This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Qadri, F.
Right arrow Articles by McGhee, J. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Qadri, F.
Right arrow Articles by McGhee, J. R.

 Previous Article  |  Next Article 

Clinical and Diagnostic Laboratory Immunology, November 1999, p. 812-818, Vol. 6, No. 6
1071-412X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Lipopolysaccharide- and Cholera Toxin-Specific Subclass Distribution of B-Cell Responses in Cholera

Firdausi Qadri,1,* Firoz Ahmed,1 M. Manjurul Karim,1 Christine Wenneras,2 Yasmin Ara Begum,1 Mohammad Abdus Salam,1 M. John Albert,1 and Jerry R. McGhee3

International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka, Bangladesh1; Department of Medical Microbiology and Immunology, Göteborg University, Göteborg, Sweden2; and Immunobiology Vaccine Center, University of Alabama at Birmingham, Birmingham, Alabama3

Received 24 March 1999/Returned for modification 29 July 1999/Accepted 23 August 1999

The immunoglobulin subclass responses to homologous lipopolysaccharide (LPS) and to cholera toxin (CT) in adult patients infected with Vibrio cholerae O1 and V. cholerae O139 were studied. LPS-specific antibody-secreting cells (ASC) of both the immunoglobulin A1 (IgA1) and IgA2 subclasses were seen, with the IgA1 ASC response predominating in both V. cholerae O1- and O139-infected patients. For antibodies in plasma, by day 11 after onset of disease, all V. cholerae O1- infected patients responded to homologous LPS with the IgA1 subclass (P = 0.001), whereas fewer (68%) responded with the IgA2 subclass (P = 0.007). About 89% of V. cholerae O139-infected patients responded with the IgA1 subclass (P = 0.003), and only 21% responded with the IgA2 subclass (not significant [NS]). Both groups of cholera patients showed significant increases in LPS-specific IgG1, IgG2, and IgG3 antibodies in plasma. In feces, the response to homologous LPS occurred in both groups of patients with the IgA1 and IgA2 subclasses, with 55 to 67% of patients showing a positive response. V. cholerae O1- and O139-infected patients showed CT-specific ASC responses of the different IgG and IgA subclasses in the circulation, and the pattern followed the order IgG1 > IgA1 > IgG2 > IgA2, with low levels of IgG3 and IgG4 ASC. Plasma anti-CT antibody responses in all subclasses were seen by day 11 after onset of disease. Although there were no increases in CT-specific ASC of the IgG3 (NS) and IgG4 (NS) subtypes, there were significant increases of these two subclasses in plasma (P <=  0.001). The response to CT in the fecal extracts was contributed to by both IgA1 and IgA2 isotypes, with 67 to 75% of the patients responding. Thus, the mucosa-derived ASC and fecal antibodies to LPS and CT were of both the IgA1 and IgA2 subclasses; in plasma, the contribution from IgA2 was lower. Very little difference in the B-cell responses to LPS and CT in the different subclasses was seen in the two groups of cholera patients. Vaccines against O1 and O139 cholera ideally should stimulate antibody subclasses that are likely to offer protection.

* Corresponding author. Mailing address: Laboratory Sciences Division, International Centre for Diarrhoeal Diseases Research, Bangladesh, GPO Box 128, Dhaka 1000, Bangladesh. Phone: 880 2 871751-60. Fax: 880 2 872529, 880 2 883116, or 880 2 886050. E-mail: fqadri{at}icddrb.org.

Clinical and Diagnostic Laboratory Immunology, November 1999, p. 812-818, Vol. 6, No. 6
1071-412X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Asaduzzaman, M., Ryan, E. T., John, M., Hang, L., Khan, A. I., Faruque, A. S. G., Taylor, R. K., Calderwood, S. B., Qadri, F. (2004). The Major Subunit of the Toxin-Coregulated Pilus TcpA Induces Mucosal and Systemic Immunoglobulin A Immune Responses in Patients with Cholera Caused by Vibrio cholerae O1 and O139. Infect. Immun. 72: 4448-4454 [Abstract] [Full Text]  
  • Meeks, M. D., Saksena, R., Ma, X., Wade, T. K., Taylor, R. K., Kovac, P., Wade, W. F. (2004). Synthetic Fragments of Vibrio cholerae O1 Inaba O-Specific Polysaccharide Bound to a Protein Carrier Are Immunogenic in Mice but Do Not Induce Protective Antibodies. Infect. Immun. 72: 4090-4101 [Abstract] [Full Text]  
  • Qadri, F, Bhuiyan, T R, Dutta, K K, Raqib, R, Alam, M S, Alam, N H, Svennerholm, A-M, Mathan, M M (2004). Acute dehydrating disease caused by Vibrio cholerae serogroups O1 and O139 induce increases in innate cells and inflammatory mediators at the mucosal surface of the gut. Gut 53: 62-69 [Abstract] [Full Text]  
  • Qadri, F., Ryan, E. T., Faruque, A. S. G., Ahmed, F., Khan, A. I., Islam, M. M., Akramuzzaman, S. M., Sack, David. A., Calderwood, S. B. (2003). Antigen-Specific Immunoglobulin A Antibodies Secreted from Circulating B Cells Are an Effective Marker for Recent Local Immune Responses in Patients with Cholera: Comparison to Antibody-Secreting Cell Responses and Other Immunological Markers. Infect. Immun. 71: 4808-4814 [Abstract] [Full Text]  
  • Qadri, F., Raqib, R., Ahmed, F., Rahman, T., Wenneras, C., Kumar Das, S., Alam, N. H., Mathan, M. M., Svennerholm, A.-M. (2002). Increased Levels of Inflammatory Mediators in Children and Adults Infected with Vibrio cholerae O1 and O139. CVI 9: 221-229 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»