TRPA1 channels mediate acute neurogenic inflammation and pain produced by bacterial endotoxins

Victor Meseguer, Yeranddy A. Alpizar, Enoch Luis, Sendoa Tajada, Bristol Denlinger, Otto Fajardo, Jan-Albert Manenschijn, Carlos Fernández-Peña, Arturo Talavera, Tatiana Kichko, Belén Navia, Alicia Sánchez, Rosa Señarís, Peter Reeh, María Teresa Pérez-García, José Ramón López-López, Thomas Voets, Carlos Belmonte, Karel Talavera and Félix Viana ()
Additional contact information
Victor Meseguer: Instituto de Neurociencias de Alicante, Universidad Miguel Hernández y CSIC
Yeranddy A. Alpizar: Laboratory of Ion Channel Research
Enoch Luis: Instituto de Neurociencias de Alicante, Universidad Miguel Hernández y CSIC
Sendoa Tajada: Universidad de Valladolid y CSIC
Bristol Denlinger: Instituto de Neurociencias de Alicante, Universidad Miguel Hernández y CSIC
Otto Fajardo: Instituto de Neurociencias de Alicante, Universidad Miguel Hernández y CSIC
Jan-Albert Manenschijn: Instituto de Neurociencias de Alicante, Universidad Miguel Hernández y CSIC
Carlos Fernández-Peña: Instituto de Neurociencias de Alicante, Universidad Miguel Hernández y CSIC
Arturo Talavera: Laboratory of Ion Channel Research
Tatiana Kichko: Institute of Physiology and Pathophysiology, University of Erlangen-Nuremberg
Belén Navia: CIMUS, University of Santiago de Compostela
Alicia Sánchez: Laboratory of Ion Channel Research
Rosa Señarís: CIMUS, University of Santiago de Compostela
Peter Reeh: Institute of Physiology and Pathophysiology, University of Erlangen-Nuremberg
María Teresa Pérez-García: Universidad de Valladolid y CSIC
José Ramón López-López: Universidad de Valladolid y CSIC
Thomas Voets: Laboratory of Ion Channel Research
Carlos Belmonte: Instituto de Neurociencias de Alicante, Universidad Miguel Hernández y CSIC
Karel Talavera: Instituto de Neurociencias de Alicante, Universidad Miguel Hernández y CSIC
Félix Viana: Instituto de Neurociencias de Alicante, Universidad Miguel Hernández y CSIC

Nature Communications, 2014, vol. 5, issue 1, 1-14

Abstract: Abstract Gram-negative bacterial infections are accompanied by inflammation and somatic or visceral pain. These symptoms are generally attributed to sensitization of nociceptors by inflammatory mediators released by immune cells. Nociceptor sensitization during inflammation occurs through activation of the Toll-like receptor 4 (TLR4) signalling pathway by lipopolysaccharide (LPS), a toxic by-product of bacterial lysis. Here we show that LPS exerts fast, membrane delimited, excitatory actions via TRPA1, a transient receptor potential cation channel that is critical for transducing environmental irritant stimuli into nociceptor activity. Moreover, we find that pain and acute vascular reactions, including neurogenic inflammation (CGRP release) caused by LPS are primarily dependent on TRPA1 channel activation in nociceptive sensory neurons, and develop independently of TLR4 activation. The identification of TRPA1 as a molecular determinant of direct LPS effects on nociceptors offers new insights into the pathogenesis of pain and neurovascular responses during bacterial infections and opens novel avenues for their treatment.

Date: 2014
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DOI: 10.1038/ncomms4125

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