The Experts below are selected from a list of 50016 Experts worldwide ranked by ideXlab platform
Hanschristian Reinecker - One of the best experts on this subject based on the ideXlab platform.
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fractalkine is an epithelial and endothelial cell derived chemoattractant for intraepithelial lymphocytes in the small Intestinal Mucosa
Journal of Immunology, 2000Co-Authors: Andreas Muehlhoefer, Daniel K Podolsky, Lawrence J Saubermann, Kerstin Luedtkeheckenkamp, Ramnik J Xavier, Richard S Blumberg, Richard P Macdermott, Hanschristian ReineckerAbstract:Fractalkine is a unique chemokine that combines properties of both chemoattractants and adhesion molecules. Fractalkine mRNA expression has been observed in the intestine. However, the role of fractalkine in the healthy intestine and during inflammatory Mucosal responses is not known. Studies were undertaken to determine the expression and function of fractalkine and the fractalkine receptor CX3CR1 in the human small Intestinal Mucosa. We identified Intestinal epithelial cells as a novel source of fractalkine. The basal expression of fractalkine mRNA and protein in the Intestinal epithelial cell line T-84 was under the control of the inflammatory mediator IL-1β. Fractalkine was shed from Intestinal epithelial cell surface upon stimulation with IL-1β. Fractalkine localized with caveolin-1 in detergent-insoluble glycolipid-enriched membrane microdomains in T-84 cells. Cellular distribution of fractalkine was regulated during polarization of T-84 cells. A subpopulation of isolated human Intestinal intraepithelial lymphocytes expressed the fractalkine receptor CX3CR1 and migrated specifically along fractalkine gradients after activation with IL-2. Immunohistochemistry demonstrated fractalkine expression in Intestinal epithelial cells and endothelial cells in normal small intestine and in active Crohn’s disease Mucosa. Furthermore, fractalkine mRNA expression was significantly up-regulated in the intestine during active Crohn’s disease. This study demonstrates that fractalkine-CX3CR1-mediated mechanism may direct lymphocyte chemoattraction and adhesion within the healthy and diseased human small Intestinal Mucosa.
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fractalkine is an epithelial and endothelial cell derived chemoattractant for intraepithelial lymphocytes in the small Intestinal Mucosa
Journal of Immunology, 2000Co-Authors: Andreas Muehlhoefer, Daniel K Podolsky, Lawrence J Saubermann, Kerstin Luedtkeheckenkamp, Ramnik J Xavier, Richard S Blumberg, Richard P Macdermott, Hanschristian ReineckerAbstract:Fractalkine is a unique chemokine that combines properties of both chemoattractants and adhesion molecules. Fractalkine mRNA expression has been observed in the intestine. However, the role of fractalkine in the healthy intestine and during inflammatory Mucosal responses is not known. Studies were undertaken to determine the expression and function of fractalkine and the fractalkine receptor CX3CR1 in the human small Intestinal Mucosa. We identified Intestinal epithelial cells as a novel source of fractalkine. The basal expression of fractalkine mRNA and protein in the Intestinal epithelial cell line T-84 was under the control of the inflammatory mediator IL-1beta. Fractalkine was shed from Intestinal epithelial cell surface upon stimulation with IL-1beta. Fractalkine localized with caveolin-1 in detergent-insoluble glycolipid-enriched membrane microdomains in T-84 cells. Cellular distribution of fractalkine was regulated during polarization of T-84 cells. A subpopulation of isolated human Intestinal intraepithelial lymphocytes expressed the fractalkine receptor CX3CR1 and migrated specifically along fractalkine gradients after activation with IL-2. Immunohistochemistry demonstrated fractalkine expression in Intestinal epithelial cells and endothelial cells in normal small intestine and in active Crohn's disease Mucosa. Furthermore, fractalkine mRNA expression was significantly up-regulated in the intestine during active Crohn's disease. This study demonstrates that fractalkine-CX3CR1-mediated mechanism may direct lymphocyte chemoattraction and adhesion within the healthy and diseased human small Intestinal Mucosa.
Richard P Macdermott - One of the best experts on this subject based on the ideXlab platform.
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fractalkine is an epithelial and endothelial cell derived chemoattractant for intraepithelial lymphocytes in the small Intestinal Mucosa
Journal of Immunology, 2000Co-Authors: Andreas Muehlhoefer, Daniel K Podolsky, Lawrence J Saubermann, Kerstin Luedtkeheckenkamp, Ramnik J Xavier, Richard S Blumberg, Richard P Macdermott, Hanschristian ReineckerAbstract:Fractalkine is a unique chemokine that combines properties of both chemoattractants and adhesion molecules. Fractalkine mRNA expression has been observed in the intestine. However, the role of fractalkine in the healthy intestine and during inflammatory Mucosal responses is not known. Studies were undertaken to determine the expression and function of fractalkine and the fractalkine receptor CX3CR1 in the human small Intestinal Mucosa. We identified Intestinal epithelial cells as a novel source of fractalkine. The basal expression of fractalkine mRNA and protein in the Intestinal epithelial cell line T-84 was under the control of the inflammatory mediator IL-1β. Fractalkine was shed from Intestinal epithelial cell surface upon stimulation with IL-1β. Fractalkine localized with caveolin-1 in detergent-insoluble glycolipid-enriched membrane microdomains in T-84 cells. Cellular distribution of fractalkine was regulated during polarization of T-84 cells. A subpopulation of isolated human Intestinal intraepithelial lymphocytes expressed the fractalkine receptor CX3CR1 and migrated specifically along fractalkine gradients after activation with IL-2. Immunohistochemistry demonstrated fractalkine expression in Intestinal epithelial cells and endothelial cells in normal small intestine and in active Crohn’s disease Mucosa. Furthermore, fractalkine mRNA expression was significantly up-regulated in the intestine during active Crohn’s disease. This study demonstrates that fractalkine-CX3CR1-mediated mechanism may direct lymphocyte chemoattraction and adhesion within the healthy and diseased human small Intestinal Mucosa.
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fractalkine is an epithelial and endothelial cell derived chemoattractant for intraepithelial lymphocytes in the small Intestinal Mucosa
Journal of Immunology, 2000Co-Authors: Andreas Muehlhoefer, Daniel K Podolsky, Lawrence J Saubermann, Kerstin Luedtkeheckenkamp, Ramnik J Xavier, Richard S Blumberg, Richard P Macdermott, Hanschristian ReineckerAbstract:Fractalkine is a unique chemokine that combines properties of both chemoattractants and adhesion molecules. Fractalkine mRNA expression has been observed in the intestine. However, the role of fractalkine in the healthy intestine and during inflammatory Mucosal responses is not known. Studies were undertaken to determine the expression and function of fractalkine and the fractalkine receptor CX3CR1 in the human small Intestinal Mucosa. We identified Intestinal epithelial cells as a novel source of fractalkine. The basal expression of fractalkine mRNA and protein in the Intestinal epithelial cell line T-84 was under the control of the inflammatory mediator IL-1beta. Fractalkine was shed from Intestinal epithelial cell surface upon stimulation with IL-1beta. Fractalkine localized with caveolin-1 in detergent-insoluble glycolipid-enriched membrane microdomains in T-84 cells. Cellular distribution of fractalkine was regulated during polarization of T-84 cells. A subpopulation of isolated human Intestinal intraepithelial lymphocytes expressed the fractalkine receptor CX3CR1 and migrated specifically along fractalkine gradients after activation with IL-2. Immunohistochemistry demonstrated fractalkine expression in Intestinal epithelial cells and endothelial cells in normal small intestine and in active Crohn's disease Mucosa. Furthermore, fractalkine mRNA expression was significantly up-regulated in the intestine during active Crohn's disease. This study demonstrates that fractalkine-CX3CR1-mediated mechanism may direct lymphocyte chemoattraction and adhesion within the healthy and diseased human small Intestinal Mucosa.
Leo Lefrancois - One of the best experts on this subject based on the ideXlab platform.
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direct analysis of the dynamics of the Intestinal Mucosa cd8 t cell response to systemic virus infection
Journal of Immunology, 2001Co-Authors: David Masopust, Jiu Jiang, Hao Shen, Leo LefrancoisAbstract:The CD8 T cell response to vesicular stomatitis virus infection was characterized in the spleen and Intestinal Mucosa using MHC tetramers. Surprisingly, the primary response persisted in the lamina propria long after the splenic response had declined. Furthermore, the response was characterized by a protracted effector phase in which cytolytic activity in the lamina propria, but not in the spleen, was maintained. The appearance of Ag-specific cells in the Intestinal Mucosa was largely, though not exclusively, a result of β7 integrin-mediated migration. Infection with Listeria monocytogenes or with vaccinia virus also led to sustained Mucosal responses. After reinfection of vesicular stomatitis virus-primed mice with a serotypically distinct virus, a sustained recall response was detected in all tissues. In CD40−/− mice, the Mucosal, but not the splenic, response was compromised, resulting in diminished Mucosal memory. The recall response was CD40 independent and correlated with memory levels, indicating that the Mucosal and systemic responses operated independently. These findings illustrated the integrated yet distinct nature of systemic vs Mucosal immune responses.
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direct analysis of the dynamics of the Intestinal Mucosa cd8 t cell response to systemic virus infection
Journal of Immunology, 2001Co-Authors: David Masopust, Jiu Jiang, Hao Shen, Leo LefrancoisAbstract:The CD8 T cell response to vesicular stomatitis virus infection was characterized in the spleen and Intestinal Mucosa using MHC tetramers. Surprisingly, the primary response persisted in the lamina propria long after the splenic response had declined. Furthermore, the response was characterized by a protracted effector phase in which cytolytic activity in the lamina propria, but not in the spleen, was maintained. The appearance of Ag-specific cells in the Intestinal Mucosa was largely, though not exclusively, a result of beta(7) integrin-mediated migration. Infection with Listeria monocytogenes or with vaccinia virus also led to sustained Mucosal responses. After reinfection of vesicular stomatitis virus-primed mice with a serotypically distinct virus, a sustained recall response was detected in all tissues. In CD40(-/-) mice, the Mucosal, but not the splenic, response was compromised, resulting in diminished Mucosal memory. The recall response was CD40 independent and correlated with memory levels, indicating that the Mucosal and systemic responses operated independently. These findings illustrated the integrated yet distinct nature of systemic vs Mucosal immune responses.
Julius Klose - One of the best experts on this subject based on the ideXlab platform.
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confocal endomicroscopy shows food associated changes in the Intestinal Mucosa of patients with irritable bowel syndrome
Gastroenterology, 2014Co-Authors: Annette Fritscherravens, Detlef Schuppan, Mark Ellrichmann, Stefan Schoch, Christoph Rocken, Jochen Brasch, Johannes Bethge, Martina Bottner, Julius KloseAbstract:Background & Aims We investigated suspected food intolerances in patients with irritable bowel syndrome (IBS) using confocal laser endomicroscopy (CLE) for real-time visualization of structural/functional changes in the Intestinal Mucosa after food challenge. Patients with functional changes after food challenge (CLE+) were placed on personalized exclusion diets and followed up for long-term symptom relief. Methods Thirty-six IBS patients with suspected food intolerance and 10 patients with Barrett's esophagus (controls) without IBS symptoms were examined by CLE at University Hospital Schleswig-Holstein (Kiel, Germany). Diluted food antigens were administered directly to the duodenal Mucosa through the working channel of the endoscope. Epithelial breaks, intervillous spaces, and the number of intraepithelial lymphocytes (IEL) were measured before and after the food challenge. CLE+ patients were placed on exclusion diets, given symptom score questionnaires, and followed up for 1 year; controls resumed their previous diet. Results CLE showed a real-time response to food antigens in 22 of 36 patients; no responses were observed in 14 of 36 patients (CLE-) or any of the controls. Baseline IELs were significantly higher in CLE+ than CLE- subjects ( P = .004); numbers increased significantly after food challenge ( P = .0008). Within 5 minutes of exposure of CLE+ patients to food antigens, IELs increased, epithelial leaks/gaps formed, and intervillous spaces widened. Epithelial leaks and intervillous spaces also increased significantly in CLE+ vs baseline (both P P = .89; r 2 = 0.027). Symptom scores improved more than 50% in CLE+ patients after a 4-week exclusion diet and increased to 74% at 12 months; symptoms continued in CLE- patients. Conclusions Based on CLE analysis of IBS patients with a suspected food intolerance, exposure to candidate food antigens caused immediate breaks, increased intervillous spaces, and increased IELs in the Intestinal Mucosa. These changes are associated with patient responses to exclusion diets. Registered at clinicaltrials.gov (registration number: NCT01692613).
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confocal endomicroscopy shows food associated changes in the Intestinal Mucosa of patients with irritable bowel syndrome
Gastroenterology, 2014Co-Authors: Annette Fritscherravens, Detlef Schuppan, Mark Ellrichmann, Stefan Schoch, Christoph Rocken, Jochen Brasch, Johannes Bethge, Martina Bottner, Julius KloseAbstract:Background & Aims We investigated suspected food intolerances in patients with irritable bowel syndrome (IBS) using confocal laser endomicroscopy (CLE) for real-time visualization of structural/functional changes in the Intestinal Mucosa after food challenge. Patients with functional changes after food challenge (CLE+) were placed on personalized exclusion diets and followed up for long-term symptom relief. Methods Thirty-six IBS patients with suspected food intolerance and 10 patients with Barrett's esophagus (controls) without IBS symptoms were examined by CLE at University Hospital Schleswig-Holstein (Kiel, Germany). Diluted food antigens were administered directly to the duodenal Mucosa through the working channel of the endoscope. Epithelial breaks, intervillous spaces, and the number of intraepithelial lymphocytes (IEL) were measured before and after the food challenge. CLE+ patients were placed on exclusion diets, given symptom score questionnaires, and followed up for 1 year; controls resumed their previous diet. Results CLE showed a real-time response to food antigens in 22 of 36 patients; no responses were observed in 14 of 36 patients (CLE-) or any of the controls. Baseline IELs were significantly higher in CLE+ than CLE- subjects (P = .004); numbers increased significantly after food challenge (P = .0008). Within 5 minutes of exposure of CLE+ patients to food antigens, IELs increased, epithelial leaks/gaps formed, and intervillous spaces widened. Epithelial leaks and intervillous spaces also increased significantly in CLE+ vs baseline (both P Conclusions Based on CLE analysis of IBS patients with a suspected food intolerance, exposure to candidate food antigens caused immediate breaks, increased intervillous spaces, and increased IELs in the Intestinal Mucosa. These changes are associated with patient responses to exclusion diets. Registered at clinicaltrials.gov (registration number: NCT01692613).
Detlef Schuppan - One of the best experts on this subject based on the ideXlab platform.
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confocal endomicroscopy shows food associated changes in the Intestinal Mucosa of patients with irritable bowel syndrome
Gastroenterology, 2014Co-Authors: Annette Fritscherravens, Detlef Schuppan, Mark Ellrichmann, Stefan Schoch, Christoph Rocken, Jochen Brasch, Johannes Bethge, Martina Bottner, Julius KloseAbstract:Background & Aims We investigated suspected food intolerances in patients with irritable bowel syndrome (IBS) using confocal laser endomicroscopy (CLE) for real-time visualization of structural/functional changes in the Intestinal Mucosa after food challenge. Patients with functional changes after food challenge (CLE+) were placed on personalized exclusion diets and followed up for long-term symptom relief. Methods Thirty-six IBS patients with suspected food intolerance and 10 patients with Barrett's esophagus (controls) without IBS symptoms were examined by CLE at University Hospital Schleswig-Holstein (Kiel, Germany). Diluted food antigens were administered directly to the duodenal Mucosa through the working channel of the endoscope. Epithelial breaks, intervillous spaces, and the number of intraepithelial lymphocytes (IEL) were measured before and after the food challenge. CLE+ patients were placed on exclusion diets, given symptom score questionnaires, and followed up for 1 year; controls resumed their previous diet. Results CLE showed a real-time response to food antigens in 22 of 36 patients; no responses were observed in 14 of 36 patients (CLE-) or any of the controls. Baseline IELs were significantly higher in CLE+ than CLE- subjects ( P = .004); numbers increased significantly after food challenge ( P = .0008). Within 5 minutes of exposure of CLE+ patients to food antigens, IELs increased, epithelial leaks/gaps formed, and intervillous spaces widened. Epithelial leaks and intervillous spaces also increased significantly in CLE+ vs baseline (both P P = .89; r 2 = 0.027). Symptom scores improved more than 50% in CLE+ patients after a 4-week exclusion diet and increased to 74% at 12 months; symptoms continued in CLE- patients. Conclusions Based on CLE analysis of IBS patients with a suspected food intolerance, exposure to candidate food antigens caused immediate breaks, increased intervillous spaces, and increased IELs in the Intestinal Mucosa. These changes are associated with patient responses to exclusion diets. Registered at clinicaltrials.gov (registration number: NCT01692613).
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confocal endomicroscopy shows food associated changes in the Intestinal Mucosa of patients with irritable bowel syndrome
Gastroenterology, 2014Co-Authors: Annette Fritscherravens, Detlef Schuppan, Mark Ellrichmann, Stefan Schoch, Christoph Rocken, Jochen Brasch, Johannes Bethge, Martina Bottner, Julius KloseAbstract:Background & Aims We investigated suspected food intolerances in patients with irritable bowel syndrome (IBS) using confocal laser endomicroscopy (CLE) for real-time visualization of structural/functional changes in the Intestinal Mucosa after food challenge. Patients with functional changes after food challenge (CLE+) were placed on personalized exclusion diets and followed up for long-term symptom relief. Methods Thirty-six IBS patients with suspected food intolerance and 10 patients with Barrett's esophagus (controls) without IBS symptoms were examined by CLE at University Hospital Schleswig-Holstein (Kiel, Germany). Diluted food antigens were administered directly to the duodenal Mucosa through the working channel of the endoscope. Epithelial breaks, intervillous spaces, and the number of intraepithelial lymphocytes (IEL) were measured before and after the food challenge. CLE+ patients were placed on exclusion diets, given symptom score questionnaires, and followed up for 1 year; controls resumed their previous diet. Results CLE showed a real-time response to food antigens in 22 of 36 patients; no responses were observed in 14 of 36 patients (CLE-) or any of the controls. Baseline IELs were significantly higher in CLE+ than CLE- subjects (P = .004); numbers increased significantly after food challenge (P = .0008). Within 5 minutes of exposure of CLE+ patients to food antigens, IELs increased, epithelial leaks/gaps formed, and intervillous spaces widened. Epithelial leaks and intervillous spaces also increased significantly in CLE+ vs baseline (both P Conclusions Based on CLE analysis of IBS patients with a suspected food intolerance, exposure to candidate food antigens caused immediate breaks, increased intervillous spaces, and increased IELs in the Intestinal Mucosa. These changes are associated with patient responses to exclusion diets. Registered at clinicaltrials.gov (registration number: NCT01692613).
