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Infection and Immunity, June 2007, p. 3150-3159, Vol. 75, No. 6
0019-9567/07/$08.00+0     doi:10.1128/IAI.00581-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Induction of Cell Signaling Events by the Cholera Toxin B Subunit in Antigen-Presenting Cells{triangledown}

Aletta C. Schnitzler,1 Jennifer M. Burke,1 and Lee M. Wetzler2*

Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts 02118,1 Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 021182

Received 7 April 2006/ Returned for modification 7 June 2006/ Accepted 3 March 2007

Cholera toxin (CT) is one of the most effective and widely studied mucosal adjuvants. Although the ADP-ribosylating A subunit has been implicated in augmenting immune responses, the receptor-binding B subunit (CT-B) has greater immunogenicity and may be a repository of adjuvant activity without potential toxicity. In order to elucidate mechanisms of immune modulation by CT-B alone, primary B cells and macrophages were assessed for responses to CT-B in vitro, as measured by the expression of cell surface markers, cellular signaling events, and cytokine secretion. Increased phosphorylation of multiple signaling molecules, including Erk1/2 and p38, was detected. CT-B also induced transactivation of the transcription elements cyclic AMP-responsive element and NF-{kappa}B, the latter of which was inhibited by phosphotyrosine inhibition. While specific inhibition of MEK1/2 did not reduce CT-B induction of cell surface marker expression, it did attenuate CT-B-mediated interleukin-6 secretion. These data show that CT-B induces a set of signaling events related to cellular activation, surface molecule expression, and cytokine production that has potential implications for elucidating CT-B adjuvant activity in the absence of enzymatically active holotoxin.

* Corresponding author. Mailing address: Evans Biomedical Research Center, Boston University School of Medicine, 650 Albany St., Rm 638, Boston, MA 02118. Phone: (617) 414-4394. Fax: (617) 414-5280. E-mail: lwetzler{at}bu.edu

{triangledown} Published ahead of print on 12 March 2007.

Editor: J. L. Flynn

Infection and Immunity, June 2007, p. 3150-3159, Vol. 75, No. 6
0019-9567/07/$08.00+0     doi:10.1128/IAI.00581-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Negri, D. R. M., Pinto, D., Vendetti, S., Patrizio, M., Sanchez, M., Riccomi, A., Ruggiero, P., Del Giudice, G., De Magistris, M. T. (2009). Cholera Toxin and Escherichia coli Heat-Labile Enterotoxin, but Not Their Nontoxic Counterparts, Improve the Antigen-Presenting Cell Function of Human B Lymphocytes. Infect. Immun. 77: 1924-1935 [Abstract] [Full Text]  


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