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Published ahead of print on January 26, 2006, doi:10.1165/rcmb.2005-0441OC

Am. J. Respir. Cell Mol. Biol., Volume 34, Number 6, June 2006, 653-660

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Submitted on December 1, 2005
Revised on January 24, 2006

ASIALOGM1 and TLR5 Cooperate in Flagellin-Induced Nucleotide Signaling to Activate ERK1/2

Nancy McNamara1*, Marianne Gallup1, Anatol Sucher1, Inna Maltseva2, David McKemy3, and Carol Basbaum1

1 Department of Anatomy, University of California, San Francisco, CA, USA, 2 School of Optometry, University of California, Berkeley, CA, USA, 3 School of Dentistry, University of Southern California, Los Angeles, CA, USA

* To whom correspondence should be addressed. E-mail: nam{at}itsa.ucsf.edu.

Bacterial flagellin can interact with both Toll-like receptor 5 (TLR5) and the cell surface glycolipid, asialoGM1 to activate an innate immune response. The induction of mucin by flagellin in human lung epithelial cells (NCIH292) is dependent on asialoGM1 ligation, ATP receptor signaling, Ca2+ mobilization and Erk1/2 activation. Conversely, the activation of NF{kappa}B by flagellin is dependent on signaling through TLR5. These results prompted us to ask whether the flagellin-induced TLR5 signaling pathway was intersecting with or mutually independent of the nucleotide receptor pathway activated downstream of asialoGM1. Herein, we demonstrate that the release of ATP induced by flagellin is dependent on a Toll signaling cascade. Although Toll was able to activate NF{kappa}B in the absence of extracellular ATP, Toll required ATP in order to activate Erk 1/2. These results suggest interdependence between the asialoGM1 and TLR5 pathways and reveal a previously unsuspected role for autocrine extracellular ATP signaling in TLR signaling.




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