Helicobacter pylori and autoimmune pancreatitis:: role of carbonic anhydrase via molecular mimicry?

被引:137
作者
Guarneri, F
Guarneri, C
Benvenga, S
机构
[1] Univ Messina, Ist Dermatol, Policlin Gaetano Martino, Messina, Italy
[2] Univ Messina, Sez Endocrinol, Dipartimento Clin Sperimentale Med & Farmacol, Messina, Italy
[3] Azienda Osped Univ Policlin Gaetano Martino, Programma Infradipartimentale Endocrinol Mol Clin, Messina, Italy
关键词
autoimmune pancreatitis; Helicobacter pylori; molecular mimicry; carbonic anhydrase; amino acid sequence analysis; in silico protein analysis;
D O I
10.1111/j.1582-4934.2005.tb00506.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Autoimmune pancreatitis is a recently defined nosological entity, which accounts for 4.6-6% of all forms of chronic pancreatitis and is often associated with other autoimmune diseases, particularly Sjogren's syndrome. Possession of the HLA DRB1*0405-DQB1*0401 genotype confers a risk for the development of autoimmune pancreatitis. Autoantibodies against carbonic anhydrase II and lactoferrin are frequently present in affected subjects and are suspected to have a pathogenic role. A link between gastric infection by Helicobacter pylori and autoimmune pancreatitis has been hypothesized. We used in silico protein analysis and search for HLA binding motifs to verify this hypothesis. We found a significant homology between human carbonic anhydrase II and alpha-carbonic anhydrase of Helicobacter pylori, an enzyme which is fundamental for the survival and proliferation of the bacterium in the gastric environment. Moreover, the homologous segments contain the binding motif of the HLA molecule DRB 1*0405. Our data strengthen the hypothesis that gastric Helicobacter pylori infection can trigger autoimmune pancreatitis in genetically predisposed subjects.
引用
收藏
页码:741 / 744
页数:4
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