Title: TRPA1 channels mediate acute neurogenic inflammation and pain produced by bacterial endotoxins
Authors: Meseguer, Victor
Aguiar Alpizar, Yeranddy
Luis, Enoch
Tajada, Sendoa
Denlinger, Bristol
Fajardo, Otto
Manenschijn, Jan-Albert
Fernandez-Pena, Carlos
Talavera, Arturo
Kichko, Tatiana
Navia, Belen
Sanchez Linde, Alicia
Senaris, Rosa
Reeh, Peter
Perez-Garcia, Maria Teresa
Lopez-Lopez, Jose Ramon
Voets, Thomas
Belmonte, Carlos
Talavera PĂ©rez, Karel #
Viana, Felix # ×
Issue Date: 2014
Series Title: Nature Communications vol:5
Article number: 3125
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) signaling pathway by lipopolysaccharide (LPS), a toxic byproduct 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.
ISSN: 2041-1723
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Laboratory of Ion Channel Research (VIB-KU Leuven Center for Brain & Disease Research)
× corresponding author
# (joint) last author

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