Augmentation of Helicobacter pylori urease activity by its specific IgG antibody: implications for bacterial colonization enhancement.
Biomed Res
; 26(1): 35-42, 2005 Feb.
Article
en En
| MEDLINE
| ID: mdl-15806982
ABSTRACT
Gastric colonization of Helicobacter pylori (H. pylori) occurs in a very early age via infected mothers having H. pylori-specific IgG antibodies that would be transplacentally transferred to infants. In addition, H. pylori urease-specific IgG was associated with chronic gastric atrophy and post-immunization gastritis is usually correlated with a strong local IgG response. These findings indicate that H. pylori-specific IgG antibodies, in particular its urease-specific IgG, may induce unfavorable influence on host resistance against H. pylori. Here, we show that we have found a unique H. pylori urease-specific IgG monoclonal antibody (MAb), termed S3, recognizing the conformational structure of the small subunit Ure-A, which enhanced the urease enzymatic activity. Such enhancement of the H. pylori urease activity induced by 1 microg of S3 was almost completely cancelled by simultaneously added the same amount of L2 MAb, which has a strong and specific inhibitory activity against H. pylori urease and recognizes a liner epitope of 8-mer peptide (F8 SIKEDVQF) within its large subunit Ure-B (Infect. Immun. 69 6597, 2001). Intravenous pre-administration of purified S3 into BALB/c mice showed significant augmentation for gastric colonization with the susceptible strain Sydney Strain-1 (SS-1). To our knowledge, this is the first demonstration that a H. pylori urease-specific IgG MAb induced an augmentation of their gastric colonization in vivo.
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Bases de datos:
MEDLINE
Asunto principal:
Ureasa
/
Helicobacter pylori
Límite:
Animals
Idioma:
En
Revista:
Biomed Res
Año:
2005
Tipo del documento:
Article
País de afiliación:
Japón