Rectal Dialysate and Fecal Concentrations of Neutrophil Gelatinase-Associated Lipocalin, Interleukin-8, and Tumor Necrosis Factor-α in Ulcerative Colitis

Nielsen, Ole Haagen; Gionchetti, Paolo; Ainsworth, Mark; Vainer, Ben; Campieri, Massimo; Borregaard, Niels; Kjeldsen, Lars

doi:10.1111/j.1572-0241.1999.01439.x

Cited by 100 publications

(31 citation statements)

References 25 publications

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“…However, these studies did not explore the functional consequences of TLR2 signaling in IEC. Our findings demonstrate that IEC are poorly responsive to a variety of TLR2 ligands with respect to proinflammatory gene expression and IL-8 secretion, two outcomes relevant to acute and chronic intestinal inflammation (92)(93)(94). Although the response to certain TLR2 ligands could be restored by transgenic expression of TLR2 and TLR6, IEC remained poorly responsive to bacterial lipopeptide suggesting that, in addition to TLR2 and TLR1, other coreceptors or signaling molecules may be functionally deficient as well.…”

Section: Discussionmentioning

confidence: 76%

Human Intestinal Epithelial Cells Are Broadly Unresponsive to Toll-Like Receptor 2-Dependent Bacterial Ligands: Implications for Host-Microbial Interactions in the Gut

Melmed¹,

Thomas²,

Lee³

et al. 2003

The Journal of Immunology

395

281

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Intestinal epithelial cells (IEC) interact with a high density of Gram-positive bacteria and are active participants in mucosal immune responses. Recognition of Gram-positive organisms by Toll-like receptor (TLR)2 induces proinflammatory gene expression by diverse cells. We hypothesized that IEC are unresponsive to Gram-positive pathogen-associated molecular patterns and sought to characterize the functional responses of IEC to TLR2-specific ligands. Human colonic epithelial cells isolated by laser capture microscopy and IEC lines (Caco-2, T84, HT-29) were analyzed for expression of TLR2, TLR6, TLR1, and Toll inhibitory protein (Tollip) mRNA by RT-PCR and quantitative real-time PCR. Response to Gram-positive bacterial ligands was measured by NF-κB reporter gene activation and IL-8 secretion. TLR2 protein expression was analyzed by immunofluorescence and flow cytometry. Colonic epithelial cells and lamina propria cells from both uninflamed and inflamed tissue demonstrate low expression of TLR2 mRNA compared with THP-1 monocytes. IECs were unresponsive to TLR2 ligands including the staphylococcal-derived Ags phenol soluble modulin, peptidoglycan, and lipotechoic acid and the mycobacterial-derived Ag soluble tuberculosis factor. Transgenic expression of TLR2 and TLR6 restored responsiveness to phenol soluble modulin and peptidoglycan in IEC. In addition to low levels of TLR2 protein expression, IEC also express high levels of the inhibitory molecule Tollip. We conclude that IEC are broadly unresponsive to TLR2 ligands secondary to deficient expression of TLR2 and TLR6. The relative absence of TLR2 protein expression by IEC and high level of Tollip expression may be important in preventing chronic proinflammatory cytokine secretion in response to commensal Gram-positive bacteria in the gut.

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Section: Discussionmentioning

confidence: 76%

Human Intestinal Epithelial Cells Are Broadly Unresponsive to Toll-Like Receptor 2-Dependent Bacterial Ligands: Implications for Host-Microbial Interactions in the Gut

Melmed¹,

Thomas²,

Lee³

et al. 2003

The Journal of Immunology

395

281

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“…Sin embargo, existe evidencia científica que confirma el papel importante del TNF-α en la CU (13), lo que apoya la posible utilidad de la terapia anti-TNF en el tratamiento de esta entidad clínica. Diversos autores han descrito altas tasas de producción local y sistémica del TNF, que se demuestra por el aumento de la producción de esta citocina en la mucosa colónica (15)(16)(17), en las heces, plasma, orina o dializado rectal de los enfermos con CU activa (18)(19)(20). Además, este aumento de concentración se correlaciona con la gravedad de la enfermedad, tanto clínica como analítica.…”

Section: Discussionunclassified

“…However, there is enough scientific evidence pointing at the important role played by TNF-α in UC (13), which supports the possible usefulness of anti-TNF-α therapy in this disease. Different authors have described active TNF-α synthesis both locally and systemically, as shown by an increased production in the colonic mucosa (15)(16)(17), and an increased detection in the stools, plasma, urine and rectal dyalisates of patients with active UC (18)(19)(20). Moreover, this increase correlates with disease severity as measured by clinical or laboratory parameters.…”

Section: Discussionmentioning

confidence: 99%

Infliximab induces clinical, endoscopic and histological responses in refractory ulcerative colitis

Bermejo

López-Sanromán²,

Hinojosa

et al. 2004

Rev. esp. enferm. dig.

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Background: infliximab is a monoclonal antiTNF-α antibody that has repeatedly shown to be effective in the management of Crohn's disease. However, data are scarce about its efficacy in ulcerative colitis.Aim: to describe the joint experience of three Spanish hospitals in the use of infliximab in patients with active refractory ulcerative colitis.Patients and methods: we present seven cases of ulcerative colitis (6 with chronic active disease despite immunosuppressive therapy, and one with acute steroid-refractory ulcerative colitis) treated with infliximab 5 mg/kg of body weight. Clinical response was evaluated by means of the Clinical Activity Index at 2, 4 and 8 weeks after initial infusion. Biochemical (erythrocyte sedimentation rate and C-reactive protein), endoscopic, and histological changes were also assessed.Results: mean age of patients was 45.8 ± 17 years (range 23-77); 4 were female. No adverse effects were recorded. Inflammatory activity diminished significantly in 6 of 7 patients (85.7%; CI 95%: 42-99%) both from a clinical (p = 0.01) and biochemical (p <0.05) point of view. Five out of six patients (83.3%; 36-99%) with corticosteroid-dependent disease could be successfully weaned off these drugs. Five patients were endoscopicly controlled both before and after therapy, and a positive endoscopic and histological response could be recorded in all of them.Conclusion: infliximab may be an effective and safe therapy for some patients with ulcerative colitis refractory to other forms of therapy, although controlled studies are needed to assess its role in the general management of this disease.

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“…Moreover, other studies have demonstrated that faecal NGAL levels are a reliable marker of UC activity 20 .…”

Section: Downloaded Frommentioning

confidence: 99%

Accuracy of Faecal Calprotectin and Neutrophil Gelatinase B-associated Lipocalin in Evaluating Subclinical Inflammation in UlceRaTIVE Colitis—the ACERTIVE study

Magro

Lopes

Coelho

et al. 2016

ECCOJC

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Rectal Dialysate and Fecal Concentrations of Neutrophil Gelatinase-Associated Lipocalin, Interleukin-8, and Tumor Necrosis Factor-α in Ulcerative Colitis

Abstract: The NGAL content in rectal dialysate and particularly in feces seems to be a reliable marker for severe disease activity in UC, whereas serum NGAL concentrations do not reflect disease activity.

Cited by 100 publications

References 25 publications

Human Intestinal Epithelial Cells Are Broadly Unresponsive to Toll-Like Receptor 2-Dependent Bacterial Ligands: Implications for Host-Microbial Interactions in the Gut

Human Intestinal Epithelial Cells Are Broadly Unresponsive to Toll-Like Receptor 2-Dependent Bacterial Ligands: Implications for Host-Microbial Interactions in the Gut

Infliximab induces clinical, endoscopic and histological responses in refractory ulcerative colitis

Accuracy of Faecal Calprotectin and Neutrophil Gelatinase B-associated Lipocalin in Evaluating Subclinical Inflammation in UlceRaTIVE Colitis—the ACERTIVE study

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