Direct secretory effect of interleukin-1 via type I receptors in human colonic mucous epithelial cells (HT29-C1.16E).

Jarry, Anne; Vallette, G.; Branka, Jean-Eric; Laboisse, Christian L.

doi:10.1136/gut.38.2.240

Cited by 24 publications

(23 citation statements)

References 8 publications

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“…Assuming that glucocorticoids decrease MPO activity [37] and the influx of inflammatory cells into the colon of TNBS rats [39], it is obvious that the changes in the local metabolism of corticosterone are not able to modulate granulocyte migration and activation. In contrast to our expectation, neither carbenoxolone nor budesonide suppressed MUC-2 expression even if colitis modulates MUC gene expression [40], and experiments performed with intestinal mucus-secreting cell lines showed modulation of transcript levels for various mucins by IL-1 and corticosteroids [41,42].…”

Section: Discussioncontrasting

confidence: 46%

Glucocorticoid Availability in Colonic Inflammation of Rat

et al. 2007

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Recent in vitro studies have shown the involvement of pro-inflammatory cytokines in the regulation of the local metabolism of glucocorticoids via 11beta-hydroxysteroid dehydrogenase type 1 and type 2 (11HSD1 and 11HSD2). However, direct in vivo evidence for a relationship among the local metabolism of glucocorticoids, inflammation and steroid enzymes is still lacking. We have therefore examined the changes in the local metabolism of glucocorticoids during colonic inflammation induced by TNBS and the consequences of corticosterone metabolism inhibition by carbenoxolone on 11HSD1, 11HSD2, cyclooxygenase 2 (COX-2), mucin 2 (MUC-2), tumor necrosis factor alpha (TNF-alpha), and interleukin 1beta (IL-1beta). The metabolism of glucocorticoids was measured in tissue slices in vitro and their 11HSD1, 11HSD2, COX-2, MUC-2, TNF-alpha, and IL-1beta mRNA abundances by quantitative reverse transcription-polymerase chain reaction. Colitis produced an up-regulation of colonic 11HSD1 and down-regulation of 11HSD2 in a dose-dependent manner, and these changes resulted in a decreased capacity of the inflamed tissue to inactivate tissue corticosterone. Similarly, 11HSD1 transcript was increased in colonic intraepithelial lymphocytes of TNBS-treated rats. Topical intracolonic application of carbenoxolone stimulated 11HSD1 mRNA and partially inhibited 11HSD2 mRNA and tissue corticosterone inactivation and these changes were blocked by RU-486. The administration of budesonide mimicked the effect of carbenoxolone. In contrast to the local metabolism of glucocorticoids, carbenoxolone neither potentiates nor diminishes gene expression for COX-2, TNF-alpha, and IL-1beta, despite the fact that budesonide down-regulated all of them. These data indicate that inflammation is associated with the down-regulation of tissue glucocorticoid catabolism. However, these changes in the local metabolism of glucocorticoids do not modulate the expression of COX-2, TNF-alpha, and IL-1beta in inflamed tissue.

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Section: Discussioncontrasting

confidence: 46%

Glucocorticoid Availability in Colonic Inflammation of Rat

et al. 2007

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“…For example, a study conducted by Marillier and colleagues demonstrated goblet cell hyperplasia is observed independent of the IL‐13/IL‐4 signalling apparatus,62 and Muc2 and Muc3 transcripts were augmented even in the absence of IL‐4 during T. spiralis infection 50. Furthermore, inflammatory cytokines have been implicated to have a role in goblet cell function during parasitic infection, including IL‐1, TNF and IL‐22,63, 64, 65 and it is yet to be defined if microbial factors, the inflammasome and adrenergic and cholinergic receptors can influence the secretion of mucins and other goblet cell‐associated products during parasitic invasion.…”

Section: Immune Control Against Gi Nematode Infectionmentioning

confidence: 99%

A sticky end for gastrointestinal helminths; the role of the mucus barrier

Sharpe

Thornton

Grencis

2018

Parasite Immunology

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SummaryGastrointestinal (GI) nematodes are a group of successful multicellular parasites that have evolved to coexist within the intestinal niche of multiple species. It is estimated that over 10% of the world's population are chronically infected by GI nematodes, making this group of parasitic nematodes a major burden to global health. Despite the large number of affected individuals, there are few effective treatments to eradicate these infections. Research into GI nematode infections has primarily focused on defining the immunological and pathological consequences on host protection. One important but neglected aspect of host protection is mucus, and the concept that mucus is just a simple barrier is no longer tenable. In fact, mucus is a highly regulated and dynamic‐secreted matrix, underpinned by a physical hydrated network of highly glycosylated mucins, which is increasingly recognized to have a key protective role against GI nematode infections. Unravelling the complex interplay between mucins, the underlying epithelium and immune cells during infection are a major challenge and are required to fully define the protective role of the mucus barrier. This review summarizes the current state of knowledge on mucins and the mucus barrier during GI nematode infections, with particular focus on murine models of infection.

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“…Receptors for the obesity associated hormone leptin are present in the colon, and activation of this receptor increases mucin and cytokine production (155–158). Pro-inflammatory stimuli such as cytokines also increase mucin production initially, likely as a defense mechanism (155, 159–162). Expression of mucin-encoding genes increases early in infection (163).…”

Section: Mucin Production Can Modulate Epithelial Exposures To Intestmentioning

confidence: 99%

Obesity-associated cancer risk: the role of intestinal microbiota in the etiology of the host proinflammatory state

Djurić

2017

Translational Research

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Obesity increases the risks of many cancers. One important mechanism behind this association is the obesity-associated pro-inflammatory state. Although the composition of the intestinal microbiome undoubtedly can contribute to the pro-inflammatory state, perhaps the most important aspect of host-microbiome interactions is host exposure to components of intestinal bacteria that stimulate the inflammatory reactions. Systemic exposures to intestinal bacteria can be modulated by dietary factors by altering both the composition of the intestinal microbiota as well as absorption of bacterial products from the intestinal lumen. In particular, high fat and high energy diets have been shown to facilitate absorption of bacterial lipopolysaccharide (LPS) from intestinal bacteria. Biomarkers of bacterial exposures that have been measured in blood include LPS-binding protein, sCD14, fatty acids characteristic of intestinal bacteria and immunoglobulins specific for bacterial LPS and flagellin. The optimal strategies to reduce these pro-inflammatory exposures, whether by altering diet composition, avoiding a positive energy balance or reducing adipose stores, likely differ in each individual. Biomarkers that assess systemic bacterial exposures therefore should be useful to optimize and personalize preventive approaches for individuals and groups with specific characteristics, and to gain insight into the possible mechanisms involved with different preventive approaches.

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Direct secretory effect of interleukin-1 via type I receptors in human colonic mucous epithelial cells (HT29-C1.16E).

Cited by 24 publications

References 8 publications

Glucocorticoid Availability in Colonic Inflammation of Rat

Glucocorticoid Availability in Colonic Inflammation of Rat

A sticky end for gastrointestinal helminths; the role of the mucus barrier

Obesity-associated cancer risk: the role of intestinal microbiota in the etiology of the host proinflammatory state

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