Detail
Článek
FT
Medvik - BMČ
  • Je něco špatně v tomto záznamu ?

Occurrence of serum antibodies against wheat alpha-amylase inhibitor 0.19 in celiac disease

D. Sánchez, S. Štěpánová Honzová, M. Hospodková, I. Hoffmanová, V. Hábová, P. Halada, H. Tlaskalová-Hogenová, L. Tučková

. 2018 ; 67 (4) : 613-622. [pub] 20180510

Jazyk angličtina Země Česko

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc19004007

The alcohol-soluble fraction of wheat gluten (gliadins) induces in genetically susceptible individuals immunologically mediated celiac disease (CLD). However, gliadins and related cereal proteins are not unique foodstuff targets of CLD patients´ immune system. Non-gluten wheat alpha-amylase inhibitor 0.19 (AAI 0.19) has been found to be capable of activating human monocyte-derived dendritic cells and inducing pro-inflammatory status in intestinal mucosa of patients with celiac disease (CLD). The possible contribution of this reactivity in incomplete remission of CLD patients on a gluten-free diet (GFD) is matter of contention. In an attempt to characterize the antigenicity of AAI 0.19 in patients with active CLD, patients on a GFD and healthy controls we developed ELISA employing wheat recombinant AAI 0.19. Using this test we revealed a significant (P<0.001) elevation of IgA anti-AAI 0.19 antibodies (Ab) in patients with active CLD (12 out of 30 patients were seropositive) but also in CLD patients on a GFD (15/46), in contrast to healthy controls (2/59). Anti-AAI 0.19 IgG Ab levels were increased (P<0.001) only in patients with active CLD (14/30) in contrast to the controls. Interestingly, the levels of anti-AAI 0.19 IgG Ab were decreased in CLD patients on a GFD (P<0.001, 1/46) compared to the controls (1/59). Notably, 20 out of 30 patients with active CLD were positive either for IgA or for IgG anti-AAI 0.19 Ab. Thus, the majority of CLD patients developed a robust IgA and IgG Ab response against AAI 0.19. These findings may contribute to the broadening of the knowledge about CLD pathogenesis.

000      
00000naa a2200000 a 4500
001      
bmc19004007
003      
CZ-PrNML
005      
20190208091451.0
007      
ta
008      
190124s2018 xr ad f 000 0|eng||
009      
AR
024    7_
$a 10.33549/physiolres.933876 $2 doi
035    __
$a (PubMed)29750882
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xr
100    1_
$a Sánchez, Daniel $u Laboratory of Cellular and Molecular Immunology, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czech Republic. sanchez@biomed.cas.cz. $7 xx0129504
245    10
$a Occurrence of serum antibodies against wheat alpha-amylase inhibitor 0.19 in celiac disease / $c D. Sánchez, S. Štěpánová Honzová, M. Hospodková, I. Hoffmanová, V. Hábová, P. Halada, H. Tlaskalová-Hogenová, L. Tučková
520    9_
$a The alcohol-soluble fraction of wheat gluten (gliadins) induces in genetically susceptible individuals immunologically mediated celiac disease (CLD). However, gliadins and related cereal proteins are not unique foodstuff targets of CLD patients´ immune system. Non-gluten wheat alpha-amylase inhibitor 0.19 (AAI 0.19) has been found to be capable of activating human monocyte-derived dendritic cells and inducing pro-inflammatory status in intestinal mucosa of patients with celiac disease (CLD). The possible contribution of this reactivity in incomplete remission of CLD patients on a gluten-free diet (GFD) is matter of contention. In an attempt to characterize the antigenicity of AAI 0.19 in patients with active CLD, patients on a GFD and healthy controls we developed ELISA employing wheat recombinant AAI 0.19. Using this test we revealed a significant (P<0.001) elevation of IgA anti-AAI 0.19 antibodies (Ab) in patients with active CLD (12 out of 30 patients were seropositive) but also in CLD patients on a GFD (15/46), in contrast to healthy controls (2/59). Anti-AAI 0.19 IgG Ab levels were increased (P<0.001) only in patients with active CLD (14/30) in contrast to the controls. Interestingly, the levels of anti-AAI 0.19 IgG Ab were decreased in CLD patients on a GFD (P<0.001, 1/46) compared to the controls (1/59). Notably, 20 out of 30 patients with active CLD were positive either for IgA or for IgG anti-AAI 0.19 Ab. Thus, the majority of CLD patients developed a robust IgA and IgG Ab response against AAI 0.19. These findings may contribute to the broadening of the knowledge about CLD pathogenesis.
650    _2
$a dospělí $7 D000328
650    _2
$a senioři $7 D000368
650    _2
$a protilátky anti-idiotypické $x krev $x imunologie $7 D000888
650    _2
$a celiakie $x krev $x diagnóza $x imunologie $7 D002446
650    _2
$a kohortové studie $7 D015331
650    _2
$a ženské pohlaví $7 D005260
650    _2
$a lidé $7 D006801
650    _2
$a imunoglobulin A $x krev $x imunologie $7 D007070
650    _2
$a imunoglobulin G $x krev $x imunologie $7 D007074
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a lidé středního věku $7 D008875
650    12
$a rostlinné proteiny $x imunologie $7 D010940
650    _2
$a mladý dospělý $7 D055815
655    _2
$a časopisecké články $7 D016428
700    1_
$a Honzová, Stanislava, $d 1953- $7 jn20001103562 $u Synlab czech Ltd., Prague, Czech Republic
700    1_
$a Hospodková, Marie $7 xx0228256 $u synlab czech Ltd., Prague, Czech Republic
700    1_
$a Hoffmanová, Iva $7 xx0101007 $u Second Department of Internal Medicine, Third Faculty of Medicine, Charles University in Pragueand University Hospital Královské Vinohrady, Prague, Czech Republic
700    1_
$a Hábová, Věra. $7 xx0073784 $u Laboratory of Cellular and Molecular Immunology, Institute of Microbiology of the CzechAcademy of Sciences, Prague, Czech Republic
700    1_
$a Halada, Petr, $d 1972- $7 xx0063115 $u Laboratory of Cellular and Molecular Immunology, Institute of Microbiology of the CzechAcademy of Sciences, Prague, Czech Republic
700    1_
$a Tlaskalová, Helena, $d 1938- $7 jn20000402365 $u Laboratory of Cellular and Molecular Immunology, Institute of Microbiology of the CzechAcademy of Sciences, Prague, Czech Republic
700    1_
$a Tučková, Ludmila, $d 1945- $7 xx0036257 $u Laboratory of Cellular and Molecular Immunology, Institute of Microbiology of the CzechAcademy of Sciences, Prague, Czech Republic
773    0_
$w MED00003824 $t Physiological research $x 1802-9973 $g Roč. 67, č. 4 (2018), s. 613-622
856    41
$u https://pubmed.ncbi.nlm.nih.gov/29750882 $y Pubmed
910    __
$a ABA008 $b A 4120 $c 266 $y 4 $z 0
990    __
$a 20190124 $b ABA008
991    __
$a 20190206110009 $b ABA008
999    __
$a ok $b bmc $g 1374796 $s 1042185
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2018 $b 67 $c 4 $d 613-622 $e 20180510 $i 1802-9973 $m Physiological research $n Physiol. Res. (Print) $x MED00003824
LZP    __
$b NLK118 $a Pubmed-20190124

Najít záznam

Citační ukazatele

Nahrávání dat...

Možnosti archivace

Nahrávání dat...