CCL

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1.

001-es BibID:BIBFORM011928
Első szerző:Caja, Sergio
Cím:Inhibition of transglutaminase 2 enzymatic activity ameliorates the anti-angiogenic effects of coeliac disease autoantibodies / Caja S., Myrsky E., Korponay-Szabo I., Nadalutti C., Sulic A. M., Lavric M., Sblattero D., Marzari R., Collighan R., Mongeot A., Griffin M., Maki M., Kaukinen K., Lindfors K.
Dátum:2010
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Scandinavian Journal of Gastroenterology. - 45 : 4 (2010), p. 421-427. -
További szerzők:Myrsky, Essi Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Nadalutti, Cristina Sulic, Ana-Marija Lavric, Miha Sblattero, Daniele Marzari, Roberto Collighan, Russell Mongeot, Alexandre Griffin, Martin Mäki, Markku Kaukinen, Katri Lindfors, Katri
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM002290
Első szerző:Garcia-Horsman, J. Arturo
Cím:Deficient activity of mammalian prolyl oligopeptidase on the immunoactive peptide digestion in coeliac disease / J. Arturo Garcia-Horsman, Jarkko I. Venäläinen, Olli Lohi, I. Seppo Auriola, Ilma R. Korponay-Szabó, Katri Kaukinen, Markku Mäki, Pekka T. Männistö
Dátum:2007
Megjegyzések:Objective. Gliadin digestion-resistant peptides are harmful in coeliac disease (CD), and initiate an autoimmune reaction that cause a cascade of symptoms. The role of the endogenous prolyl oligopeptidase (POP) is still not clear, and its activity over gliadin immunoactive peptides has not been fully established. Our objective was therefore to determine the endogenous POP protein level, tissue distribution and total activity in normal and CD epithelia, to evaluate tissue peptidase activity over gliadin peptides, and compare this with activities of mammalian POP and rat intestinal extracts. Material and methods. POP was assayed in biopsy preparations enzymatically and by Western blot analysis. Distribution was studied by immunohistochemistry using a specific POP antibody. Peptide cleavage was followed by mass spectroscopy-highperformance liquid chromatography (MS-HPLC). Results. There was no difference in POP activity between normal and CD samples, but those from active CD subjects had an even higher ability to degrade the 33-mer peptide than those from treated CD and healthy humans. POP locates intracellularly in epithelia, similarly to dipeptidyl peptidase IV (DPPIV), but the latter is clearly found in normal microvilli but less so in diseased microvilli. Mammalian POP is unable to digest 33-mer peptide, which, conversely, is a POP inhibitor. Rat intestine is more effective than human intestine in cleaving the 33-mer peptide. However, the products are still harmful epitopes. A surplus of POP eliminates 12-mer and 19-mer peptide products. Conclusions. The results rule out a causative role of POP in the pathogenesis of CD and strongly suggest that other peptidases are needed to eliminate gliadin-derived, immunoactive and toxic peptides larger than 33-mer, which is a POP inhibitor.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
coeliac disease
digestion
gliadin
peptidase
prolyl oligopeptidase
Megjelenés:Scandinavian Journal of Gastroenterology 42 : 5 (2007), p. 562-571. -
További szerzők:Venäläinen, Jarkko I. Lohi, Olli Auriola, I. Seppo Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Kaukinen, Katri Mäki, Markku Männistö, Pekka T.
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3.

001-es BibID:BIBFORM044301
Első szerző:Kaukinen, Katri
Cím:Small-bowel mucosal transglutaminase 2-specific IgA deposits in coeliac disease without villous atrophy : a prospective and randomized clinical study / Kaukinen Katri, Peräaho Markku, Collin Pekka, Partanen Jukka, Woolley Nina, Kaartinen Tanja, Nuutinen Tuula, Halttunen Tuula, Mäki Markku, Korponay-Szabo Ilma
Dátum:2005
ISSN:0036-5521
Megjegyzések:OBJECTIVE:In coeliac disease, autoantibodies directed against transglutaminase 2 are produced in small-bowel mucosa, and they have been found to be deposited extracellularly. The aim of this study was to investigate whether such mucosal IgA deposits are important in the diagnostic work-up of early-stage coeliac disease without small-bowel mucosal villous atrophy.MATERIAL AND METHODS:Forty-one adults suspected of coeliac disease owing to increased density of mucosal gamma(delta)+ intraepithelial lymphocytes but normal villous morphology were randomized to gluten challenge or a gluten-free diet for 6 months. Clinically and histologically verified gluten dependency was compared with existence of small-bowel mucosal transglutaminase 2-specific extracellular IgA deposits and (coeliac disease-type) HLA DQ2 and DQ8; 34 non-coeliac subjects and 18 patients with classical coeliac disease served as controls.RESULTS:Of the 41 patients, 5 in the challenge group and 6 in the gluten-free diet group were clinically gluten sensitive; all 11 had HLA DQ2 or DQ8. Ten of these 11 patients showed transglutaminase 2-targeted mucosal IgA deposits, which were dependent on gluten consumption. Minimal IgA deposits were seen in only 3 out of 30 patients with suspected coeliac disease without any clinically detected gluten dependency. The deposits were found in all classical coeliac patients and in none of the non-coeliac control subjects.CONCLUSIONS:Clinically pertinent coeliac disease exists despite normal small-bowel mucosal villous architecture. Mucosal transglutaminase 2-specific IgA deposits can be utilized in detecting such patients with genetic gluten intolerance
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Scandinavian Journal Of Gastroenterology. - 40 : 5 (2005), p. 564-572. -
További szerzők:Peräaho, Markku Collin, Pekka Partanen, Jukka Woolley, Nina Kaartinen, Tanja Nuutinen, Tuula Halttunen, Tuula Mäki, Markku Korponay-Szabó Ilma (1959-) (gyermekgyógyász)
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4.

001-es BibID:BIBFORM025026
Első szerző:Myrsky, Essi
Cím:Altered small-bowel mucosal vascular network in untreated coeliac disease / Myrsky E., Syrjänen M., Korponay-Szabo I. R., Mäki M., Kaukinen K., Lindfors K.
Dátum:2009
ISSN:0036-5521
Megjegyzések:It has recently been shown that serum autoantibodies targeted against transglutaminase 2 derived from untreated coeliac patients can disturb several steps of angiogenesis in vitro. The purpose of this study was to establish whether the small-bowel mucosal vasculature is altered in coeliac disease and whether the putative changes are gluten dependent. MATERIAL AND METHODS: The small-bowel mucosal microvessel architecture was examined in duodenal biopsy samples from coeliac patients before and after a gluten-free diet and from non-coeliac controls. In addition, the vasculature was subjected to a detailed morphometric analysis. Double immunofluorescent stainings of the vasculature with anti- alpha-smooth muscle actin antibody were performed in order to assess the maturity of mucosal vessels. Coeliac disease-specific transglutaminase 2-targeted autoantibody deposits in the vessel wall were studied using triple immunofluorescent stainings. RESULTS: On a gluten-containing diet the mucosal vasculature in the small intestine of untreated coeliac disease patients was altered in overall organization as well as in the number and maturity of the vessels when compared to healthy subjects. In patients on a gluten-free diet, the vasculature normalized parallel to mucosal recovery. CONCLUSIONS: In coeliac disease, ingestion of gluten leads to altered appearance of small-bowel mucosal microvasculature. It is thus conceivable that the small-bowel mucosal vascular biology might be involved in the pathogenesis of coeliac disease.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Scandinavian Journal Of Gastroenterology. - 44 : 2 (2009), p. 162-167. -
További szerzők:Syrjänen, Mari Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Mäki, Markku Kaukinen, Katri Lindfors, Katri
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