Helicobacter pylori heat shock protein B (HspB) localizes in vivo in the gastric mucosa and MALT lymphoma

被引:9
作者
De Luca, Antonio [1 ]
De Falco, Maria [2 ]
Manente, Lucrezia [3 ]
Dattilo, Doriana [1 ]
Lucariello, Angela [1 ]
Esposito, Vincenzo [4 ]
Gnarini, Mariarosaria [4 ]
Citro, Gennaro [5 ]
Baldi, Alfonso [6 ]
Tufano, Maria Antonietta [3 ]
Iaquinto, Gaetano [7 ]
机构
[1] Univ Naples 2, Dept Med & Publ Hlth, I-80138 Naples, Italy
[2] Univ Naples Federico II, Dept Biol Sci, Sect Evolutionary & Comparat Biol, Naples, Italy
[3] Univ Naples 2, Dept Expt Med, I-80138 Naples, Italy
[4] III Div AO D Cotugno, Naples, Italy
[5] Regina Elena Inst Canc Res, SAFU Dept, Rome, Italy
[6] Univ Naples 2, Dept Biochem & Biophys F Cedrangolo, Sect Anat Pathol, I-80138 Naples, Italy
[7] San G Moscati Hosp, Div Gastroenterol, Avellino, Italy
关键词
D O I
10.1002/jcp.21376
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Heat shock protein B (HspB) is one of the dominant proteins recognized by most Helicobacter pylori-infected persons and is being considered as potential candidates for subunit vaccines. In the present study we describe the generation of an antibody against HspB and its use in immunohistochemical assays on gastric biopsies. We have demonstrated that our rabbit polyclonal antibody against HspB did not recognize any protein in lysates from a lung human epithelial cell (H1299) line and did not cross-react with the other members of human heat shock proteins. Secondly, we have observed that in gastric biopsies, HspB immunostaining was present inside the cytoplasm of human epithelial cells with a particular localization in the apical portion of gastric epithelial cells other than in the extracellular spaces among gastric cells of human stomach. Finally, we have demonstrated a cytoplasmic HspB immunostaining in groups of neoplastic cells of MALT lymphoma. In conclusion, our observations suggest a possible involvement of HspB in the pathogenesis of H. pylori-related pathologies such as gastritis, ulcer and gastric cancer.
引用
收藏
页码:78 / 82
页数:5
相关论文
共 51 条
[1]   Disruption of the epithelial apical-junctional complex by Helicobacter pylori CagA [J].
Amieva, MR ;
Vogelmann, R ;
Covacci, A ;
Tompkins, LS ;
Nelson, WJ ;
Falkow, S .
SCIENCE, 2003, 300 (5624) :1430-1434
[2]   Helicobacter pylori enter and survive within multivesicular vacuoles of epithelial cells [J].
Amieva, MR ;
Salama, NR ;
Tompkins, LS ;
Falkow, S .
CELLULAR MICROBIOLOGY, 2002, 4 (10) :677-690
[3]   Helicobacter pylori CagA induces a transition from polarized to invasive phenotypes in MDCK cells [J].
Bagnoli, F ;
Buti, L ;
Tompkins, L ;
Covacci, A ;
Amieva, MR .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (45) :16339-16344
[4]  
Barton SGRG, 1998, CLIN EXP IMMUNOL, V112, P490
[5]   Helicobacter pylori:: resurrection of the cancer link [J].
Björkholm, B ;
Falk, P ;
Engstrand, L ;
Nyrén, O .
JOURNAL OF INTERNAL MEDICINE, 2003, 253 (02) :102-119
[6]  
Björkholm N, 2000, HELICOBACTER, V5, P148
[7]   HYPOTHESES ON THE PATHOGENESIS AND NATURAL-HISTORY OF HELICOBACTER-PYLORI INDUCED INFLAMMATION [J].
BLASER, MJ .
GASTROENTEROLOGY, 1992, 102 (02) :720-727
[8]   cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors [J].
Censini, S ;
Lange, C ;
Xiang, ZY ;
Crabtree, JE ;
Ghiara, P ;
Borodovsky, M ;
Rappuoli, R ;
Covacci, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (25) :14648-14653
[9]   Interaction with CagF is required for translocation of CagA into the host via the Helicobacter pylori type IV secretion system [J].
Couturier, MR ;
Tasca, E ;
Montecucco, C ;
Stein, M .
INFECTION AND IMMUNITY, 2006, 74 (01) :273-281
[10]   Pattern of expression of HtrA1 during mouse development [J].
De Luca, A ;
De Falco, M ;
De Luca, L ;
Penta, R ;
Shridhar, V ;
Baldi, F ;
Campioni, M ;
Paggi, MG ;
Baldi, A .
JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY, 2004, 52 (12) :1609-1617