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

0492455 - MBÚ 2019 RIV CZ eng J - Journal Article
Sánchez, Daniel - Štěpánová Honzová, S. - Hospodková, M. - Hoffmanová, I. - Hábová, V. - Halada, Petr - Tlaskalová-Hogenová, Helena - Tučková, Ludmila
Occurrence of serum antibodies against wheat alpha-amylase inhibitor 0.19 in celiac disease.
Physiological Research. Roč. 67, č. 4 (2018), s. 613-622. ISSN 0862-8408. E-ISSN 1802-9973
R&D Projects: GA ČR GA13-14608S; GA TA ČR TA04010762; GA TA ČR(CZ) TH03010019
Grant - others:COST Association(CZ) COST Action FA1402 ImARAS
Institutional support: RVO:61388971
Keywords : alpha-amylase inhibitor 0.19 * celiac disease * gluten-free diet
OECD category: Immunology
Impact factor: 1.701, year: 2018

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.
Permanent Link: http://hdl.handle.net/11104/0286002