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22 results on '"Rogier, R.L."'

1. Supplementation of diet with non-digestible oligosaccharides alters the intestinal microbiota, but not arthritis development, in IL-1 receptor antagonist deficient mice

Author

Rogier, R.L., Ederveen, T.H., Wopereis, H., Hartog, Anita, Boekhorst, J., Hijum, S.A.F.T. van, Walgreen, B., Helsen, M.M.A., Kraan, P.M. van der, Lent, P.L.E.M. van, Loo, F.A.J. van de, Abdollahi-Roodsaz, S., Koenders, M.I., Rogier, R.L., Ederveen, T.H., Wopereis, H., Hartog, Anita, Boekhorst, J., Hijum, S.A.F.T. van, Walgreen, B., Helsen, M.M.A., Kraan, P.M. van der, Lent, P.L.E.M. van, Loo, F.A.J. van de, Abdollahi-Roodsaz, S., and Koenders, M.I.

Abstract

Contains fulltext : 208073.pdf (publisher's version ) (Open Access)

Published
2019

2. The role of intestinal microbiota in T cell-mediated experimental arthritis. Lessons from the mouse gut

Author

Kraan, P.M. van der, Berg, W.B. van den, Abdollahi-Roodsaz, S., Koenders, M.I., Rogier, R.L., Kraan, P.M. van der, Berg, W.B. van den, Abdollahi-Roodsaz, S., Koenders, M.I., and Rogier, R.L.

Abstract

Radboud University, 19 februari 2019, Promotores : Kraan, P.M. van der, Berg, W.B. van den Co-promotores : Abdollahi-Roodsaz, S., Koenders, M.I., Contains fulltext : 200684.pdf (publisher's version ) (Open Access)

Published
2019

3. Supplementation of diet with non-digestible oligosaccharides alters the intestinal microbiota, but not arthritis development, in IL-1 receptor antagonist deficient mice

Author

Rogier, R.L., Ederveen, T.H., Wopereis, H., Hartog, Anita, Boekhorst, J., Hijum, S.A.F.T. van, Walgreen, B., Helsen, M.M.A., Kraan, P.M. van der, Lent, P.L.E.M. van, Loo, F.A.J. van de, Abdollahi-Roodsaz, S., Koenders, M.I., Rogier, R.L., Ederveen, T.H., Wopereis, H., Hartog, Anita, Boekhorst, J., Hijum, S.A.F.T. van, Walgreen, B., Helsen, M.M.A., Kraan, P.M. van der, Lent, P.L.E.M. van, Loo, F.A.J. van de, Abdollahi-Roodsaz, S., and Koenders, M.I.

Abstract

Contains fulltext : 208073.pdf (publisher's version ) (Open Access)

Published
2019

4. The role of intestinal microbiota in T cell-mediated experimental arthritis. Lessons from the mouse gut

Author

Kraan, P.M. van der, Berg, W.B. van den, Abdollahi-Roodsaz, S., Koenders, M.I., Rogier, R.L., Kraan, P.M. van der, Berg, W.B. van den, Abdollahi-Roodsaz, S., Koenders, M.I., and Rogier, R.L.

Abstract

Radboud University, 19 februari 2019, Promotores : Kraan, P.M. van der, Berg, W.B. van den Co-promotores : Abdollahi-Roodsaz, S., Koenders, M.I., Contains fulltext : 200684.pdf (publisher's version ) (Open Access)

Published
2019

5. The role of intestinal microbiota in T cell-mediated experimental arthritis. Lessons from the mouse gut

Author

Kraan, P.M. van der, Berg, W.B. van den, Abdollahi-Roodsaz, S., Koenders, M.I., Rogier, R.L., Kraan, P.M. van der, Berg, W.B. van den, Abdollahi-Roodsaz, S., Koenders, M.I., and Rogier, R.L.

Abstract

Radboud University, 19 februari 2019, Promotores : Kraan, P.M. van der, Berg, W.B. van den Co-promotores : Abdollahi-Roodsaz, S., Koenders, M.I., Contains fulltext : 200684.pdf (publisher's version ) (Open Access)

Published
2019

6. Supplementation of diet with non-digestible oligosaccharides alters the intestinal microbiota, but not arthritis development, in IL-1 receptor antagonist deficient mice

Author

Rogier, R.L., Ederveen, T.H., Wopereis, H., Hartog, Anita, Boekhorst, J., Hijum, S.A.F.T. van, Walgreen, B., Helsen, M.M.A., Kraan, P.M. van der, Lent, P.L.E.M. van, Loo, F.A.J. van de, Abdollahi-Roodsaz, S., Koenders, M.I., Rogier, R.L., Ederveen, T.H., Wopereis, H., Hartog, Anita, Boekhorst, J., Hijum, S.A.F.T. van, Walgreen, B., Helsen, M.M.A., Kraan, P.M. van der, Lent, P.L.E.M. van, Loo, F.A.J. van de, Abdollahi-Roodsaz, S., and Koenders, M.I.

Abstract

Contains fulltext : 208073.pdf (publisher's version ) (Open Access)

Published
2019

8. Supplementation of diet with non-digestible oligosaccharides alters the intestinal microbiota, but not arthritis development, in IL-1 receptor antagonist deficient mice.

Author

Rogier, R.L. and Rogier, R.L.

Subjects
All institutes and research themes of the Radboud University Medical Center., Molecular Biology., Radboudumc 4: lnfectious Diseases and Global Health RIMLS: Radboud Institute for Molecular Life Sciences., Radboudumc 5: Inflammatory diseases RIMLS: Radboud Institute for Molecular Life Sciences.
Published
2019

9. Microbiota-Dependent Involvement of Th17 Cells in Murine Models of Inflammatory Arthritis

Author

Evans-Marin, Heather, Rogier, R.L., Koralov, Sergei B., Manasson, Julia, Roeleveld, D.M., Kraan, P.M. van der, Koenders, M.I., Abdollahi-Roodsaz, S., Evans-Marin, Heather, Rogier, R.L., Koralov, Sergei B., Manasson, Julia, Roeleveld, D.M., Kraan, P.M. van der, Koenders, M.I., and Abdollahi-Roodsaz, S.

Abstract

Contains fulltext : 199029.pdf (Publisher’s version ) (Open Access)

Published
2018

10. Microbiota-Dependent Involvement of Th17 Cells in Murine Models of Inflammatory Arthritis

Author

Evans-Marin, Heather, Rogier, R.L., Koralov, Sergei B., Manasson, Julia, Roeleveld, D.M., Kraan, P.M. van der, Koenders, M.I., Abdollahi-Roodsaz, S., Evans-Marin, Heather, Rogier, R.L., Koralov, Sergei B., Manasson, Julia, Roeleveld, D.M., Kraan, P.M. van der, Koenders, M.I., and Abdollahi-Roodsaz, S.

Abstract

Contains fulltext : 199029.pdf (Publisher’s version ) (Open Access)

Published
2018

11. Microbiota-Dependent Involvement of Th17 Cells in Murine Models of Inflammatory Arthritis

Author

Evans-Marin, Heather, Rogier, R.L., Koralov, Sergei B., Manasson, Julia, Roeleveld, D.M., Kraan, P.M. van der, Koenders, M.I., Abdollahi-Roodsaz, S., Evans-Marin, Heather, Rogier, R.L., Koralov, Sergei B., Manasson, Julia, Roeleveld, D.M., Kraan, P.M. van der, Koenders, M.I., and Abdollahi-Roodsaz, S.

Abstract

Contains fulltext : 199029.pdf (Publisher’s version ) (Open Access)

Published
2018

12. Aberrant intestinal microbiota due to IL-1 receptor antagonist deficiency promotes IL-17- and TLR4-dependent arthritis

Author

Rogier, R.L., Ederveen, T.H., Boekhorst, J., Wopereis, H., Scher, J.U., Manasson, J., Frambach, S.J.C.M., Knol, J., Garssen, J., Kraan, P.M. van der, Koenders, M.I., Berg, W.B. van den, Hijum, S.A. van, Abdollahi-Roodsaz, S., Rogier, R.L., Ederveen, T.H., Boekhorst, J., Wopereis, H., Scher, J.U., Manasson, J., Frambach, S.J.C.M., Knol, J., Garssen, J., Kraan, P.M. van der, Koenders, M.I., Berg, W.B. van den, Hijum, S.A. van, and Abdollahi-Roodsaz, S.

Abstract

Contains fulltext : 174148.pdf (publisher's version ) (Open Access), BACKGROUND: Perturbation of commensal intestinal microbiota has been associated with several autoimmune diseases. Mice deficient in interleukin-1 receptor antagonist (Il1rn -/- mice) spontaneously develop autoimmune arthritis and are susceptible to other autoimmune diseases such as psoriasis, diabetes, and encephalomyelitis; however, the mechanisms of increased susceptibility to these autoimmune phenotypes are poorly understood. We investigated the role of interleukin-1 receptor antagonist (IL-1Ra) in regulation of commensal intestinal microbiota, and assessed the involvement of microbiota subsets and innate and adaptive mucosal immune responses that underlie the development of spontaneous arthritis in Il1rn -/- mice. RESULTS: Using high-throughput 16S rRNA gene sequencing, we show that IL-1Ra critically maintains the diversity and regulates the composition of intestinal microbiota in mice. IL-1Ra deficiency reduced the intestinal microbial diversity and richness, and caused specific taxonomic alterations characterized by overrepresented Helicobacter and underrepresented Ruminococcus and Prevotella. Notably, the aberrant intestinal microbiota in IL1rn -/- mice specifically potentiated IL-17 production by intestinal lamina propria (LP) lymphocytes and skewed the LP T cell balance in favor of T helper 17 (Th17) cells, an effect transferable to WT mice by fecal microbiota. Importantly, LP Th17 cell expansion and the development of spontaneous autoimmune arthritis in IL1rn -/- mice were attenuated under germ-free condition. Selective antibiotic treatment revealed that tobramycin-induced alterations of commensal intestinal microbiota, i.e., reduced Helicobacter, Flexispira, Clostridium, and Dehalobacterium, suppressed arthritis in IL1rn -/- mice. The arthritis phenotype in IL1rn -/- mice was previously shown to depend on Toll-like receptor 4 (TLR4). Using the ablation of both IL-1Ra and TLR4, we here show that the aberrations in the IL1rn -/- microbiota are partly TLR4-d

Published
2017

13. Alteration of the intestinal microbiome characterizes preclinical inflammatory arthritis in mice and its modulation attenuates established arthritis

Author

Rogier, R.L., Evans-Marin, Heather, Manasson, Julia, Kraan, P.M. van der, Walgreen, B., Helsen, M.M.A., Bersselaar, L.A.M. van den, Loo, F.A.J. van de, Lent, P.L. van, Berg, W.B. van den, Koenders, M.I., Scher, Jose U., Abdollahi-Roodsaz, S., Rogier, R.L., Evans-Marin, Heather, Manasson, Julia, Kraan, P.M. van der, Walgreen, B., Helsen, M.M.A., Bersselaar, L.A.M. van den, Loo, F.A.J. van de, Lent, P.L. van, Berg, W.B. van den, Koenders, M.I., Scher, Jose U., and Abdollahi-Roodsaz, S.

Abstract

Contains fulltext : 179543.pdf (publisher's version ) (Open Access)

Published
2017

14. Aberrant intestinal microbiota due to IL-1 receptor antagonist deficiency promotes IL-17- and TLR4-dependent arthritis

Author

Rogier, R.L., Ederveen, T.H., Boekhorst, J., Wopereis, H., Scher, J.U., Manasson, J., Frambach, S.J.C.M., Knol, J., Garssen, J., Kraan, P.M. van der, Koenders, M.I., Berg, W.B. van den, Hijum, S.A. van, Abdollahi-Roodsaz, S., Rogier, R.L., Ederveen, T.H., Boekhorst, J., Wopereis, H., Scher, J.U., Manasson, J., Frambach, S.J.C.M., Knol, J., Garssen, J., Kraan, P.M. van der, Koenders, M.I., Berg, W.B. van den, Hijum, S.A. van, and Abdollahi-Roodsaz, S.

Abstract

Contains fulltext : 174148.pdf (publisher's version ) (Open Access), BACKGROUND: Perturbation of commensal intestinal microbiota has been associated with several autoimmune diseases. Mice deficient in interleukin-1 receptor antagonist (Il1rn -/- mice) spontaneously develop autoimmune arthritis and are susceptible to other autoimmune diseases such as psoriasis, diabetes, and encephalomyelitis; however, the mechanisms of increased susceptibility to these autoimmune phenotypes are poorly understood. We investigated the role of interleukin-1 receptor antagonist (IL-1Ra) in regulation of commensal intestinal microbiota, and assessed the involvement of microbiota subsets and innate and adaptive mucosal immune responses that underlie the development of spontaneous arthritis in Il1rn -/- mice. RESULTS: Using high-throughput 16S rRNA gene sequencing, we show that IL-1Ra critically maintains the diversity and regulates the composition of intestinal microbiota in mice. IL-1Ra deficiency reduced the intestinal microbial diversity and richness, and caused specific taxonomic alterations characterized by overrepresented Helicobacter and underrepresented Ruminococcus and Prevotella. Notably, the aberrant intestinal microbiota in IL1rn -/- mice specifically potentiated IL-17 production by intestinal lamina propria (LP) lymphocytes and skewed the LP T cell balance in favor of T helper 17 (Th17) cells, an effect transferable to WT mice by fecal microbiota. Importantly, LP Th17 cell expansion and the development of spontaneous autoimmune arthritis in IL1rn -/- mice were attenuated under germ-free condition. Selective antibiotic treatment revealed that tobramycin-induced alterations of commensal intestinal microbiota, i.e., reduced Helicobacter, Flexispira, Clostridium, and Dehalobacterium, suppressed arthritis in IL1rn -/- mice. The arthritis phenotype in IL1rn -/- mice was previously shown to depend on Toll-like receptor 4 (TLR4). Using the ablation of both IL-1Ra and TLR4, we here show that the aberrations in the IL1rn -/- microbiota are partly TLR4-d

Published
2017

15. Alteration of the intestinal microbiome characterizes preclinical inflammatory arthritis in mice and its modulation attenuates established arthritis

Author

Rogier, R.L., Evans-Marin, Heather, Manasson, Julia, Kraan, P.M. van der, Walgreen, B., Helsen, M.M.A., Bersselaar, L.A.M. van den, Loo, F.A.J. van de, Lent, P.L. van, Berg, W.B. van den, Koenders, M.I., Scher, Jose U., Abdollahi-Roodsaz, S., Rogier, R.L., Evans-Marin, Heather, Manasson, Julia, Kraan, P.M. van der, Walgreen, B., Helsen, M.M.A., Bersselaar, L.A.M. van den, Loo, F.A.J. van de, Lent, P.L. van, Berg, W.B. van den, Koenders, M.I., Scher, Jose U., and Abdollahi-Roodsaz, S.

Abstract

Contains fulltext : 179543.pdf (publisher's version ) (Open Access)

Published
2017

16. Aberrant intestinal microbiota due to IL-1 receptor antagonist deficiency promotes IL-17- and TLR4-dependent arthritis

Author

Rogier, R.L., Ederveen, T.H., Boekhorst, J., Wopereis, H., Scher, J.U., Manasson, J., Frambach, S.J.C.M., Knol, J., Garssen, J., Kraan, P.M. van der, Koenders, M.I., Berg, W.B. van den, Hijum, S.A. van, Abdollahi-Roodsaz, S., Rogier, R.L., Ederveen, T.H., Boekhorst, J., Wopereis, H., Scher, J.U., Manasson, J., Frambach, S.J.C.M., Knol, J., Garssen, J., Kraan, P.M. van der, Koenders, M.I., Berg, W.B. van den, Hijum, S.A. van, and Abdollahi-Roodsaz, S.

Abstract

Contains fulltext : 174148.pdf (publisher's version ) (Open Access), BACKGROUND: Perturbation of commensal intestinal microbiota has been associated with several autoimmune diseases. Mice deficient in interleukin-1 receptor antagonist (Il1rn -/- mice) spontaneously develop autoimmune arthritis and are susceptible to other autoimmune diseases such as psoriasis, diabetes, and encephalomyelitis; however, the mechanisms of increased susceptibility to these autoimmune phenotypes are poorly understood. We investigated the role of interleukin-1 receptor antagonist (IL-1Ra) in regulation of commensal intestinal microbiota, and assessed the involvement of microbiota subsets and innate and adaptive mucosal immune responses that underlie the development of spontaneous arthritis in Il1rn -/- mice. RESULTS: Using high-throughput 16S rRNA gene sequencing, we show that IL-1Ra critically maintains the diversity and regulates the composition of intestinal microbiota in mice. IL-1Ra deficiency reduced the intestinal microbial diversity and richness, and caused specific taxonomic alterations characterized by overrepresented Helicobacter and underrepresented Ruminococcus and Prevotella. Notably, the aberrant intestinal microbiota in IL1rn -/- mice specifically potentiated IL-17 production by intestinal lamina propria (LP) lymphocytes and skewed the LP T cell balance in favor of T helper 17 (Th17) cells, an effect transferable to WT mice by fecal microbiota. Importantly, LP Th17 cell expansion and the development of spontaneous autoimmune arthritis in IL1rn -/- mice were attenuated under germ-free condition. Selective antibiotic treatment revealed that tobramycin-induced alterations of commensal intestinal microbiota, i.e., reduced Helicobacter, Flexispira, Clostridium, and Dehalobacterium, suppressed arthritis in IL1rn -/- mice. The arthritis phenotype in IL1rn -/- mice was previously shown to depend on Toll-like receptor 4 (TLR4). Using the ablation of both IL-1Ra and TLR4, we here show that the aberrations in the IL1rn -/- microbiota are partly TLR4-d

Published
2017

18. Aberrant intestinal microbiota due to IL-1 receptor antagonist deficiency promotes IL-17- and TLR4-dependent arthritis.

Author

Rogier, R.L. and Rogier, R.L.

Subjects
Radboudumc 11: Renal disorders RIMLS: Radboud Institute for Molecular Life Sciences., Radboudumc 4: lnfectious Diseases and Global Health RIMLS: Radboud Institute for Molecular Life Sciences., Radboudumc 5: Inflammatory diseases RIMLS: Radboud Institute for Molecular Life Sciences., Radboudumc 6: Metabolic Disorders RIMLS: Radboud Institute for Molecular Life Sciences.
Published
2017

19. Toll-like receptor mediated modulation of T cell response by commensal intestinal microbiota as a trigger for autoimmune arthritis

Author

Rogier, R.L., Koenders, M.I., Abdollahi-Roodsaz, S., Rogier, R.L., Koenders, M.I., and Abdollahi-Roodsaz, S.

Abstract

Contains fulltext : 154313.pdf (publisher's version ) (Open Access), In autoimmune diseases, a disturbance of the balance between T helper 17 (Th17) and regulatory T cells (Tregs) is often observed. This disturbed balance is also the case in rheumatoid arthritis (RA). Genetic predisposition to RA confers the presence of several polymorphisms mainly regulating activation of T lymphocytes. However, the presence of susceptibility factors is neither necessary nor sufficient to explain the disease development, emphasizing the importance of environmental factors. Multiple studies have shown that commensal gut microbiota is of great influence on immune homeostasis and can trigger the development of autoimmune diseases by favoring induction of Th17 cells over Tregs. However the mechanism by which intestinal microbiota influences the Th cell balance is not completely understood. Here we review the current evidence supporting the involvement of commensal intestinal microbiota in rheumatoid arthritis, along with a potential role of Toll-like receptors (TLRs) in modulating the relevant Th cell responses to trigger autoimmunity. A better understanding of TLR triggering by intestinal microbiota and subsequent T cell activation might offer new perspectives for manipulating the T cell response in RA patients and may lead to the discovery of new therapeutic targets or even preventive measures.

Published
2015

20. Toll-like receptor mediated modulation of T cell response by commensal intestinal microbiota as a trigger for autoimmune arthritis

Author

Rogier, R.L., Koenders, M.I., Abdollahi-Roodsaz, S., Rogier, R.L., Koenders, M.I., and Abdollahi-Roodsaz, S.

Abstract

Contains fulltext : 154313.pdf (publisher's version ) (Open Access), In autoimmune diseases, a disturbance of the balance between T helper 17 (Th17) and regulatory T cells (Tregs) is often observed. This disturbed balance is also the case in rheumatoid arthritis (RA). Genetic predisposition to RA confers the presence of several polymorphisms mainly regulating activation of T lymphocytes. However, the presence of susceptibility factors is neither necessary nor sufficient to explain the disease development, emphasizing the importance of environmental factors. Multiple studies have shown that commensal gut microbiota is of great influence on immune homeostasis and can trigger the development of autoimmune diseases by favoring induction of Th17 cells over Tregs. However the mechanism by which intestinal microbiota influences the Th cell balance is not completely understood. Here we review the current evidence supporting the involvement of commensal intestinal microbiota in rheumatoid arthritis, along with a potential role of Toll-like receptors (TLRs) in modulating the relevant Th cell responses to trigger autoimmunity. A better understanding of TLR triggering by intestinal microbiota and subsequent T cell activation might offer new perspectives for manipulating the T cell response in RA patients and may lead to the discovery of new therapeutic targets or even preventive measures.

Published
2015

21. Toll-like receptor mediated modulation of T cell response by commensal intestinal microbiota as a trigger for autoimmune arthritis

Author

Rogier, R.L., Koenders, M.I., Abdollahi-Roodsaz, S., Rogier, R.L., Koenders, M.I., and Abdollahi-Roodsaz, S.

Abstract

Contains fulltext : 154313.pdf (publisher's version ) (Open Access), In autoimmune diseases, a disturbance of the balance between T helper 17 (Th17) and regulatory T cells (Tregs) is often observed. This disturbed balance is also the case in rheumatoid arthritis (RA). Genetic predisposition to RA confers the presence of several polymorphisms mainly regulating activation of T lymphocytes. However, the presence of susceptibility factors is neither necessary nor sufficient to explain the disease development, emphasizing the importance of environmental factors. Multiple studies have shown that commensal gut microbiota is of great influence on immune homeostasis and can trigger the development of autoimmune diseases by favoring induction of Th17 cells over Tregs. However the mechanism by which intestinal microbiota influences the Th cell balance is not completely understood. Here we review the current evidence supporting the involvement of commensal intestinal microbiota in rheumatoid arthritis, along with a potential role of Toll-like receptors (TLRs) in modulating the relevant Th cell responses to trigger autoimmunity. A better understanding of TLR triggering by intestinal microbiota and subsequent T cell activation might offer new perspectives for manipulating the T cell response in RA patients and may lead to the discovery of new therapeutic targets or even preventive measures.

Published
2015

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