This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Bhat, N. Articles by Perez-Perez, G. Search for Related Content PubMed PubMed Citation Articles by Bhat, N. Articles by Perez-Perez, G.

 Previous Article  |  Next Article 

Clinical and Diagnostic Laboratory Immunology, December 2005, p. 1393-1400, Vol. 12, No. 12
1071-412X/05/$08.00+0     doi:10.1128/CDLI.12.12.1393-1400.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Local and Systemic Immune and Inflammatory Responses to Helicobacter pylori Strains

Niranjan Bhat,^1, James Gaensbauer,^1, Richard M. Peek,^2,3 Karen Bloch,¹ Kyi-Toe Tham,^2,4 Martin J. Blaser,^5,6 and Guillermo Perez-Perez^5*

Division of Infectious Diseases, Vanderbilt University School of Medicine, Nashville, Tennessee,¹ Veterans Affairs Medical Center, Nashville, Tennessee,² Division of Gastroenterology, Vanderbilt University School of Medicine, Nashville, Tennessee,³ Department of Pathology, Vanderbilt University School of Medicine, Nashville, Tennessee,⁴ Departments of Medicine and Microbiology, New York University School of Medicine, New York, New York,⁵ Veterans Affairs Medical Center, New York, New York⁶

Received 19 July 2005/ Returned for modification 28 July 2005/ Accepted 4 October 2005

Colonization with Helicobacter pylori eventuates in varied clinical outcomes, which relate to both bacterial and host factors. Here we examine the relationships between cagA status, serum and gastric juice antibody responses, and gastric inflammation in dyspeptic patients. Serum, gastric juice, and gastric biopsy specimens were obtained from 89 patients undergoing endoscopy. H. pylori colonization and cagA status were determined by histology, culture, and PCR methods, and acute inflammation and chronic inflammation in the gastric mucosa were scored by a single pathologist. Serum and gastric juice antibodies to H. pylori whole-cell and CagA antigens were determined by enzyme-linked immunosorbent assay. Relationships between variables were sequentially analyzed using univariate and multivariate statistical methods. Of the 89 subjects, 62 were colonized by H. pylori. By univariate analyses, levels of serum immunoglobulin G (IgG) and IgA and gastric juice IgA antibodies against whole-cell and CagA antigens each were significantly higher in the H. pylori-positive group than in the H. pylori-negative group (P < 0.001). H. pylori and CagA seropositivities were both significantly associated with enhanced inflammation in gastric antrum and body (P < 0.02). The presence of gastric juice antibodies to H. pylori antigens was associated with more severe gastric inflammation. However, in multivariate analyses, only the presence of serum antibodies against CagA and, to a lesser extent, whole-cell antigens remained significantly associated with acute and chronic inflammation in antrum and body (P < 0.05). Thus, serum antibody response to CagA correlates with severity of gastric inflammation. Furthermore, given the relationships demonstrated by multivariate analysis, determination of gastric juice antibodies may provide a better representation of serum, rather than secretory, immune response.

N.B. and J.G. contributed equally to this study.