C P Kelly

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint Clostridium difficile infection
    C P Kelly
    Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    Annu Rev Med 49:375-90. 1998
  2. pmc p38 MAP kinase activation by Clostridium difficile toxin A mediates monocyte necrosis, IL-8 production, and enteritis
    M Warny
    Gastroenterology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    J Clin Invest 105:1147-56. 2000
  3. ncbi request reprint cag+ Helicobacter pylori induce transactivation of the epidermal growth factor receptor in AGS gastric epithelial cells
    S Keates
    Division of Gastroenterology and Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    J Biol Chem 276:48127-34. 2001
  4. ncbi request reprint ZBP-89, Sp1, and nuclear factor-kappa B regulate epithelial neutrophil-activating peptide-78 gene expression in Caco-2 human colonic epithelial cells
    A C Keates
    Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    J Biol Chem 276:43713-22. 2001
  5. ncbi request reprint Differential activation of mitogen-activated protein kinases in AGS gastric epithelial cells by cag+ and cag- Helicobacter pylori
    S Keates
    Gastroenterology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    J Immunol 163:5552-9. 1999
  6. doi request reprint Larazotide acetate in patients with coeliac disease undergoing a gluten challenge: a randomised placebo-controlled study
    C P Kelly
    Celiac Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    Aliment Pharmacol Ther 37:252-62. 2013
  7. doi request reprint Body mass index and the risk of obesity in coeliac disease treated with the gluten-free diet
    T A Kabbani
    Department of Medicine and Division of Gastroenterology, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Boston, MA 02215, USA
    Aliment Pharmacol Ther 35:723-9. 2012
  8. ncbi request reprint Association between antibody response to toxin A and protection against recurrent Clostridium difficile diarrhoea
    L Kyne
    Gerontology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    Lancet 357:189-93. 2001
  9. ncbi request reprint Interleukin 16 is up-regulated in Crohn's disease and participates in TNBS colitis in mice
    A C Keates
    Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    Gastroenterology 119:972-82. 2000
  10. pmc Helicobacter pylori infection stimulates plasminogen activator inhibitor 1 production by gastric epithelial cells
    A C Keates
    Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    Infect Immun 76:3992-9. 2008

Collaborators

Detail Information

Publications28

  1. ncbi request reprint Clostridium difficile infection
    C P Kelly
    Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    Annu Rev Med 49:375-90. 1998
    ..Diarrhea and colitis usually improve within three days after a patient starts taking metronidazole or vancomycin, but 20% suffer a relapse of diarrhea when these agents are discontinued...
  2. pmc p38 MAP kinase activation by Clostridium difficile toxin A mediates monocyte necrosis, IL-8 production, and enteritis
    M Warny
    Gastroenterology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    J Clin Invest 105:1147-56. 2000
    ..p38 MAP kinase also mediates intestinal inflammation and mucosal damage induced by toxin A...
  3. ncbi request reprint cag+ Helicobacter pylori induce transactivation of the epidermal growth factor receptor in AGS gastric epithelial cells
    S Keates
    Division of Gastroenterology and Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    J Biol Chem 276:48127-34. 2001
    ..Transactivation of gastric epithelial cell EGF receptors may be instrumental in regulating both proliferative and inflammatory responses induced by cag+ H. pylori infection...
  4. ncbi request reprint ZBP-89, Sp1, and nuclear factor-kappa B regulate epithelial neutrophil-activating peptide-78 gene expression in Caco-2 human colonic epithelial cells
    A C Keates
    Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    J Biol Chem 276:43713-22. 2001
    ..This study demonstrates that ENA-78 gene expression in Caco-2 intestinal epithelial cells is subject to complex regulation involving the coordinate binding of ZBP-89, Sp1, and nuclear factor-kappaB to the ENA-78 promoter...
  5. ncbi request reprint Differential activation of mitogen-activated protein kinases in AGS gastric epithelial cells by cag+ and cag- Helicobacter pylori
    S Keates
    Gastroenterology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    J Immunol 163:5552-9. 1999
    ..pylori cag+ strains may be instrumental in inducing gastroduodenal inflammation, ulceration, and neoplasia...
  6. doi request reprint Larazotide acetate in patients with coeliac disease undergoing a gluten challenge: a randomised placebo-controlled study
    C P Kelly
    Celiac Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    Aliment Pharmacol Ther 37:252-62. 2013
    ..Larazotide acetate is a first-in-class oral peptide that prevents tight junction opening, and may reduce gluten uptake and associated sequelae...
  7. doi request reprint Body mass index and the risk of obesity in coeliac disease treated with the gluten-free diet
    T A Kabbani
    Department of Medicine and Division of Gastroenterology, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Boston, MA 02215, USA
    Aliment Pharmacol Ther 35:723-9. 2012
    ..Coeliac disease is increasingly diagnosed and weight changes are common after adoption of a gluten-free diet (GFD), however data on body mass index (BMI) changes are limited...
  8. ncbi request reprint Association between antibody response to toxin A and protection against recurrent Clostridium difficile diarrhoea
    L Kyne
    Gerontology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    Lancet 357:189-93. 2001
    ..The aim of this study was to determine whether an acquired immune response to toxin A, during an episode of C. difficile diarrhoea, influences risk of recurrence...
  9. ncbi request reprint Interleukin 16 is up-regulated in Crohn's disease and participates in TNBS colitis in mice
    A C Keates
    Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    Gastroenterology 119:972-82. 2000
    ..The aim of this study was to determine whether IL-16 production is increased in inflammatory bowel disease and whether IL-16 participates in trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice...
  10. pmc Helicobacter pylori infection stimulates plasminogen activator inhibitor 1 production by gastric epithelial cells
    A C Keates
    Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    Infect Immun 76:3992-9. 2008
    ..pylori-mediated PAI-1 upregulation. These findings suggest that the upregulation of PAI-1 in H. pylori-infected gastric epithelial cells may contribute to the carcinogenic process...
  11. pmc Saccharomyces boulardii stimulates intestinal immunoglobulin A immune response to Clostridium difficile toxin A in mice
    A Qamar
    Gastroenterology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    Infect Immun 69:2762-5. 2001
    ..003) and a 4.4-fold increase in specific intestinal anti-toxin A levels (P < 0.001). Enhancing host intestinal immune responses may be an important mechanism for S. boulardii-mediated protection against diarrheal illnesses...
  12. pmc Gliadin-primed CD4+CD45RBlowCD25- T cells drive gluten-dependent small intestinal damage after adoptive transfer into lymphopenic mice
    T L Freitag
    Beth Israel Deaconess Medical Center, Boston, MA 02215, USA
    Gut 58:1597-605. 2009
    ..We aimed to assess the pathogenic role of gluten-reactive T cells and to generate a model of gluten-induced enteropathy...
  13. ncbi request reprint Clostridium difficile
    L Kyne
    Harvard Medical School, Gerontology Division, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
    Gastroenterol Clin North Am 30:753-77, ix-x. 2001
    ..Ultimately, active or passive immunization against C. difficile may be an effective means of controlling the growing problem of nosocomial C. difficile diarrhea and colitis...
  14. ncbi request reprint Gastric mucosal alpha(4)beta(7)-integrin-positive CD4 T lymphocytes and immune protection against helicobacter infection in mice
    M Michetti
    Division of Gastroenterology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA
    Gastroenterology 119:109-18. 2000
    ..This study examined the ability of alpha(4)beta(7)(hi) CD4(+) T lymphocytes to home to the stomach and their role in immunization-mediated protection against Helicobacter felis infection...
  15. pmc A randomized, double-blind study of larazotide acetate to prevent the activation of celiac disease during gluten challenge
    Daniel A Leffler
    Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    Am J Gastroenterol 107:1554-62. 2012
    ..The aim of this study was to evaluate the efficacy and tolerability of larazotide acetate in protecting against gluten-induced intestinal permeability and gastrointestinal symptom severity in patients with celiac disease...
  16. ncbi request reprint Signal transduction pathways mediating neurotensin-stimulated interleukin-8 expression in human colonocytes
    D Zhao
    Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    J Biol Chem 276:44464-71. 2001
    ..We speculate that these NT-related proinflammatory pathways are important in the pathophysiology of colonic inflammation...
  17. ncbi request reprint Monocytic cell necrosis is mediated by potassium depletion and caspase-like proteases
    M Warny
    Gastroenterology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    Am J Physiol 276:C717-24. 1999
    ..Thus, in monocytic cells, necrosis is a cell death pathway mediated by passive K+ efflux and activation of caspase-like proteases...
  18. pmc Safety and efficacy of low dose Escherichia coli enterotoxin adjuvant for urease based oral immunisation against Helicobacter pylori in healthy volunteers
    S Banerjee
    Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA
    Gut 51:634-40. 2002
    ..This study was undertaken to establish a safe and effective dose of LT, to confirm the safety of recombinant urease, and to compare the immunogenicity of orally compared with enterically delivered urease...
  19. doi request reprint Can we identify patients at high risk of recurrent Clostridium difficile infection?
    C P Kelly
    Gastroenterology Division, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA
    Clin Microbiol Infect 18:21-7. 2012
    ....
  20. ncbi request reprint P2Y(6) nucleotide receptor mediates monocyte interleukin-8 production in response to UDP or lipopolysaccharide
    M Warny
    Gastroenterology Divison, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    J Biol Chem 276:26051-6. 2001
    ..Furthermore, lipopolysaccharide mediates IL-8 production at least in part by autocrine P2Y(6) activation. These findings indicate a novel role for P2Y(6) in innate immune defenses...
  21. pmc Transactivation of the epidermal growth factor receptor by cag+ Helicobacter pylori induces upregulation of the early growth response gene Egr-1 in gastric epithelial cells
    S Keates
    Division of Gastroenterology, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA
    Gut 54:1363-9. 2005
    ....
  22. pmc Interaction between psychiatric and autoimmune disorders in coeliac disease patients in the Northeastern United States
    S Garud
    The Celiac Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    Aliment Pharmacol Ther 29:898-905. 2009
    ..Previous studies yielded conflicting results regarding the presence of an association between coeliac disease (CD) and psychiatric disorders including depression. This association has not been studied in the United States...
  23. ncbi request reprint P-glycoprotein-170 inhibition significantly reduces cortisol and ciclosporin efflux from human intestinal epithelial cells and T lymphocytes
    R J Farrell
    Department of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    Aliment Pharmacol Ther 16:1021-31. 2002
    ..To assess the role of P-glycoprotein-170 (P-gp) in transporting cortisol and ciclosporin from human intestinal epithelium and T lymphocytes...
  24. doi request reprint Noncoeliac enteropathy: the differential diagnosis of villous atrophy in contemporary clinical practice
    K Pallav
    Department of Gastroenterology, Beth Israel Deaconess Medical Center, Boston, MA, USA
    Aliment Pharmacol Ther 35:380-90. 2012
    ..Duodenal villous atrophy (DVA) is a key diagnostic finding in coeliac disease (CD). However, the differential diagnosis for this finding is broad...
  25. ncbi request reprint Diagnosis of celiac sprue
    R J Farrell
    Gastroenterology Division, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA
    Am J Gastroenterol 96:3237-46. 2001
    ..We review the wide spectrum of celiac sprue, its variable clinical manifestations, and the current approach to diagnosis...
  26. ncbi request reprint Enterocytes are the primary source of the chemokine ENA-78 in normal colon and ulcerative colitis
    S Keates
    Gastroenterology Division, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA
    Am J Physiol 273:G75-82. 1997
    ..ENA-78 as an enterocyte-derived, neutrophil-activating chemokine may be especially important in neutrophil recruitment from the lamina propria into the epithelial layer...
  27. ncbi request reprint A prospective comparative study of five measures of gluten-free diet adherence in adults with coeliac disease
    D A Leffler
    The Celiac Center, Beth Israel Deaconess Medical Center, Department of Gastroenterology, Boston, MA 02215, USA
    Aliment Pharmacol Ther 26:1227-35. 2007
    ..The only accepted treatment for coeliac disease is lifelong adherence to a strict gluten-free diet (GFD). Individuals' ability to adhere to the GFD varies, but systematic studies guiding the assessment of adherence are currently lacking...
  28. ncbi request reprint Prolapsing mucosal polyps: an underrecognized form of colonic polyp--a clinicopathological study of 15 cases
    D A Tendler
    Division of Gastroenterogy, Duke University Medical Center, Durham, North Carolina 7710, USA
    Am J Gastroenterol 97:370-6. 2002
    ..Prolapsing intestinal mucosa occurs in many forms throughout the GI tract. We describe 15 patients with polypoid masses in the sigmoid colon and histological features of mucosal prolapse...