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Comment
. 2017 Jun 1:324:45-50.
doi: 10.1016/j.taap.2017.03.007. Epub 2017 Mar 8.

TRPA1: Acrolein meets its target

Satyanarayana Achanta  1 , Sven-Eric Jordt  2
Affiliations
Comment

TRPA1: Acrolein meets its target

Satyanarayana Achanta et al. Toxicol Appl Pharmacol. .
No abstract available

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Figures

Fig. 1
Fig. 1. Acrolein causes cardiopulmonary effects through the activation of TRPA1 ion channels
Sources of environmental acrolein are diesel exhaust, cigarette smoke, burning of organic matter, industrial sources or overheated cooking oil. At the molecular level, acrolein reacts with N-terminal amino acid residues of TRPA1 channels in sensory nerve endings, triggering nerve excitation and calcium influx, followed by activation of intracellular inflammatory signaling involving ATP release and NF-ƙB pathways. Acrolein activates trigeminal sensory nerve endings in the cornea and upper airways, resulting in eye irritation, the lachrymatory reflex, tingling, sneezing, painful and burning sensations, and increased nasal secretions. Activation of vagal laryngeal sensory nerve endings in the throat triggers the cough reflex and the sensations of coarseness and burning pain. TRPA1 activation stimulates the neuronal release of the pro-inflammatory neuropeptides, Substance P (SP) and Calcitonin Gene-Related Peptide (CGRP), among others. These peptides increase mucus production from goblet cells (blue) and submucosal glands and increase the contractility of airway smooth muscle cells increasing airway resistance. The release of CGRP acts on pulmonary vasculature resulting in increased vasodilation and permeability leading to plasma extravasation, edema and neutrophil infiltration. In addition to pulmonary effects, acrolein also causes cardiac arrhythmia through increased excitability of sensory nerves and autonomic imbalance.
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