanced in mice after a challenge with endotoxin. The results indicate that LBP is present at the mucosal surface of the intestine, a phenomenon for which secretion and transport of LBP by intestinal epithelial cells may be responsible.

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Section: The Lbp Content Of Mucus Is Enhanced During Endotoxemiamentioning

confidence: 98%

“…Enhanced concentrations of these cytokines are present in the subepithelial tissue during inflammatory bowel diseases (7) and during systemic inflammation (8,9). This implicates that epithelial cells are exposed to cytokines at their basolateral cell surface.…”

mentioning

confidence: 96%

Lipopolysaccharide-Binding Protein Is Vectorially Secreted and Transported by Cultured Intestinal Epithelial Cells and Is Present in the Intestinal Mucus of Mice

Vreugdenhil

Snoek

Greve

et al. 2000

The Journal of Immunology

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“…ple, mucosal production of certain acute phase proteins (28,29,47,50) and cytokines (13,25,27,49) is increased in these conditions, and some of these substances may influence mucosal integrity and regulate intestinal permeability (15,51).…”

mentioning

confidence: 99%

Proteasome inhibitors induce heat shock response and increase IL-6 expression in human intestinal epithelial cells

Pritts

Hungness²,

Hershko

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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In previous studies, the heat shock response, induced by hyperthermia or sodium arsenite, increased interleukin (IL)-6 production in intestinal mucosa and cultured human enterocytes. A novel way to induce the heat shock response, documented in other cell types, is treatment with proteasome inhibitors. It is not known if proteasome inhibition induces heat shock in enterocytes or influences IL-6 production. Here we tested the hypothesis that treatment of cultured Caco-2 cells, a human intestinal epithelial cell line, with proteasome inhibitors induces the heat shock response and stimulates IL-6 production. Treatment of Caco-2 cells with one of the proteasome inhibitors MG-132 or lactacystin activated the transcription factor heat shock factors (HSF)-1 and -2 and upregulated cellular levels of the 72-kDa heat shock protein HSP-72. The same treatment resulted in increased gene and protein expression of IL-6, a response that was blocked by quercetin. Additional experiments revealed that the IL-6 gene promoter contains a HSF-responsive element and that the IL-6 gene may be regulated by the heat shock response. The present results suggest that proteasome inhibition induces heat shock response and IL-6 production in enterocytes and that IL-6 may be a heat shock-responsive gene, at least under certain circumstances. The observations are important considering the multiple biological roles of IL-6, both locally in the gut mucosa and systemically, and considering recent proposals in the literature to use proteasome inhibitors in the clinical setting to induce the heat shock response.

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“…A similar mechanism may be responsible for the observed decrease in the Na/ K-ATPase along with the enhanced activity of TNF-α and IL-6 of the present study, in etoposide treated rats. Furthermore, the level of TNF α indicates the extent of inflammation [24]. Recent studies have suggested that the biological effects of TNF α are caused by direct actions on multiple target tissues and the induction of other cytokines, such as IL 1, IL 6 and IL 8 [34].…”

Section: Discussionmentioning

confidence: 99%

“…Results of earlier studies also suggest that the production of proinflammatory cytokines is increased in the local gut mucosa of mice with endotoxemia or sepsis [3,24] and that the intestine might be a significant source of tissue TNF-alpha during stress [10]. Therefore, this study was designed to assess the effect of Spondias pinnata on etoposide induced intestinal mucositis in rat model.…”

Section: Introductionmentioning

confidence: 99%

oral-ingestion-of-spondias-pinnata-bark-extract-trim-down-severity-of-small-intestinal-mucositis

C¹,

Shetty²,

Rao³

2015

J Cancer Sci Ther

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Intestinal Production of Interleukin-1α during Endotoxemia in the Mouse

Cited by 64 publications

References 0 publications

Lipopolysaccharide-Binding Protein Is Vectorially Secreted and Transported by Cultured Intestinal Epithelial Cells and Is Present in the Intestinal Mucus of Mice

Lipopolysaccharide-Binding Protein Is Vectorially Secreted and Transported by Cultured Intestinal Epithelial Cells and Is Present in the Intestinal Mucus of Mice

Proteasome inhibitors induce heat shock response and increase IL-6 expression in human intestinal epithelial cells

oral-ingestion-of-spondias-pinnata-bark-extract-trim-down-severity-of-small-intestinal-mucositis

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