Exposure of intestinal epithelial cell HT29 to bile acids and ammonia enhances Mac-1-mediated neutrophil adhesion

Miyata, Ryukou; Iwabuchi, Kazuhisa; Watanabe, Sumio; Sato, Nobuhiro; Nagaoka, Isao

doi:10.1007/s000110050458

Cited by 7 publications

(3 citation statements)

References 32 publications

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“…For analysis of existing membrane-associated protein moieties, epithelial cells were pretreated with proteinase K (50 to 250 g/ml, 10 min at 37°C) (41) (Roche Corp., Mannheim, Germany) in a volume of 1 ml of PBS in the presence or absence of cycloheximide (for inhibition of de novo protein synthesis [1 to 100 g/ml, 60 min at 37°C]) (43). Initial concentrations of each reagent were based on published reports for other cells (1,25,41,43,49); additional concentrations were used when no effects were observed. Controls included epithelial cells incubated in PBS alone.…”

Section: Methodsmentioning

confidence: 99%

Potential Role for a Carbohydrate Moiety in Anti-CandidaActivity of Human Oral Epithelial Cells

et al. 2001

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Candida albicans is both a commensal and a pathogen at the oral mucosa. Although an intricate network of host defense mechanisms are expected for protection against oropharyngeal candidiasis, anti-Candida host defense mechanisms at the oral mucosa are poorly understood. Our laboratory recently showed that primary epithelial cells from human oral mucosa, as well as an oral epithelial cell line, inhibit the growth of blastoconidia and/or hyphal phases of several Candida species in vitro with a requirement for cell contact and with no demonstrable role for soluble factors. In the present study, we show that oral epithelial cell-mediated anti-Candida activity is resistant to gamma-irradiation and is not mediated by phagocytosis, nitric oxide, hydrogen peroxide, and superoxide oxidative inhibitory pathways or by nonoxidative components such as soluble defensin and calprotectin peptides. In contrast, epithelial cell-mediated anti-Candida activity was sensitive to heat, paraformaldehyde fixation, and detergents, but these treatments were accompanied by a significant loss in epithelial cell viability. Treatments that removed existing membrane protein or lipid moieties in the presence or absence of protein synthesis inhibitors had no effect on epithelial cell inhibitory activity. In contrast, the epithelial cell-mediated anti-Candida activity was abrogated after treatment of the epithelial cells with periodic acid, suggesting a role for carbohydrates. Adherence of C. albicans to oral epithelial cells was unaffected, indicating that the carbohydrate moiety is exclusively associated with the growth inhibition activity. Subsequent studies that evaluated specific membrane carbohydrate moieties, however, showed no role for sulfated polysaccharides, sialic acid residues, or glucose-and mannose-containing carbohydrates. These results suggest that oral epithelial cell-mediated anti-Candida activity occurs exclusively with viable epithelial cells through contact with C. albicans by an as-yet-undefined carbohydrate moiety.

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Section: Methodsmentioning

confidence: 99%

Potential Role for a Carbohydrate Moiety in Anti-CandidaActivity of Human Oral Epithelial Cells

et al. 2001

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“…They activate mast cells, causing their degranulation and the release of mediators (eg, histamine) [40], which then act either directly on epithelial cells or indirectly through recruitment of the enteric nervous system to promote ion and fl uid secretion. Through stimulation of epithelial cytokine synthesis, bile acids can recruit phagocytes to the mucosa and simultaneously induce the expression of proteins (eg, CD11b/CD18), which promote neutrophil adhesion to epithelial cells [31,48]. These actions may contribute to immune surveillance in the mucosa but may also underlie mucosal infl ammatory responses that can occur during conditions of bile acid malabsorption.…”

Section: Bile Acids In Regulation Of the Enteric Nervous And Mucosal mentioning

confidence: 97%

Bile acids in regulation of intestinal physiology

Keating¹,

Keely

2009

Curr Gastroenterol Rep

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In addition to their roles in facilitating lipid digestion and absorption, bile acids are recognized as important regulators of intestinal function. Exposure to bile acids can dramatically influence intestinal transport and barrier properties; in recent years, they have also become appreciated as important factors in regulating cell growth and survival. Indeed, few cells reside within the intestinal mucosa that are not altered to some degree by exposure to bile acids. The past decade saw great advances in the knowledge of how bile acids exert their actions at the cellular and molecular levels. In this review, we summarize the current understanding of the role of bile acids in regulation of intestinal physiology.

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“…Specific cell surface moieties on vaginal epithelial cells were examined in a manner similar to human oral epithelial cells (39). For examination of existing membrane-associated protein moieties, murine vaginal epithelial cells were pretreated with proteinase K for 10 min at 37°C (25 g/ml; Roche Corp, Mannheim, Germany) in a volume of 1 ml of PBS (28,39). The control included epithelial cells incubated in PBS alone.…”

Section: Growth Inhibition Assay (I) [mentioning

confidence: 99%