R B Sartor

Summary

Affiliation: University of North Carolina
Country: USA

Publications

  1. pmc Luminal and mucosal-associated intestinal microbiota in patients with diarrhea-predominant irritable bowel syndrome
    Ian M Carroll
    Division of Gastroenterology and Hepatology, Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
    Gut Pathog 2:19. 2010
  2. pmc Lactobacillus GG in inducing and maintaining remission of Crohn's disease
    Michael Schultz
    Department of Internal Medicine I, University of Regensburg, Regensburg, Germany
    BMC Gastroenterol 4:5. 2004
  3. doi request reprint Microbial influences in inflammatory bowel diseases
    R Balfour Sartor
    Department of Medicine, Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
    Gastroenterology 134:577-94. 2008
  4. doi request reprint Key questions to guide a better understanding of host-commensal microbiota interactions in intestinal inflammation
    R B Sartor
    Department of Medicine Division of Gastroenterology and Hepatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
    Mucosal Immunol 4:127-32. 2011
  5. ncbi request reprint Bacteria in Crohn's disease: mechanisms of inflammation and therapeutic implications
    R Balfour Sartor
    Department of Medicine, Division of Gastroenterology and Hepatology, University of North Carolina, Chapel Hill, NC 27599, USA
    J Clin Gastroenterol 41:S37-43. 2007
  6. doi request reprint Microbial-host interactions in inflammatory bowel diseases and experimental colitis
    R Balfour Sartor
    Departments of Medicine, Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27599, USA
    Nestle Nutr Workshop Ser Pediatr Program 64:121-32; discussion 132-7, 251-7. 2009
  7. ncbi request reprint Microbial host interactions in IBD: implications for pathogenesis and therapy
    R Balfour Sartor
    Department of Medicine, Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, CB 7032, Room 7309, Medical Biomolecular Research Building, Chapel Hill, NC 27599, USA
    Curr Gastroenterol Rep 9:497-507. 2007
  8. ncbi request reprint Therapeutic manipulation of the enteric microflora in inflammatory bowel diseases: antibiotics, probiotics, and prebiotics
    R Balfour Sartor
    Department of Medicine, Microbiology and Immunology, Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill, North Carolina 27599 7032 USA
    Gastroenterology 126:1620-33. 2004
  9. ncbi request reprint Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis
    R Balfour Sartor
    Department of Medicine, University of North Carolina, Chapel Hill, NC 27599 7032, USA
    Nat Clin Pract Gastroenterol Hepatol 3:390-407. 2006
  10. ncbi request reprint Role of commensal enteric bacteria in the pathogenesis of immune-mediated intestinal inflammation: lessons from animal models and implications for translational research
    R Balfour Sartor
    University of North Carolina, Chapel Hill, North Carolina, USA
    J Pediatr Gastroenterol Nutr 40:S30-1. 2005

Detail Information

Publications80

  1. pmc Luminal and mucosal-associated intestinal microbiota in patients with diarrhea-predominant irritable bowel syndrome
    Ian M Carroll
    Division of Gastroenterology and Hepatology, Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
    Gut Pathog 2:19. 2010
    ..abstract:..
  2. pmc Lactobacillus GG in inducing and maintaining remission of Crohn's disease
    Michael Schultz
    Department of Internal Medicine I, University of Regensburg, Regensburg, Germany
    BMC Gastroenterol 4:5. 2004
    ..The aim of this randomized, placebo-controlled trial was to determine the effect of oral Lactobacillus GG (L. GG) to induce or maintain medically induced remission...
  3. doi request reprint Microbial influences in inflammatory bowel diseases
    R Balfour Sartor
    Department of Medicine, Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
    Gastroenterology 134:577-94. 2008
    ..Identification of these host and microbial alterations in individual patients should lead to selective targeted interventions that correct underlying abnormalities and induce sustained and predictable therapeutic responses...
  4. doi request reprint Key questions to guide a better understanding of host-commensal microbiota interactions in intestinal inflammation
    R B Sartor
    Department of Medicine Division of Gastroenterology and Hepatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
    Mucosal Immunol 4:127-32. 2011
    ..These questions are designed to stimulate research that will promote a better understanding of host-microbial interactions in the intestine and promote targeted novel therapeutic interventions...
  5. ncbi request reprint Bacteria in Crohn's disease: mechanisms of inflammation and therapeutic implications
    R Balfour Sartor
    Department of Medicine, Division of Gastroenterology and Hepatology, University of North Carolina, Chapel Hill, NC 27599, USA
    J Clin Gastroenterol 41:S37-43. 2007
    ....
  6. doi request reprint Microbial-host interactions in inflammatory bowel diseases and experimental colitis
    R Balfour Sartor
    Departments of Medicine, Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27599, USA
    Nestle Nutr Workshop Ser Pediatr Program 64:121-32; discussion 132-7, 251-7. 2009
    ..Adherent/invasive Escherichia coli that adhere to and invade epithelial cells and resist killing by macrophages are increased in ileal CD...
  7. ncbi request reprint Microbial host interactions in IBD: implications for pathogenesis and therapy
    R Balfour Sartor
    Department of Medicine, Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, CB 7032, Room 7309, Medical Biomolecular Research Building, Chapel Hill, NC 27599, USA
    Curr Gastroenterol Rep 9:497-507. 2007
    ....
  8. ncbi request reprint Therapeutic manipulation of the enteric microflora in inflammatory bowel diseases: antibiotics, probiotics, and prebiotics
    R Balfour Sartor
    Department of Medicine, Microbiology and Immunology, Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill, North Carolina 27599 7032 USA
    Gastroenterology 126:1620-33. 2004
    ..These agents likely will become an integral component of treating IBD in combination with traditional anti-inflammatory and immunosuppressive agents...
  9. ncbi request reprint Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis
    R Balfour Sartor
    Department of Medicine, University of North Carolina, Chapel Hill, NC 27599 7032, USA
    Nat Clin Pract Gastroenterol Hepatol 3:390-407. 2006
    ..These new insights will help develop better diagnostic approaches that identify clinically important subsets of patients for whom the natural history of disease and response to treatment are predictable...
  10. ncbi request reprint Role of commensal enteric bacteria in the pathogenesis of immune-mediated intestinal inflammation: lessons from animal models and implications for translational research
    R Balfour Sartor
    University of North Carolina, Chapel Hill, North Carolina, USA
    J Pediatr Gastroenterol Nutr 40:S30-1. 2005
  11. ncbi request reprint Probiotic therapy of intestinal inflammation and infections
    R Balfour Sartor
    Department of Medicine, UNC, Chapel Hill, North Carolina 27599 7032, USA
    Curr Opin Gastroenterol 21:44-50. 2005
    ..The author presents evidence published during the past year regarding treatment of clinical and experimental intestinal inflammation and infections by probiotic agents...
  12. pmc Does Mycobacterium avium subspecies paratuberculosis cause Crohn's disease?
    R Balfour Sartor
    UNC Department of Medicine Division of Gastroenterology and Hepatology, CB 7032, Room 7309 Biomolecular Bldg MBRB, Chapel Hill, NC 27599 7032, USA
    Gut 54:896-8. 2005
    ..Reassessing this persistent theory in light of advances in molecular microbial detection and genetic pathogenesis of disease...
  13. ncbi request reprint Colitis in HLA-B27/beta 2 microglobulin transgenic rats
    R B Sartor
    University of North Carolina, Chapel Hill 27599 7038, USA
    Int Rev Immunol 19:39-50. 2000
    ....
  14. pmc Reduced ratio of protective versus proinflammatory cytokine responses to commensal bacteria in HLA-B27 transgenic rats
    L A Dieleman
    Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill, NC, USA
    Clin Exp Immunol 136:30-9. 2004
    ..However, B cell cytokine production in response to components of commensal intestinal microorganisms occurs in the absence of intestinal inflammation...
  15. pmc Adoptive transfer of nontransgenic mesenteric lymph node cells induces colitis in athymic HLA-B27 transgenic nude rats
    F Hoentjen
    Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill, NC, USA
    Clin Exp Immunol 143:474-83. 2006
    ....
  16. ncbi request reprint Variable phenotypes of enterocolitis in interleukin 10-deficient mice monoassociated with two different commensal bacteria
    Sandra C Kim
    Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill, NC 27599 7032, USA
    Gastroenterology 128:891-906. 2005
    ....
  17. ncbi request reprint TNF receptor-associated factor-2 is involved in both IL-1 beta and TNF-alpha signaling cascades leading to NF-kappa B activation and IL-8 expression in human intestinal epithelial cells
    C Jobin
    Department of Medicine, Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill 27599, USA
    J Immunol 162:4447-54. 1999
    ..In addition, our data suggest that TRAF-2 is involved in IL-1 beta signaling in HT-29 cells. Manipulation of cytokine signaling pathways represents a new approach for inhibiting proinflammatory gene expression in IEC...
  18. pmc Lactobacillus GG prevents recurrence of colitis in HLA-B27 transgenic rats after antibiotic treatment
    L A Dieleman
    Center for Gastrointestinal Biology and Disease and Division of Digestive Diseases, University of North Carolina at Chapel Hill, North Carolina 27599 7038, USA
    Gut 52:370-6. 2003
    ....
  19. ncbi request reprint Continuous stimulation by normal luminal bacteria is essential for the development and perpetuation of colitis in Tg(epsilon26) mice
    C Veltkamp
    Center for GI Biology and Disease, University of North Carolina, Chapel Hill, North Carolina 27599-7038, USA
    Gastroenterology 120:900-13. 2001
    ..Moreover, pathogenic T cells require the continuous presence of colonic bacteria to sustain colitis...
  20. ncbi request reprint Curcumin blocks cytokine-mediated NF-kappa B activation and proinflammatory gene expression by inhibiting inhibitory factor I-kappa B kinase activity
    C Jobin
    Department of Medicine, Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill 27599, USA
    J Immunol 163:3474-83. 1999
    ..Therefore, curcumin blocks a signal upstream of NF-kappa B-inducing kinase and IKK. We conclude that curcumin potently inhibits cytokine-mediated NF-kappa B activation by blocking a signal leading to IKK activity...
  21. pmc Differential effect of immune cells on non-pathogenic Gram-negative bacteria-induced nuclear factor-kappaB activation and pro-inflammatory gene expression in intestinal epithelial cells
    D Haller
    Department of Medicine and the Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill, USA
    Immunology 112:310-20. 2004
    ....
  22. pmc Different subsets of enteric bacteria induce and perpetuate experimental colitis in rats and mice
    H C Rath
    Center for GI Biology and Disease, University of North Carolina, Chapel Hill, North Carolina, USA
    Infect Immun 69:2277-85. 2001
    ....
  23. ncbi request reprint Lactobacillus plantarum 299V in the treatment and prevention of spontaneous colitis in interleukin-10-deficient mice
    Michael Schultz
    Center for GI Biology and Disease, Department of Medicine, University of North Carolina, Chapel Hill, NC 27599 7038, U S A
    Inflamm Bowel Dis 8:71-80. 2002
    ..These results demonstrate that L. plantarum can attenuate immune-mediated colitis and suggest a potential therapeutic role for this agent in clinical inflammatory bowel diseases...
  24. pmc Induction of persistent colitis by a human commensal, enterotoxigenic Bacteroides fragilis, in wild-type C57BL/6 mice
    Ki Jong Rhee
    Section of Digestive Diseases and Nutrition MC716, Department of Medicine, University of Illinois at Chicago, Room 741, Clinical Sciences Building, 840 South Wood Street, Chicago, IL 60612 7323, USA
    Infect Immun 77:1708-18. 2009
    ..Our data support the hypothesis that chronic colonization with the human commensal ETBF can induce persistent, subclinical colitis in humans...
  25. pmc Dysregulated luminal bacterial antigen-specific T-cell responses and antigen-presenting cell function in HLA-B27 transgenic rats with chronic colitis
    Bi Feng Qian
    Center for Gastrointestinal Biology and Disease, Department of Medicine, University of North Carolina, Chapel Hill, NC 27599, USA
    Immunology 116:112-21. 2005
    ..Alterations in the production of IFN-gamma, and in responses to this cytokine, as well as possible resistance of TG cells to suppressive regulation could together contribute to the development of chronic colitis in TG rats...
  26. pmc Endogenous antigen presenting cell-derived IL-10 inhibits T lymphocyte responses to commensal enteric bacteria
    Carol A Albright
    Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill, USA
    Immunol Lett 123:77-87. 2009
    ..Cytokines produced by APC are an important determinant of pathogenic versus protective mucosal immune responses to colonic bacterial stimulation...
  27. pmc Bifidobacterium animalis causes extensive duodenitis and mild colonic inflammation in monoassociated interleukin-10-deficient mice
    James P Moran
    Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill, North Carolina, USA
    Inflamm Bowel Dis 15:1022-31. 2009
    ..Here we tested the ability of this organism to cause T-cell-mediated intestinal inflammation by introducing it into germ-free (GF) IL-10-/- mice...
  28. ncbi request reprint Enhanced survival and mucosal repair after dextran sodium sulfate-induced colitis in transgenic mice that overexpress growth hormone
    K L Williams
    Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 7545, USA
    Gastroenterology 120:925-37. 2001
    ..Transgenic mice overexpressing GH (MT1-bGH-TG) were used to test whether increased plasma GH levels alter inflammation or crypt damage during dextran sodium sulfate (DSS)-induced colitis...
  29. ncbi request reprint Interleukin-10 signaling blocks inhibitor of kappaB kinase activity and nuclear factor kappaB DNA binding
    A J Schottelius
    Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina 27599 7295, USA
    J Biol Chem 274:31868-74. 1999
    ..This is the first evidence of an anti-inflammatory protein inhibiting IKK activity and demonstrates that IKK is a logical target for blocking inflammatory diseases...
  30. doi request reprint Aberrant innate immune responses in TLR-ligand activated HLA-B27 transgenic rat cells
    Bi Feng Qian
    Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill, NC 27599, USA
    Inflamm Bowel Dis 14:1358-65. 2008
    ..However, the role of the innate immune response to bacterial components has not been established...
  31. doi request reprint Reduced responsiveness of HLA-B27 transgenic rat cells to TGF-beta and IL-10-mediated regulation of IFN-gamma production
    Bi Feng Qian
    Center for Gastrointestinal Biology and Disease, Department of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599, USA
    Inflamm Bowel Dis 14:921-30. 2008
    ....
  32. pmc Antibiotics with a selective aerobic or anaerobic spectrum have different therapeutic activities in various regions of the colon in interleukin 10 gene deficient mice
    F Hoentjen
    Department of Gastroenterology, Free University Amsterdam, The Netherlands
    Gut 52:1721-7. 2003
    ..We investigated whether broad or narrow spectrum antibiotics affect onset and progression of disease in various regions of IL-10(-/-) mice...
  33. ncbi request reprint Dendritic cells in germ-free and specific pathogen-free mice have similar phenotypes and in vitro antigen presenting function
    Kristen L W Walton
    Department of Medicine, CB 7032, 7317 MBRB, University of North Carolina, Chapel Hill, NC 27599 7032, USA
    Immunol Lett 102:16-24. 2006
    ..In addition, splenic APC from GF mice are fully competent to stimulate naïve T-cell proliferation in vitro...
  34. pmc Altered macrophage function contributes to colitis in mice defective in the phosphoinositide-3 kinase subunit p110δ
    Jennifer K Uno
    Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, North Carolina, USA
    Gastroenterology 139:1642-53, 1653.e1-6. 2010
    ..Here, we further characterize features of inflammatory bowel diseases in these mice and investigate underlying innate immune defects...
  35. ncbi request reprint STAT3 regulates NF-kappaB recruitment to the IL-12p40 promoter in dendritic cells
    Frank Hoentjen
    Center for Gastrointestinal Biology and Diseases, University of North Carolina at Chapel Hill, USA
    Blood 105:689-96. 2005
    ..In conclusion, dysregulated LPS-induced IL-12p40 gene expression in IL-10(-/-) mice is due to enhanced NF-kappaB recruitment to the IL-12p40 promoter in the absence of activated STAT3...
  36. ncbi request reprint Treatment of inflammatory bowel disease with antibiotics
    Kim L Isaacs
    Division of Gastroenterology and Hepatology, Department of Medicine, University of North Carolina at Chapel Hill, 27599 7080, USA
    Gastroenterol Clin North Am 33:335-45, x. 2004
    ..This article summarizes published studies of antibiotics in IBD patients and reviews available data for the use of antibiotic therapy in Crohn's disease and ulcerative colitis...
  37. pmc The role of mucosal immunity and host genetics in defining intestinal commensal bacteria
    Jonathan Hansen
    Center for Gastrointestinal Biology and Disease, Division of Gastroenterology and Hepatology, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 7032, USA
    Curr Opin Gastroenterol 26:564-71. 2010
    ....
  38. ncbi request reprint Dual-association of gnotobiotic IL-10-/- mice with 2 nonpathogenic commensal bacteria induces aggressive pancolitis
    Sandra C Kim
    Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill, NC, USA
    Inflamm Bowel Dis 13:1457-66. 2007
    ..faecalis: late onset, distal colonic; E. coli: early onset, cecal). Hypothesis: E. faecalis and E. coli act in an additive manner to induce more aggressive colitis than disease induced by each bacterial species independently...
  39. ncbi request reprint IGF-I and procollagen alpha1(I) are coexpressed in a subset of mesenchymal cells in active Crohn's disease
    J B Pucilowska
    Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 7545, USA
    Am J Physiol Gastrointest Liver Physiol 279:G1307-22. 2000
    ..We conclude that increased IGF-I expression in multiple mesenchymal cell subtypes and increased numbers of cells with fibroblast/myofibroblast phenotype are involved in fibrosis associated with CD...
  40. doi request reprint Interplay of commensal and pathogenic bacteria, genetic mutations, and immunoregulatory defects in the pathogenesis of inflammatory bowel diseases
    C D Packey
    Department of Medicine, Program of Digestive Health, Unviersity of North Carolina at Chapel Hill, Chapell Hill, NC 27599 7032, USA
    J Intern Med 263:597-606. 2008
    ..Future therapies for these heterogeneous diseases should be individualized based on the patient-specific subset...
  41. ncbi request reprint IL-2-deficient mice raised under germfree conditions develop delayed mild focal intestinal inflammation
    M Schultz
    Center for Gastrointestinal Biology and Disease, Department of Medicine, University of North Carolina, Chapel Hill, NC 27599, USA
    Am J Physiol 276:G1461-72. 1999
    ..In contrast to other genetically engineered rodents, IL-2 -/- mice develop mild focal gastrointestinal and active portal tract inflammation in the absence of viable bacteria...
  42. pmc Commensal bacteria, traditional and opportunistic pathogens, dysbiosis and bacterial killing in inflammatory bowel diseases
    Christopher D Packey
    Department of Medicine, Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
    Curr Opin Infect Dis 22:292-301. 2009
    ..The authors present evidence published during the past 2 years of the roles of commensal and pathogenic bacteria in the pathogenesis of the inflammatory bowel diseases...
  43. ncbi request reprint CD4(+) T lymphocytes mediate colitis in HLA-B27 transgenic rats monoassociated with nonpathogenic Bacteroides vulgatus
    Frank Hoentjen
    Division of Gastroenterology and Hepatology, University of North Carolina, Chapel Hill, North Carolina, USA
    Inflamm Bowel Dis 13:317-24. 2007
    ..The aim of this study was therefore to investigate the role of T cells in the development of colitis in B. vulgatus-monoassociated HLA-B27 TG rats...
  44. pmc Lipopolysaccharide activates innate immune responses in murine intestinal myofibroblasts through multiple signaling pathways
    Kristen L W Walton
    Department of Medicine, Center for Gastrointestinal Biology, University of North Carolina, Chapel Hill, NC, USA
    Am J Physiol Gastrointest Liver Physiol 296:G601-11. 2009
    ..These data support the hypothesis that MF are a component of the innate immune system and may exert paracrine effects on adjacent epithelial and immune cells by responding to luminal bacterial adjuvants...
  45. ncbi request reprint IKK beta and phosphatidylinositol 3-kinase/Akt participate in non-pathogenic Gram-negative enteric bacteria-induced RelA phosphorylation and NF-kappa B activation in both primary and intestinal epithelial cell lines
    Dirk Haller
    Department of Medicine and the Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill, North Carolina 27599 7080, USA
    J Biol Chem 277:38168-78. 2002
    ..We propose that non-pathogenic B. vulgatus activates the NF-kappa B signaling pathway through both I kappa B degradation and RelA phosphorylation but that immune cells mediate tolerance of IEC to this commensal bacteria...
  46. pmc Gene expression patterns in experimental colitis in IL-10-deficient mice
    Jonathan J Hansen
    Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
    Inflamm Bowel Dis 15:890-9. 2009
    ....
  47. ncbi request reprint Clinical applications of advances in the genetics of IBD
    R Balfour Sartor
    Departments of Medicine, Microbiology, and Immunology Division of Digestive Diseases, University of North Carolina, Chapel Hill, NC, USA
    Rev Gastroenterol Disord 3:S9-17. 2003
    ..One can anticipate that it will become feasible to prospectively determine a patient's genotype and to individualize a drug regimen, leading to highly effective, safe treatments for IBD patients on a rational, rather than empiric, basis...
  48. ncbi request reprint The I kappa B/NF-kappa B system: a key determinant of mucosalinflammation and protection
    C Jobin
    Department of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599
    Am J Physiol Cell Physiol 278:C451-62. 2000
    ..The key role of NF-kappa B in regulating expression of a number of proinflammatory genes makes this protein an attractive target for selective therapeutic intervention...
  49. pmc Helicobacter hepaticus does not induce or potentiate colitis in interleukin-10-deficient mice
    L A Dieleman
    Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 7080, USA
    Infect Immun 68:5107-13. 2000
    ..hepaticus. We conclude that H. hepaticus does not induce or potentiate disease in our IL-10(-/-) mice and therefore is not required to induce colitis in genetically susceptible hosts...
  50. ncbi request reprint Bradykinin receptor antagonists type 2 attenuate the inflammatory changes in peptidoglycan-induced acute arthritis in the Lewis rat
    A B Uknis
    Sol Sherry Thrombosis Research Center, Department of Medicine, Temple University School of Medicine, Philadelphia, PA 19140, USA
    Inflamm Res 50:149-55. 2001
    ..CONCLUSIONS: These results indicate that the systemic inflammation is due in part to BK generation which can be blocked by B2-RA, while inhibiting the B1 receptor prevents an anti-inflammatory response...
  51. pmc Disrupted B-lymphocyte development and survival in interleukin-2-deficient mice
    M Schultz
    Center for Gastrointestinal Biology and Disease, Department of Medicine, University of North Carolina, Chapel Hill, NC, USA
    Immunology 104:127-34. 2001
    ..We conclude that conventional B cells in older IL-2-/- mice are lost by attrition owing to a derangement in B-cell development. Because B1 cells are less dependent on the bone marrow, a separate mechanism for their loss is suggested...
  52. ncbi request reprint Transforming growth factor-beta 1 inhibits non-pathogenic Gram negative bacteria-induced NF-kappa B recruitment to the interleukin-6 gene promoter in intestinal epithelial cells through modulation of histone acetylation
    Dirk Haller
    Department of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599, USA
    J Biol Chem 278:23851-60. 2003
    ..We concluded that the TGF-beta1/Smad signaling pathway helps maintain normal intestinal homeostasis to commensal luminal enteric bacteria by regulating NF-kappaB signaling in IEC through altered histone acetylation...
  53. ncbi request reprint NF-kappaB-inducing kinase restores defective IkappaB kinase activity and NF-kappaB signaling in intestinal epithelial cells
    Maria Pia Russo
    Department of Medicine, Division of Gastroenterology and Hepatology, CB 7032, Medical Biomolecular Research Building, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7080, USA
    Cell Signal 16:741-50. 2004
    ..These data show that altered NF-kappaB signaling is associated with impaired stimulation of an upstream IKK activator...
  54. pmc Impaired mucosal defense to acute colonic injury in mice lacking cyclooxygenase-1 or cyclooxygenase-2
    O Morteau
    Department of Medicine, University of North Carolina Chapel Hill, Chapel Hill, North Carolina 27599, USA
    J Clin Invest 105:469-78. 2000
    ....
  55. ncbi request reprint Expression and localization of IL-1beta mRNA is interrelated with cytoskeletal rearrangement in monocytes stimulated by adherence: a light microscopy in situ hybridization study
    U Bocker
    Center for Gastrointestinal Biology and Diseases, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
    Immunol Cell Biol 79:444-53. 2001
    ..The present study demonstrates that IL-1beta mRNA expression and localization in adherent monocytes is interrelated with the cytoskeletal rearrangement upon adherence, spreading and polarization...
  56. ncbi request reprint CCFA microbial-host interactions workshop: highlights and key observations
    R Balfour Sartor
    University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
    Inflamm Bowel Dis 13:600-19. 2007
    ....
  57. ncbi request reprint Innate immunity in the pathogenesis and therapy of IBD
    R Balfour Sartor
    Department of Medicine, Division of Digestive Diseases, CB 7038, Room 032, Glaxo Building, University of North Carolina, Chapel Hill, NC 27599 7038, USA
    J Gastroenterol 38:43-7. 2003
  58. ncbi request reprint Elevated vasoactive intestinal peptide concentrations in patients with irritable bowel syndrome
    Olafur S Palsson
    Division of Gastroenterology and Hepatology and Center for Functional Gastrointestinal and Motility Disorders, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
    Dig Dis Sci 49:1236-43. 2004
    ....
  59. pmc Specific microbiota direct the differentiation of IL-17-producing T-helper cells in the mucosa of the small intestine
    Ivaylo I Ivanov
    Kimmel Center for Biology and Medicine of the Skirball Institute, Department of Microbiology, New York University School of Medicine, New York, NY 10016, USA
    Cell Host Microbe 4:337-49. 2008
    ..Our results suggest that composition of intestinal microbiota regulates the Th17:Treg balance in the LP and may thus influence intestinal immunity, tolerance, and susceptibility to inflammatory bowel diseases...
  60. ncbi request reprint A novel human fibroblast growth factor treats experimental intestinal inflammation
    Michael Jeffers
    CuraGen Corporation, New Haven, Connecticut 06405, USA
    Gastroenterology 123:1151-62. 2002
    ..In the present study, we examined the activity of this protein in 2 animal models of acute intestinal inflammation and in mechanistic studies in vitro...
  61. pmc Alcohol, intestinal bacterial growth, intestinal permeability to endotoxin, and medical consequences: summary of a symposium
    Vishnudutt Purohit
    Division of Metabolism and Health Effects, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, 5635 Fishers Lane, Room 2035, MSC 9304, Bethesda, MD 20892 9304, USA
    Alcohol 42:349-61. 2008
    ..Thus reducing the number of intestinal Gram-negative bacteria and preserving intestinal permeability to endotoxin may attenuate alcoholic liver and other organ injuries...
  62. pmc Villous B cells of the small intestine are specialized for invariant NK T cell dependence
    Peter Velazquez
    Department of Pathology and Laboratory Medicine, University of California, Los Angeles, CA 90095, USA
    J Immunol 180:4629-38. 2008
    ..These findings define a distinct population of conventional B cells in small intestinal villi, and suggest an immunologic link between CD1-restricted invariant NK T cells and this B cell population...
  63. ncbi request reprint Bacterial symbionts induce a FUT2-dependent fucosylated niche on colonic epithelium via ERK and JNK signaling
    Di Meng
    Developmental Gastroenterology Laboratory, Massachusetts General Hospital East, 114 16th St, Rm 3650, Charlestown, MA 02129, USA
    Am J Physiol Gastrointest Liver Physiol 293:G780-7. 2007
    ....
  64. ncbi request reprint IL-10 gene-deficient mice lack TGF-beta/Smad-mediated TLR2 degradation and fail to inhibit proinflammatory gene expression in intestinal epithelial cells under conditions of chronic inflammation
    Pedro A Ruiz
    Else Kroener Fresenius Centre for Experimental Nutritional Medicine, Technical University of Munich, 85350 Freising Weihenstephan, Germany
    Ann N Y Acad Sci 1072:389-94. 2006
    ....
  65. ncbi request reprint Growth hormone reduces the severity of fibrosis associated with chronic intestinal inflammation
    Arianne L Theiss
    Department of Cell and Molecular Pathology, The Univesity of North Carolina at Chapel Hill, 27599 7545, USA
    Gastroenterology 129:204-19. 2005
    ..We tested if GH treatment altered inflammation or fibrosis during chronic, experimental granulomatous enterocolitis...
  66. ncbi request reprint Interleukin 10-deficient mice exhibit defective colonic Muc2 synthesis before and after induction of colitis by commensal bacteria
    Nicole M J Schwerbrock
    Pediatric Gastroenterology and Nutrition, Department of Pediatrics, Erasmus Medical Center, Rotterdam, The Netherlands
    Inflamm Bowel Dis 10:811-23. 2004
    ..These quantitative and structural aberrations in Muc2 in IL-10 mice likely reduce the ability of their mucosa to cope with nonpathogenic commensal bacteria and may contribute to their susceptibility to develop colitis...
  67. ncbi request reprint IL-10 gene-deficient mice lack TGF-beta/Smad signaling and fail to inhibit proinflammatory gene expression in intestinal epithelial cells after the colonization with colitogenic Enterococcus faecalis
    Pedro A Ruiz
    Centre for Nutrition and Food Research, Immunobiology of Nutrition, Technical University of Munich, Freising Weihenstephan, Germany
    J Immunol 174:2990-9. 2005
    ....
  68. ncbi request reprint Interleukin-10 blocked endoplasmic reticulum stress in intestinal epithelial cells: impact on chronic inflammation
    Anna Shkoda
    Else Kroener Fresenius Center for Experimental Nutritional Medicine, Technical University of Munich, 85350 Freising Weihenstephan, Germany
    Gastroenterology 132:190-207. 2007
    ..The aim of the study was to use functional epithelial cell proteomics to characterize anti-inflammatory mechanisms of interleukin 10 (IL-10)...
  69. ncbi request reprint 15-deoxy-delta12,14-prostaglandin J2-mediated ERK signaling inhibits gram-negative bacteria-induced RelA phosphorylation and interleukin-6 gene expression in intestinal epithelial cells through modulation of protein phosphatase 2A activity
    Pedro A Ruiz
    Centre for Nutrition and Food Research, Immunobiology of Nutrition, Technical University of Munich, 85350 Freising Weihenstephan, Germany
    J Biol Chem 279:36103-11. 2004
    ..We concluded that 15d-PGJ(2) may help to control NF-kappaB signaling and normal intestinal homeostasis to the enteric microflora by modulating RelA phosphorylation in IEC through altered protein phosphatase 2A activity...
  70. ncbi request reprint CD4+CD25+ cell depletion from the normal CD4+ T cell pool prevents tolerance toward the intestinal flora and leads to chronic colitis in immunodeficient mice
    Claudia Veltkamp
    Department of Gastroenterology, Ruprecht Karls University, Heidelberg, Germany
    Inflamm Bowel Dis 12:437-46. 2006
    ....
  71. ncbi request reprint Are we losing control? Medical costs can no longer be ignored
    R Balfour Sartor
    Gastroenterology 129:1149. 2005
  72. ncbi request reprint The hedgehog signalling pathway in the gastrointestinal tract: implications for development, homeostasis, and disease
    Charlie Lees
    Gastrointestinal Unit, School of Molecular and Clinical Medicine, Western General Hospital, University of Edinburgh, Edinburgh, United Kingdom
    Gastroenterology 129:1696-710. 2005
    ..We summarize the available evidence demonstrating that this developmental pathway has continuing roles in adult homeostasis and is dysregulated in malignancy and inflammation of the gastrointestinal tract...
  73. ncbi request reprint Kininogen deficiency modulates chronic intestinal inflammation in genetically susceptible rats
    Irma Isordia-Salas
    The Sol Sherry Thrombosis Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA
    Am J Physiol Gastrointest Liver Physiol 283:G180-6. 2002
    ..Plasma T-kininogen was significantly less in F5HKd. These results indicate the importance of the kallikrein-kinin system in this model of chronic enterocolitis and systemic inflammation...
  74. ncbi request reprint Challenges in IBD Research: updating the scientific agendas
    Charles O Elson
    Division of Gastroenterology, Inflammatory Bowel Disease Center, University of Alabama at Birmingham, USA
    Inflamm Bowel Dis 9:137-53. 2003
  75. ncbi request reprint Antithrombotic activity of kininogen is mediated by inhibitory effects of domain 3 during arterial injury in vivo
    Sarmina Hassan
    Sol Sherry Thrombosis Research Center, Temple Univeristy School of Medicine, 3400 N Broad St, Rm 418 OMS, Philadelphia, PA 19140, USA
    Am J Physiol Heart Circ Physiol 292:H2959-65. 2007
    ..We conclude that HKd rats are prothrombotic and that HKa, kininogen D3, and its fragment E7CP modulate arterial thrombosis after endothelial injury...
  76. ncbi request reprint Inflammatory-mediated repression of the rat ileal sodium-dependent bile acid transporter by c-fos nuclear translocation
    Frank Chen
    Division of Pediatric Gastroenterology, Nutrition and Liver Diseases, Department of Pediatrics and the Immunobiology Center, Mount Sinai School of Medicine, New York, New York 10029, USA
    Gastroenterology 123:2005-16. 2002
    ..Ileal malabsorption of bile salts is observed in Crohn's ileitis. We define the transcriptional mechanisms involved in cytokine-mediated repression of the rat apical sodium-dependent bile acid transporter (ASBT)...
  77. ncbi request reprint Episodic retreatment versus scheduled maintenance therapy of crohn's disease with infliximab: not so far apart
    R Balfour Sartor
    Gastroenterology 126:598-601. 2004
  78. pmc Intestinal heat shock protein 110 regulates expression of CD1d on intestinal epithelial cells
    Sean P Colgan
    Center for Experimental Therapeutics, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    J Clin Invest 112:745-54. 2003
    ..These data support the presence of a novel autocrine pathway of CD1d regulation by Hsp110...
  79. ncbi request reprint The mutation Ser511Asn leads to N-glycosylation and increases the cleavage of high molecular weight kininogen in rats genetically susceptible to inflammation
    Irma Isordia-Salas
    The Sol Sherry Thrombosis Research Center, Temple University School of Medicine, 3400 North Broad St, Philadelphia, PA 19140, USA
    Blood 102:2835-42. 2003
    ..When CHO cells were cultured in the presence of tunicamycin, the kallikrein-induced cleavage rate of Lewis HK was not increased. This molecular alteration might be one contributing factor resulting in chronic inflammation in Lewis rats...
  80. ncbi request reprint VSL#3 probiotic-mixture induces remission in patients with active ulcerative colitis
    Rodrigo Bibiloni
    Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada
    Am J Gastroenterol 100:1539-46. 2005
    ..We evaluated the safety and efficacy of VSL#3 and the components, and the composition of the biopsy-associated microbiota in patients with active mild to moderate ulcerative colitis (UC)...

Research Grants49

  1. GASTROENTEROLOGY RESEARCH TRAINING
    RYAN SARTOR; Fiscal Year: 2007
    ..least two years of intensive training in molecular techniques and basic pathophysiology in a diverse but integrated investigative environment that yields broadly trained independent investigators capable of adapting to rapid advances in ..
  2. Colitis Induced by immune responses to luminal bacteria-mouse
    RYAN BALFOUR SARTOR; Fiscal Year: 2010
    ....
  3. National Gnotobiotic Rodent Resource Center
    RYAN SARTOR; Fiscal Year: 2007
    ..abstract_text> ..
  4. COLITIS INDUCED BY IMMUNE RESPONSES TO LUMINAL BACTERIA
    RYAN SARTOR; Fiscal Year: 2007
    ..abstract_text> ..
  5. Non-Invasive Approaches to Assessing Inflammation (RMI)
    RYAN SARTOR; Fiscal Year: 2006
    ..This project will create a new program involving investigators who have not previously worked together, while building on institutional strengths and programmatic initiatives. ..
  6. COLITIS INDUCED BY IMMUNE RESPONSES TO LUMINAL BACTERIA
    RYAN SARTOR; Fiscal Year: 2006
    ..abstract_text> ..
  7. National Gnotobiotic Rodent Resource Center
    RYAN SARTOR; Fiscal Year: 2004
    ..abstract not provided..
  8. MECHANISMS OF COLITIS INDUCED BY DEFINED BACTERIAL FLORA
    RYAN SARTOR; Fiscal Year: 2007
    ..These innovative, mechanistic studies take advantage of our unique gnotobiotic rodent facilities, a proven multidisciplinary investigative team, and novel preliminary data. ..
  9. MECHANISMS OF COLITIS INDUCED BY DEFINED BACTERIAL FLORA
    RYAN SARTOR; Fiscal Year: 2007
    ..abstract_text> ..
  10. MECHANISMS OF COLITIS INDUCED BY DEFINED BACTERIAL FLORA
    RYAN BALFOUR SARTOR; Fiscal Year: 2010
    ..These innovative, mechanistic studies take advantage of our unique gnotobiotic rodent facilities, a proven multidisciplinary investigative team, and novel preliminary data. ..
  11. National Gnotobiotic Rodent Resource Center
    RYAN BALFOUR SARTOR; Fiscal Year: 2010
    ..In addition, it permits investigators to obtain preliminary data to submit competitive grant applications. In the past funding cycle these preliminary data and access to our facility resulted in 6 new funded grants. ..
  12. GASTROENTEROLOGY RESEARCH TRAINING
    RYAN SARTOR; Fiscal Year: 2007
    ..of intensive training in molecular techniques and basic pathophysiology in a diverse but integrated investigative environment that yields broadly trained independent investigators capable of adapting to rapid advances in ..
  13. MECHANISMS OF COLITIS INDUCED BY DEFINED BACTERIAL FLORA
    RYAN SARTOR; Fiscal Year: 2004
    ..These studies will generate novel insights into the pathogenesis of IBD and open new opportunities for novel therapeutic interventions to block induction of antigen-specific immune response to luminal bacteria. ..
  14. COLITIS INDUCED BY IMMUNE RESPONSES TO LUMINAL BACTERIA
    RYAN SARTOR; Fiscal Year: 2003
    ..abstract_text> ..
  15. COLITIS INDUCED BY IMMUNE RESPONSES TO LUMINAL BACTERIA
    RYAN SARTOR; Fiscal Year: 2001
    ..Successful completion of these specific aims will provide essential insights into the pathogenesis of IBD and suggest novel therapeutic approaches targeting etiologic mechanisms. ..
  16. REGULATION OF IMMUNOSUPPRESSIVE MOLECULES IN IBD
    RYAN SARTOR; Fiscal Year: 2001
    ....
  17. REGULATION OF IMMUNOSUPPRESSIVE MOLECULES IN IBD
    RYAN SARTOR; Fiscal Year: 1993
    ..Our ultimate goal is to treat and prevent IBD by augmenting endogenous inhibitory pathways either by gene therapy or pharmacologic stimulation...
  18. BACTERIAL CELL WALL-INDUCED GRANULOMATOUS ENTEROCOLITIS
    RYAN SARTOR; Fiscal Year: 1993
    ....