期刊论文详细信息
BMC Gastroenterology
Serum parameters in the spectrum of coeliac disease: beyond standard antibody testing - a cohort study
Marco W J Schreurs4  Chris J J Mulder2  Petra Bonnet1  Veerle M H Coupe3  Hedayat Amini1  B Mary E Von Blomberg1  Roy L J van Wanrooij2  Greetje J Tack2 
[1] Department of Pathology, VU University Medical Centre, Amsterdam The Netherlands;Department of Gastroenterology and Hepatology, VU University Medical Centre, PO Box 7057, Amsterdam 1007 MB, The Netherlands;Department of Epidemiology and Biostatistics, VU University Medical Centre, Amsterdam The Netherlands;Department of Immunology, Erasmus MC, University Medical Centre, Rotterdam, The Netherlands
关键词: Immunological and biochemical parameters;    Cytokines;    Enteropathy associated T-cell lymphoma;    Refractory coeliac disease;    Coeliac disease;   
Others  :  858305
DOI  :  10.1186/1471-230X-12-159
 received in 2012-05-21, accepted in 2012-11-04,  发布年份 2012
PDF
【 摘 要 】

Background

Invasive techniques are still required to distinguish between uncomplicated and complicated forms of CD.

Methods

We set out to investigate the potential use of novel serum parameters, including IL-6, IL-8, IL-17, IL-22, sCD25, sCD27, granzyme-B, sMICA and sCTLA-4 in patients diagnosed with active CD, CD on a GFD, Refractory coeliac disease (RCD) type I and II, and enteropathy associated T-cell lymphoma (EATL).

Results

In both active CD and RCDI-II elevated levels of the proinflammatory IL-8, IL-17 and sCD25 were observed. In addition, RCDII patients displayed higher serum levels of soluble granzyme-B and IL-6 in comparison to active CD patients. In contrast, no differences between RCDI and active CD or RCDII were observed. Furthermore, EATL patients displayed higher levels of IL-6 as compared to all other groups.

Conclusions

A series of novel serum parameters reveal distinctive immunological characteristics of RCDII and EATL in comparison to uncomplicated CD and RCDI.

【 授权许可】

   
2012 Tack et al.; licensee BioMed Central Ltd.

【 预 览 】
附件列表
Files Size Format View
20140723100806591.pdf 284KB PDF download
21KB Image download
56KB Image download
【 图 表 】

【 参考文献 】
  • [1]Jabri B, Sollid LM: Tissue-mediated control of immunopathology in coeliac disease. Nat Rev Immunol 2009, 9(12):858-870.
  • [2]Nilsen EM, Jahnsen FL, Lundin KE, Johansen FE, Fausa O, Sollid LM, Jahnsen J, Scott H, Brandtzaeg P: Gluten induces an intestinal cytokine response strongly dominated by interferon gamma in patients with celiac disease. Gastroenterology 1998, 115(3):551-563.
  • [3]Fernandez S, Molina IJ, Romero P, Gonzalez R, Pena J, Sanchez F, Reynoso FR, Perez-Navero JL, Estevez O, Ortega C, Santamaria M: Characterization of gliadin-specific Th17 cells from the mucosa of celiac disease patients. Am J Gastroenterol 2011, 106(3):528-538.
  • [4]Monteleone I, Sarra M, Del Vecchio BG, Paoluzi OA, Franze E, Fina D, Fabrizi A, MacDonald TT, Pallone F, Monteleone G: Characterization of IL-17A-producing cells in celiac disease mucosa. J Immunol 2010, 184(4):2211-2218.
  • [5]Sapone A, Lammers KM, Mazzarella G, Mikhailenko I, Carteni M, Casolaro V, Fasano A: Differential mucosal IL-17 expression in two gliadin-induced disorders: gluten sensitivity and the autoimmune enteropathy celiac disease. Int Arch Allergy Immunol 2010, 152(1):75-80.
  • [6]Hue S, Mention JJ, Monteiro RC, Zhang S, Cellier C, Schmitz J, Verkarre V, Fodil N, Bahram S, Cerf-Bensussan N, Caillat-Zucman S: A direct role for NKG2D/MICA interaction in villous atrophy during celiac disease. Immunity 2004, 21(3):367-377.
  • [7]Meresse B, Chen Z, Ciszewski C, Tretiakova M, Bhagat G, Krausz TN, Raulet DH, Lanier LL, Groh V, Spies T, Ebert EC, Green PH, Jabri B: Coordinated induction by IL15 of a TCR-independent NKG2D signaling pathway converts CTL into lymphokine-activated killer cells in celiac disease. Immunity 2004, 21(3):357-366.
  • [8]Daum S, Cellier C, Mulder CJ: Refractory coeliac disease. Best Pract Res Clin Gastroenterol 2005, 19(3):413-424.
  • [9]Rubio-Tapia A, Murray JA: Classification and management of refractory coeliac disease. Gut 2010, 59(4):547-557.
  • [10]Verbeek WH, Goerres MS, von Blomberg BM, Oudejans JJ, Scholten PE, Hadithi M, Al-Toma A, Schreurs MW, Mulder CJ: Flow cytometric determination of aberrant intra-epithelial lymphocytes predicts T-cell lymphoma development more accurately than T-cell clonality analysis in Refractory Celiac Disease. Clin Immunol 2008, 126(1):48-56.
  • [11]Cellier C, Patey N, Mauvieux L, Jabri B, Delabesse E, Cervoni JP, Burtin ML, Guy-Grand D, Bouhnik Y, Modigliani R, Barbier JP, Macintyre E, Brousse N, Cerf-Bensussan N: Abnormal intestinal intraepithelial lymphocytes in refractory sprue. Gastroenterology 1998, 114(3):471-481.
  • [12]Tack GJ, van Wanrooij RL, Langerak AW, Tjon JM, von Blomberg BM, Heideman DA, van BJ, Koning F, Bouma G, Mulder CJ, Schreurs MW: Origin and immunophenotype of aberrant IEL in RCDII patients. Mol Immunol 2012, 50(4):262-270.
  • [13]de Bruin PC, Connolly CE, Oudejans JJ, Kummer JA, Jansen W, McCarthy CF, Meijer CJ: Enteropathy-associated T-cell lymphomas have a cytotoxic T-cell phenotype. Histopathology 1997, 31(4):313-317.
  • [14]Al-Toma A, Verbeek WH, Hadithi M, von Blomberg BM, Mulder CJ: Survival in refractory coeliac disease and enteropathy-associated T-cell lymphoma: retrospective evaluation of single-centre experience. Gut 2007, 56(10):1373-1378.
  • [15]Daum S, Ipczynski R, Schumann M, Wahnschaffe U, Zeitz M, Ullrich R: High rates of complications and substantial mortality in both types of refractory sprue. Eur J Gastroenterol Hepatol 2009, 21(1):66-70.
  • [16]Malamut G, Afchain P, Verkarre V, Lecomte T, Amiot A, Damotte D, Bouhnik Y, Colombel JF, Delchier JC, Allez M, Cosnes J, Lavergne-Slove A, Meresse B, Trinquart L, Macintyre E, Radford-Weiss I, Hermine O, Brousse N, Cerf-Bensussan N, Cellier C: Presentation and long-term follow-up of refractory celiac disease: comparison of type I with type II. Gastroenterology 2009, 136(1):81-90.
  • [17]Rubio-Tapia A, Kelly DG, Lahr BD, Dogan A, Wu TT, Murray JA: Clinical staging and survival in refractory celiac disease: a single center experience. Gastroenterology 2009, 136(1):99-107.
  • [18]Walker-Smith JA, Guandalini S, Schmitz J: Revised criteria for diagnosis of coeliac disease. Report of Working Group of European Society of Paediatric Gastroenterology and Nutrition. Arch Dis Child 1990, 65(8):909-911.
  • [19]Oberhuber G, Granditsch G, Vogelsang H: The histopathology of coeliac disease: time for a standardized report scheme for pathologists. Eur J Gastroenterol Hepatol 1999, 11(10):1185-1194.
  • [20]Manavalan JS, Hernandez L, Shah JG, Konikkara J, Naiyer AJ, Lee AR, Ciaccio E, Minaya MT, Green PH, Bhagat G: Serum cytokine elevations in celiac disease: association with disease presentation. Hum Immunol 2010, 71(1):50-57.
  • [21]Kerttula TO, Hallstrom O, Maki M: Phenotypical characterization of peripheral blood T cells in patients with coeliac disease: elevation of antigen-primed CD45RO + T lymphocytes. Immunology 1995, 86(1):104-109.
  • [22]Lahat N, Shapiro S, Karban A, Gerstein R, Kinarty A, Lerner A: Cytokine profile in coeliac disease. Scand J Immunol 1999, 49(4):441-446.
  • [23]Nilsen EM, Lundin KE, Krajci P, Scott H, Sollid LM, Brandtzaeg P: Gluten specific, HLA-DQ restricted T cells from coeliac mucosa produce cytokines with Th1 or Th0 profile dominated by interferon gamma. Gut 1995, 37(6):766-776.
  • [24]Hall RP III, Benbenisty KM, Mickle C, Takeuchi F, Streilein RD: Serum IL-8 in patients with dermatitis herpetiformis is produced in response to dietary gluten. J Invest Dermatol 2007, 127(9):2158-2165.
  • [25]Blanco A, Garrote JA, Arranz E, Alonso M, Clavo C: Increased serum IL-2R levels in coeliac disease are related to CD4 but not CD8 antigens. J Pediatr Gastroenterol Nutr 1992, 15(4):413-417.
  • [26]Romaldini CC, Barbieri D, Okay TS, Raiz R Jr, Cancado EL: Serum soluble interleukin-2 receptor, interleukin-6, and tumor necrosis factor-alpha levels in children with celiac disease: response to treatment. J Pediatr Gastroenterol Nutr 2002, 35(4):513-517.
  • [27]Srivastava MD, Rossi TM, Lebenthal E: Serum soluble interleukin-2 receptor, soluble CD8 and soluble intercellular adhesion molecule-1 levels in Crohn’s disease, celiac disease, and systemic lupus erythematosus. Res Commun Mol Pathol Pharmacol 1995, 87(1):21-26.
  • [28]Fornari MC, Pedreira S, Niveloni S, Gonzalez D, Diez RA, Vazquez H, Mazure R, Sugai E, Smecuol E, Boerr L, Maurino E, Bai JC: Pre- and post-treatment serum levels of cytokines IL-1beta, IL-6, and IL-1 receptor antagonist in celiac disease. Are they related to the associated osteopenia? Am J Gastroenterol 1998, 93(3):413-418.
  • [29]Bettelli E, Carrier Y, Gao W, Korn T, Strom TB, Oukka M, Weiner HL, Kuchroo VK: Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells. Nature 2006, 441(7090):235-238.
  • [30]Strober W, Fuss IJ: Proinflammatory cytokines in the pathogenesis of inflammatory bowel diseases. Gastroenterology 2011, 140(6):1756-1767.
  • [31]Trifari S, Kaplan CD, Tran EH, Crellin NK, Spits H: Identification of a human helper T cell population that has abundant production of interleukin 22 and is distinct from T(H)-17, T(H)1 and T(H)2 cells. Nat Immunol 2009, 10(8):864-871.
  • [32]Brand S, Beigel F, Olszak T, Zitzmann K, Eichhorst ST, Otte JM, Diepolder H, Marquardt A, Jagla W, Popp A, Leclair S, Herrmann K, Seiderer J, Ochsenkuhn T, Goke B, Auernhammer CJ, Dambacher J: IL-22 is increased in active Crohn’s disease and promotes proinflammatory gene expression and intestinal epithelial cell migration. Am J Physiol Gastrointest Liver Physiol 2006, 290(4):G827-G838.
  • [33]Bodd M, Raki M, Tollefsen S, Fallang LE, Bergseng E, Lundin KE, Sollid LM: HLA-DQ2-restricted gluten-reactive T cells produce IL-21 but not IL-17 or IL-22. Mucosal Immunol 2010, 3(6):594-601.
  • [34]Font J, Pallares L, Martorell J, Martinez E, Gaya A, Vives J, Ingelmo M: Elevated soluble CD27 levels in serum of patients with systemic lupus erythematosus. Clin Immunol Immunopathol 1996, 81(3):239-243.
  • [35]Tak PP, Hintzen RQ, Teunissen JJ, Smeets TJ, Daha MR, van Lier RA, Kluin PM, Meinders AE, Swaak AJ, Breedveld FC: Expression of the activation antigen CD27 in rheumatoid arthritis. Clin Immunol Immunopathol 1996, 80(2):129-138.
  • [36]Swaak AJ, Hintzen RQ, Huysen V, van den Brink HG, Smeenk JT: Serum levels of soluble forms of T cell activation antigens CD27 and CD25 in systemic lupus erythematosus in relation with lymphocytes count and disease course. Clin Rheumatol 1995, 14(3):293-300.
  • [37]Metkar SS, Naresh KN, Manna PP, Srinivas V, Advani SH, Nadkarni JJ: Circulating levels of TNF alpha and TNF receptor superfamily members in lymphoid neoplasia. Am J Hematol 2000, 65(2):105-110.
  • [38]Rubin LA, Nelson DL: The soluble interleukin-2 receptor: biology, function, and clinical application. Ann Intern Med 1990, 113(8):619-627.
  • [39]Tack GJ, Verbeek WH, Van De Water JM, von Blomberg BM, Bhola SL, Ylstra B, Mulder CJ, Schreurs MW: Phenotypic and genomic analysis of an exceptional case of enteropathy associated T-cell lymphoma. Leuk Res 2010, 34(8):e183-e189.
  • [40]Groh V, Wu J, Yee C, Spies T: Tumour-derived soluble MIC ligands impair expression of NKG2D and T-cell activation. Nature 2002, 419(6908):734-738.
  • [41]Salih HR, Antropius H, Gieseke F, Lutz SZ, Kanz L, Rammensee HG, Steinle A: Functional expression and release of ligands for the activating immunoreceptor NKG2D in leukemia. Blood 2003, 102(4):1389-1396.
  • [42]Kurzrock R, Redman J, Cabanillas F, Jones D, Rothberg J, Talpaz M: Serum interleukin 6 levels are elevated in lymphoma patients and correlate with survival in advanced Hodgkin’s disease and with B symptoms. Cancer Res 1993, 53(9):2118-2122.
  • [43]Gustot T, Lemmers A, Louis E, Nicaise C, Quertinmont E, Belaiche J, Roland S, Van GA, Deviere J, Franchimont D: Profile of soluble cytokine receptors in Crohn’s disease. Gut 2005, 54(4):488-495.
  • [44]Haghazali M, Molaei M, Mashayekhi R, Zojaji H, Pourhoseingholi MA, Shooshtarizadeh T, Mirsattari D, Zali MR: Proinflammatory cytokines and thrombomodulin in patients with peptic ulcer disease and gastric cancer, infected with Helicobacter pylori. Indian J Pathol Microbiol 2011, 54(1):103-106.
  文献评价指标  
  下载次数:17次 浏览次数:1次