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Infection and Immunity, October 2007, p. 4998-5003, Vol. 75, No. 10
0019-9567/07/$08.00+0     doi:10.1128/IAI.00545-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Lipopolysaccharide from Salmonella enterica Activates NF-{kappa}B through both Classical and Alternative Pathways in Primary B Lymphocytes{triangledown}

Vongthip Souvannavong,1,2* Nabila Saidji,2 and Richard Chaby1,2

CNRS, Institut de Biochimie Biophysique Moléculaire et Cellulaire, UMR 8619,1 Université Paris-Sud, Laboratoire Activation Cellulaire et Transduction de Signaux, Orsay F-91405, France2

Received 16 April 2007/ Returned for modification 11 June 2007/ Accepted 29 July 2007

Lipopolysaccharides (LPS) are potent polyclonal B-lymphocyte activators. Recently, we have shown that LPS inhibits both spontaneous and drug-induced apoptosis in mature B lymphocytes, through cytosolic retention of Bax, a proapoptotic protein of the Bcl-2 family, by preventing its translocation to mitochondria. Research within the last few years has revealed that members of the NF-{kappa}B transcription factor regulate cell viability by activating genes involved in mitochondrion-dependent apoptosis. In this report, we examined the effect of sustained LPS stimulation on cytosolic and nuclear proteins of the I{kappa}B/NF-{kappa}B family to determine which NF-{kappa}B pathway, canonical (classical) or noncanonical (alternative), is activated by this agent in mature B cells. Immunoblotting analyses showed that LPS induced a time-dependent degradation of the NF-{kappa}B inhibitors I{kappa}Bß and I{kappa}B{varepsilon} (preferentially to isoform I{kappa}B{alpha}), via I{kappa}B kinase ß. In addition, we observed that LPS triggered the processing of NF-{kappa}B p105 to p50 and that of NF-{kappa}B p100 to p52 in parallel with nuclear translocation of active p50 and p52, as NF-{kappa}Bp50/RelA and NF-{kappa}Bp52/RelB heterodimers, respectively. These results suggest that sustained stimulation with LPS can activate NF-{kappa}B through both classical and alternative pathways.

* Corresponding author. Mailing address: CNRS, IBBMC, UMR 8619, Université Paris-Sud, Bat. 430, 91405 Orsay cedex, France. Phone: 33-1 69 15 48 45. Fax: 33-1 69 85 37 15. E-mail: vongthip.souvannavong{at}u-psud.fr

{triangledown} Published ahead of print on 13 August 2007.

Editor: A. Camilli

Infection and Immunity, October 2007, p. 4998-5003, Vol. 75, No. 10
0019-9567/07/$08.00+0     doi:10.1128/IAI.00545-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.





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