Gliadin peptides activate blood monocytes from patients with celiac disease

被引:84
作者
Cinova, Jana
Palova-Jelinkova, Lenka
Smythies, Lesley E.
Cerna, Marie
Pecharova, Barbara
Dvorak, Milos
Fruhauf, Pavel
Tlaskalova-Hogenova, Helena
Smith, Phillip D.
Tuckova, Ludmila
机构
[1] Univ Alabama Birmingham, Dept Med Gastroenterol, Birmingham, AL 35294 USA
[2] Acad Sci Czech Republ, Inst Microbiol, Prague, Czech Republic
[3] Charles Univ Prague, Fac Med 3, Prague, Czech Republic
[4] Charles Univ Prague, Fac Med 1, Prague, Czech Republic
[5] VA Med Ctr, Birmingham, AL USA
关键词
celiac disease; innate immunity; blood monocytes;
D O I
10.1007/s10875-006-9061-z
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
To elucidate the role of innate immune responses in celiac disease, we investigated the effect of gliadin on blood monocytes from patients with celiac disease. Gliadin induced substantial TNF-alpha and IL-8 production by monocytes from patients with active celiac disease, lower levels by monocytes from patients with inactive celiac disease, and even lower levels by monocytes from healthy donors. In healthy donor monocytes gliadin induced IL-8 from monocytes expressing HLA-DQ2 and increased monocyte expression of the costimulatory molecules CD80 and CD86, the dendritic cell marker CD83, and the activation marker CD40. Gliadin also increased DNA binding activity of NF-kappa B p50 and p65 subunits in monocytes from celiac patients, and NF-kappa B inhibitors reduced both DNA binding activity and cytokine production. Thus, gliadin activation of HLA-DQ(2+) monocytes leading to chemokine and proinflammatory cytokine production may contribute to the host innate immune response in celiac disease.
引用
收藏
页码:201 / 209
页数:9
相关论文
共 55 条
[1]   Value of serologic markers for clinical diagnosis and population studies of coeliac disease [J].
Ascher, H ;
HahnZoric, M ;
Hanson, LA ;
Kilander, AF ;
Nilsson, LA ;
Tlaskalova, H .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 1996, 31 (01) :61-67
[2]   The NF-kappa B and I kappa B proteins: New discoveries and insights [J].
Baldwin, AS .
ANNUAL REVIEW OF IMMUNOLOGY, 1996, 14 :649-683
[3]   Plasma cytokine profiles in patients with celiac disease and selective IgA deficiency [J].
Cataldo, F ;
Lio, D ;
Marino, V ;
Scola, L ;
Crivello, A ;
Corazza, GR .
PEDIATRIC ALLERGY AND IMMUNOLOGY, 2003, 14 (04) :320-324
[4]   The immune recognition of gluten in coeliac disease [J].
Ciccocioppo, R ;
Di Sabatino, A ;
Corazza, GR .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2005, 140 (03) :408-416
[5]   The role of NF-κB, IRF-1, and STAT-1α transcription factors in the iNOS gene induction by gliadin and IFN-γ in RAW 264.7 macrophages [J].
De Stefano, D ;
Maiuri, MC ;
Iovine, B ;
Ialenti, A ;
Bevilacqua, M ;
Carnuccio, R .
JOURNAL OF MOLECULAR MEDICINE-JMM, 2006, 84 (01) :65-74
[6]   Autoantibodies to tissue transglutaminase as predictors of celiac disease [J].
Dieterich, W ;
Laag, E ;
Schöpper, H ;
Volta, U ;
Ferguson, A ;
Gillett, H ;
Riecken, EO ;
Schuppan, D .
GASTROENTEROLOGY, 1998, 115 (06) :1317-1321
[7]  
Ding ZQ, 2001, J LEUKOCYTE BIOL, V69, P458
[8]   Gliadin, zonulin and gut permeability: Effects on celiac and non- celiac intestinal mucosa and intestinal cell lines [J].
Drago, S ;
El Asmar, R ;
Di Pierro, M ;
Clemente, MG ;
Tripathi, A ;
Sapone, A ;
Thakar, M ;
Iacono, G ;
Carroccio, A ;
D'Agate, C ;
Not, T ;
Zampini, L ;
Catassi, C ;
Fasano, A .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 2006, 41 (04) :408-419
[9]  
Eiras P, 2000, SCAND J IMMUNOL, V52, P1
[10]   NF-κB and rel proteins:: Evolutionarily conserved mediators of immune responses [J].
Ghosh, S ;
May, MJ ;
Kopp, EB .
ANNUAL REVIEW OF IMMUNOLOGY, 1998, 16 :225-260