Effect of cigarette smoking on cough reflex induced by TRPV1 and TRPA1 stimulations

Kanezaki, Masashi; Ebihara, Satoru; Gui, Peijun; Ebihara, Takae; Kohzuki, Masahiro

doi:10.1016/j.rmed.2011.12.007

Cited by 44 publications

(30 citation statements)

References 39 publications

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“…Our findings are in line with the results of previous epidemiological studies on chronic cough [25,31]. Smoking is an important risk factor for chronic cough and current smokers are known to have an increased cough frequency [32,33]. Also, GORD has been reported as the third most important medical condition associated with chronic cough in Europe [11].…”

Section: Prevalent Chronic Cough N=1073supporting

confidence: 91%

Prevalence and incidence of, and risk factors for chronic cough in the adult population: the Rotterdam Study

et al. 2020

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Chronic cough is a common complaint in the general population but there are no precise data on the incidence of, and prospectively examined risk factors for chronic cough in a population-based setting. Therefore, we investigated the period prevalence, incidence and risk factors for chronic cough in adult subjects.In a prospective population-based cohort study among subjects aged ≥45 years, data on chronic cough were collected on two separate occasions using a standardised questionnaire. Chronic cough was defined as daily coughing for at least 3 months duration during the preceding 2 years. Potential risk factors were gathered by interview, physical examination and several investigations.Of the 9824 participants in this study, 1073 (10.9%) subjects had chronic cough at baseline. The prevalence of chronic cough increased with age and peaked in the eighth decade. In subjects aged <70 years, chronic cough was more common in women. During an average follow-up of 6 years, 439 incident cases of chronic cough occurred with an overall incidence rate of 11.6 per 1000 person-years (95% CI 10.6–12.8). In current smokers, the incidence of chronic cough was higher in men. In the multivariable analysis, current smoking, gastro-oesophageal reflux disease (GORD), asthma and COPD were identified as risk factors for chronic cough.Chronic cough is common among adults and highly prevalent in the older population. Current smoking, GORD, asthma and COPD are independent risk factors for chronic cough. Individuals at risk of developing chronic cough may benefit from smoking cessation and control of the underlying disease.

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Section: Prevalent Chronic Cough N=1073supporting

confidence: 91%

Prevalence and incidence of, and risk factors for chronic cough in the adult population: the Rotterdam Study

et al. 2020

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“…Capsaicin and extracellular acidification are direct stimulators of TRPV1 [32, 45] and activation of bradykinin B2 receptors has been shown to gate TRPV1 channels via second messenger systems [35, 46, 47], thus inhibition of TRPV1 reduces cough by these agents. In humans, inhalation of C fiber stimulants evokes cough and ‘urge-to-cough’ sensations [48, 49]. However, selective stimulation of nodose C fibers fails to evoke cough [44].…”

Section: Sensory Afferent Nerves Involved In Coughmentioning

confidence: 99%

Role of reactive oxygen species and TRP channels in the cough reflex

Taylor‐Clark

2016

Cell Calcium

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The cough reflex is evoked by noxious stimuli in the airways. Although this reflex is essential for health, it can be triggered chronically in inflammatory and infectious airway disease. Neuronal transient receptor potential (TRP) channels such as ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1) are polymodal receptors expressed on airway nociceptive afferent nerves. Reactive oxygen species (ROS) and other reactive compounds are associated with inflammation, from either NADPH oxidase or mitochondria. These reactive compounds cause activation and hyperexcitability of nociceptive afferents innervating the airways, and evidence suggests key contributions of TRPA1 and TRPV1.

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“…These features indicate changes in, and excess activity of peptidergic sensory fibers (Patterson et al, 2007). The large-pore cation channels TRPV1 and TRPA1 are activated by exogenous chemical irritants, such as cigarette smoke (Kanezaki et al, 2012) and also directly and indirectly via GPCR- and receptor tyrosine kinase-coupling by many endogenous ligands generated during inflammation, including protons, lipids, endogenous cannabinoids, bradykinin and NGF (Szallasi et al, 2007). Stimulation of nociceptor peripheral terminals results in calcium-mediated vesicular release of neuropeptides like substance P and calcitonin gene related peptide (CGRP), to generate neurogenic inflammation, which is characterized by increased vascular permeability and vasodilatation.…”

Section: Introductionmentioning

confidence: 99%

Silencing Nociceptor Neurons Reduces Allergic Airway Inflammation

Talbot

Abdulnour

Burkett

et al. 2015

Neuron

325

407

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Summary Lung nociceptors initiate cough and bronchoconstriction. To elucidate if these fibers also contribute to allergic airway inflammation we stimulated lung nociceptors with capsaicin and observed increased neuropeptide release and immune cell infiltration. In contrast, ablating Nav1.8+ sensory neurons or silencing them with QX-314, a charged sodium channel inhibitor that enters via large pore ion channels to specifically block nociceptors, substantially reduced ovalbumin or house dust mite-induced airway inflammation and bronchial hyperresponsiveness. We also discovered that IL-5, a cytokine produced by activated immune cells, acts directly on nociceptors to induce release of vasoactive intestinal peptide (VIP). VIP then stimulates CD4+ and resident innate lymphoid type 2 cells, creating an inflammatory signaling loop that promotes allergic inflammation. Our results indicate that nociceptors amplify pathological adaptive immune responses and that silencing these neurons with QX-314 interrupts this neuro-immune interplay, revealing a potential new therapeutic strategy for asthma.

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Effect of cigarette smoking on cough reflex induced by TRPV1 and TRPA1 stimulations

Abstract: The study suggests that smoking has a differential effect on cough responses between TRPV1 and TRPA1 stimulations.

Cited by 44 publications

References 39 publications

Prevalence and incidence of, and risk factors for chronic cough in the adult population: the Rotterdam Study

Prevalence and incidence of, and risk factors for chronic cough in the adult population: the Rotterdam Study

Role of reactive oxygen species and TRP channels in the cough reflex

Silencing Nociceptor Neurons Reduces Allergic Airway Inflammation

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