Heat- and Formalin-Inactivated Probiotic Bacteria Induce Comparable Cytokine Patterns in Intestinal Epithelial Cell–Leucocyte Cocultures

The mode of inactivation of probiotic bacteria may profoundly affect their immune-modulatory properties to the point of reversal of effects in in vitro human intestinal epithelial-like cell cultures (Caco-2). To further investigate the influence of inactivation treatment on cytokine production, three probiotic strains were evaluated—live, heat-inactivated, and formalininactivated strains—for their impact on interleukin (IL) 6, IL-8, and IL-10 production in Caco-2–leucocyte cocultures. The tested bacteria induced strain-specific production of IL-6, IL-8, and IL-10. No suppressive effects on cytokine synthesis were observed. Live microorganisms seemed to be slightly more potent inducers of cytokine production than nonviable strains, but differences to inactivated bacteria were not statistically significant. Our results indicate that heat and formalin treatments of probiotic microorganisms are equivalent inactivation methods in terms of induction of IL-6, IL-8, and IL-10 production in Caco-2–peripheral blood mononuclear cell cocultures and do not invert immune-modulatory effects.

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Isoflavones inhibit intestinal epithelial cell proliferation and induce apoptosis in vitro

British Journal of Cancer ◽

10.1038/sj.bjc.6690559 ◽

1999 ◽

Vol 80 (10) ◽

pp. 1550-1557 ◽

Cited By ~ 61

Author(s):

C Booth ◽

D F Hargreaves ◽

J A Hadfield ◽

A T McGown ◽

C S Potten

Keyword(s):

Cell Proliferation ◽

Epithelial Cell ◽

Intestinal Epithelial Cell ◽

Intestinal Epithelial ◽

Epithelial Cell Proliferation

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Effects of lactoferrin on intestinal epithelial cell growth and differentiation: an in vivo and in vitro study

BioMetals ◽

10.1007/s10534-014-9779-7 ◽

2014 ◽

Vol 27 (5) ◽

pp. 857-874 ◽

Cited By ~ 21

Author(s):

Anne Blais ◽

Cuibai Fan ◽

Thierry Voisin ◽

Najat Aattouri ◽

Michel Dubarry ◽

...

Keyword(s):

Cell Growth ◽

Epithelial Cell ◽

Intestinal Epithelial Cell ◽

In Vitro Study ◽

Vitro Study ◽

Intestinal Epithelial ◽

Cell Growth And Differentiation

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Effects of Ethanol and Acetaldehyde on Tight Junction Integrity: In Vitro Study in a Three Dimensional Intestinal Epithelial Cell Culture Model

PLoS ONE ◽

10.1371/journal.pone.0035008 ◽

2012 ◽

Vol 7 (4) ◽

pp. e35008 ◽

Cited By ~ 60

Author(s):

Elhaseen Elamin ◽

Daisy Jonkers ◽

Kati Juuti-Uusitalo ◽

Sven van IJzendoorn ◽

Freddy Troost ◽

...

Keyword(s):

Cell Culture ◽

Epithelial Cell ◽

Intestinal Epithelial Cell ◽

Three Dimensional ◽

In Vitro Study ◽

Intestinal Epithelial ◽

Cell Culture Model ◽

Epithelial Cell Culture ◽

Culture Model

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Deficiency in the anti-apoptotic protein DJ-1 promotes intestinal epithelial cell apoptosis and aggravates inflammatory bowel disease via p53

Journal of Biological Chemistry ◽

10.1074/jbc.ra119.010143 ◽

2020 ◽

Vol 295 (13) ◽

pp. 4237-4251 ◽

Cited By ~ 1

Author(s):

Jie Zhang ◽

Min Xu ◽

Weihua Zhou ◽

Dejian Li ◽

Hong Zhang ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Epithelial Cell ◽

Bowel Disease ◽

Intestinal Epithelial Cell ◽

Intestinal Inflammation ◽

Intestinal Epithelial ◽

P53 Expression ◽

Inflammatory Bowel

Parkinson disease autosomal recessive, early onset 7 (PARK7 or DJ-1) is involved in multiple physiological processes and exerts anti-apoptotic effects on multiple cell types. Increased intestinal epithelial cell (IEC) apoptosis and excessive activation of the p53 signaling pathway is a hallmark of inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn's disease (CD). However, whether DJ-1 plays a role in colitis is unclear. To determine whether DJ-1 deficiency is involved in the p53 activation that results in IEC apoptosis in colitis, here we performed immunostaining, real-time PCR, and immunoblotting analyses to assess DJ-1 expression in human UC and CD samples. In the inflamed intestines of individuals with IBD, DJ-1 expression was decreased and negatively correlated with p53 expression. DJ-1 deficiency significantly aggravated colitis, evidenced by increased intestinal inflammation and exacerbated IEC apoptosis. Moreover, DJ-1 directly interacted with p53, and reduced DJ-1 levels increased p53 levels both in vivo and in vitro and were associated with decreased p53 degradation via the lysosomal pathway. We also induced experimental colitis with dextran sulfate sodium in mice and found that compared with DJ-1−/− mice, DJ-1−/−p53−/− mice have reduced apoptosis and inflammation and increased epithelial barrier integrity. Furthermore, pharmacological inhibition of p53 relieved inflammation in the DJ-1−/− mice. In conclusion, reduced DJ-1 expression promotes inflammation and IEC apoptosis via p53 in colitis, suggesting that the modulation of DJ-1 expression may be a potential therapeutic strategy for managing colitis.

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Absorption of Hemoglobin Iron: The Role of Xanthine Oxidase in the Intestinal Heme-Splitting Reaction

Blood ◽

10.1182/blood.v35.1.94.94 ◽

1970 ◽

Vol 35 (1) ◽

pp. 94-103 ◽

Cited By ~ 26

Author(s):

R. BEN DAWSON ◽

SHEILA RAFAL ◽

LEWIS R. WEINTRAUB

Keyword(s):

Epithelial Cell ◽

Xanthine Oxidase ◽

Intestinal Epithelial Cell ◽

Oxidase Inhibitor ◽

Small Intestinal Mucosa ◽

Intestinal Epithelial ◽

Sephadex Column ◽

Xanthine Oxidase Inhibitor

Abstract Heme from ingested hemoglobin—59Fe is taken into the epithelial cell of the small intestinal mucosa of the dog and the 59Fe subsequently appears in the plasma bound to transferrin. A substance was demonstrated in homogenates of the mucosa which releases iron from a hemoglobin substrate in vitro. Thus: (1) The addition of catalase to the mucosal homogenate reduces the "heme-splitting" reaction. In contrast, sodium azide, a catalase inhibitor, potentiates the reaction. This suggests that a peroxide generating system participates in the "heme-splitting" reaction. (2) Xanthine oxidase, an enzyme present in the intestinal epithelial cell, produces H2O2 by oxidation of its substrate. The addition of allopurinol, a xanthine oxidase inhibitor, to the intestinal mucosal homogenate diminishes the "heme-splitting" reaction. (3) Fractionation of the 50,000 Gm. supernatant of the mucosal homogenate on a G-200 Sephadex column shows the "heme-splitting" activity to have the same elution volume as xanthine oxidase, indicating a similar molecular weight. (4) The addition of a mucosal homogenate to a xanthine substrate results in the production of uric acid. These data suggest that xanthine oxidase in the intestinal epithelial cell is important in the release of iron from absorbed heme. The enzyme mediates the "heme-splitting" reaction by the generation of peroxides which, in turn, oxidize the alpha-methene bridge of the heme ring releasing iron and forming biliverdin.

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Human intestinal epithelial cell survival: differentiation state-specific control mechanisms

AJP Cell Physiology ◽

10.1152/ajpcell.2001.280.6.c1540 ◽

2001 ◽

Vol 280 (6) ◽

pp. C1540-C1554 ◽

Cited By ~ 68

Author(s):

Rémy Gauthier ◽

Charlène Harnois ◽

Jean-François Drolet ◽

John C. Reed ◽

Anne Vézina ◽

...

Keyword(s):

Epithelial Cell ◽

Cell Survival ◽

Intestinal Epithelial Cell ◽

The State ◽

Control Mechanisms ◽

Intestinal Epithelial ◽

Human Intestinal Epithelial Cell ◽

Expression Levels ◽

Specific Control

To investigate whether human intestinal epithelial cell survival involves distinct control mechanisms depending on the state of differentiation, we analyzed the in vitro effects of insulin, pharmacological inhibitors of Fak, MEK/Erk, and PI3-K/Akt, and integrin (β1, β4)-blocking antibodies on the survival of the well-established human Caco-2 enterocyte-like and HIEC-6 cryptlike cell models. In addition, relative expression levels of six Bcl-2 homologs (Bcl-2, Bcl-XL, Mcl-1, Bax, Bak, and Bad) and activation levels of Fak, Erk-2, and Akt were analyzed. Herein, we report that 1) the enterocytic differentiation process results in the establishment of distinct profiles of Bcl-2 homolog expression levels, as well as p125Fak, p42Erk-2, and p57Aktactivated levels; 2) the inhibition of Fak, of the MEK/Erk pathway, or of PI3-K, have distinct impacts on enterocytic cell survival in undifferentiated (subconfluent Caco-2, confluent HIEC-6) and differentiated (30 days postconfluent Caco-2) cells; 3) exposure to insulin and the inhibition of Fak, MEK, and PI3-K resulted in differentiation state-distinct modulations in the expression of each Bcl-2 homolog analyzed; and 4) Fak, β1 and β4 integrins, as well as the MEK/Erk and PI3-K/Akt pathways, are distinctively involved in cell survival depending on the state of cell differentiation. Taken together, these data indicate that human intestinal epithelial cell survival is regulated according to differentiation state-specific control mechanisms.

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