Non-invasive assessment of barrier integrity and function of the human gut

Grootjans, Joep; Thuijls, Geertje; Verdam, Froukje J.; Derikx, Joep P. M.; Lenaerts, Kaatje; Buurman, Wim A.

doi:10.4240/wjgs.v2.i3.61

Cited by 182 publications

(168 citation statements)

References 71 publications

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“…inflammation in the intestine by increasing the antigenic load traversing the intestinal barrier. To this end, we first measured transcript levels of a number of the gap junction proteins of the claudin family and of JAM3, which have all been shown to modulate intestinal barrier integrity (59,60). As compared with Conv.R and Col.GF conditions, vehicle-treated GF mice had lower mRNA levels of claudin 2, 3, and 15, and of Jam3 (Figure 4, A-D), a finding consistent with the capacity of the microbiota to induce gap junction protein gene expression (61).…”

Section: Resultsmentioning

confidence: 99%

Sex steroid deficiency–associated bone loss is microbiota dependent and prevented by probiotics

Li¹,

Chassaing²,

Tyagi³

et al. 2016

Journal of Clinical Investigation

491

610

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Section: Resultsmentioning

confidence: 99%

Sex steroid deficiency–associated bone loss is microbiota dependent and prevented by probiotics

Li¹,

Chassaing²,

Tyagi³

et al. 2016

Journal of Clinical Investigation

491

610

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“…GSTs show differential expression dependent on the tissue type and even on different parts of the same tissue. Different expression levels of GST expression result in different exposure to carcinogens (Grootjans et al, 2010;Mannervik, 2012;Rotunno et al, 2012). In addition to that, studies conducted so far indicate that the rate of activation and deactivation of xenobiotics also effect carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

GSTT1 is Deregulated in Left Colon Tumors

Çoşkunpınar

Canbay²,

Oltulu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Our aim was to determine GSTT1 expression levels in left colon tumors and paired normal tissue in order to identify specific alterations in GSTT1 mRNA levels. Alterations in GSTT1 expression in twenty-four leftsided colon tumors and paired cancer free tissue were determined by qRT-PCR. Significant fold changes were determined with t-test. When compared with cancer free tissue, left colon cancers showed a significant decrease in GSTT1 expression. However, GSTT1 mRNA levels among different grades increased gradually in correlation with tumor grade. Our results suggest that downregulation of GSTT1 in left-sided colon cancers is an early event and is reversed with cancer progression, probably due to cellular defense mechanisms as a response to changes in the microenvironment.

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“…This finding was also confirmed by immunohistochemical analysis of I-FABP, a protein that is expressed by intestinal epithelial cells and is released upon epithelial injury. 28,29 We then assessed whether selective IL-1α exposure to different fetal compartments resulted in impaired gut development. Maturation of the fetal gut was assessed by immunohistochemical staining of I-FABP 30 and by the size of vacuoles in the intestinal epithelium.…”

Section: Il-1α-driven Fetal Gut Inflammationmentioning

confidence: 99%

Selective IL-1α exposure to the fetal gut, lung, and chorioamnion/skin causes intestinal inflammatory and developmental changes in fetal sheep

Nikiforou

Kemp

Gorp

et al. 2016

Laboratory Investigation

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Chorioamnionitis, caused by intra-amniotic exposure to bacteria and their toxic components, is associated with fetal gut inflammation and mucosal injury. In a translational ovine model, we have shown that these adverse intestinal outcomes to chorioamnionitis were the combined result of local gut and pulmonary-driven systemic immune responses. Chorioamnionitis-induced gut inflammation and injury was largely prevented by inhibiting interleukin-1 (IL-1) signaling. Therefore, we investigated whether local (gut-derived) IL-1α signaling or systemic IL-1α-driven immune responses (lung or chorioamnion/skin-derived) were sufficient for intestinal inflammation and mucosal injury in the course of chorioamnionitis. Fetal surgery was performed in sheep to isolate the lung, gastrointestinal tract, and chorioamnion/skin, and IL-1α or saline was given into the trachea, stomach, or amniotic cavity 1 or 6 days before preterm delivery. Selective IL-1α exposure to the lung, gut, or chorioamnion/skin increased the CD3+ cell numbers in the fetal gut. Direct IL-1α exposure to the gut impaired intestinal zonula occludens protein-1 expression, induced villus atrophy, changed the expression pattern of intestinal fatty acid-binding protein along the villus, and increased the CD68, IL-1, and TNF-α mRNA levels in the fetal ileum. With lung or chorioamnion/skin exposure to IL-1α, intestinal inflammation was associated with increased numbers of blood leukocytes without induction of intestinal injury or immaturity. We concluded that local IL-1α signaling was required for intestinal inflammation, disturbed gut maturation, and mucosal injury in the context of chorioamnionitis. Intrauterine infection is the most frequent cause of preterm birth 1 before 28 weeks of gestation. 2 Chorioamnionitis, which is commonly caused by intrauterine bacterial infection, is defined as an inflammation of the fetal membranes, amniotic fluid and placenta. [3][4][5] Bacterial infection of the amniotic cavity results in direct exposure of the lung (by fetal breathing), gastrointestinal tract (by swallowing), skin, and chorioamnion to bacteria and their inflammatory components in the contaminated amniotic fluid. The fetal inflammatory response to chorioamnionitis is associated with multiorgan dysfunction, 6,7 which increase the incidence of periventricular leukomalacia, 8 bronchopulmonary dysplasia, 9 and necrotizing enterocolitis. 10,11 We have used a translational ovine model of chorioamnionitis to investigate the impact of intrauterine inflammation on fetal organs. Using this model, we have shown that intraamniotic (IA) delivery of Escherichia coli lipopolysaccharide (LPS) resulted in an acute inflammatory response in the chorioamnion and increased the influx of inflammatory cells in the respiratory tract within 5 h. 12,13 These immune alterations were rapidly followed by systemic inflammation at the same time point and fetal skin inflammation 12 h after LPS exposure. 13,14 The first signs of intestinal inflammation were detected 2 days after IA delivery of LPS, an...

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Non-invasive assessment of barrier integrity and function of the human gut

Cited by 182 publications

References 71 publications

Sex steroid deficiency–associated bone loss is microbiota dependent and prevented by probiotics

Sex steroid deficiency–associated bone loss is microbiota dependent and prevented by probiotics

GSTT1 is Deregulated in Left Colon Tumors

Selective IL-1α exposure to the fetal gut, lung, and chorioamnion/skin causes intestinal inflammatory and developmental changes in fetal sheep

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