Neurophysiology of the cough reflex

Jg, Widdicombe

doi:10.1183/09031936.95.08071193

Cited by 343 publications

(221 citation statements)

References 82 publications

(106 reference statements)

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“…With a diameter of 4 mm, these structures are approximately 15 times larger than single virus particles, which are typically 100-300 nm in size (Griffin, 2007). Such structures are probably derived from vesicles of cellular debris extruded from MV-infected cells and may be readily expelled into the air by coughing triggered directly by stimulation of cough receptors in damaged epithelium below the level of the larynx in the trachea or lungs (Eccles, 2005;Widdicombe, 1995). Alternatively, the generalized inflammatory response initiated by the high level of MV infection in tonsillar tissue in the URT may also trigger a cough response in epithelium below the larynx.…”

Section: Discussionmentioning

confidence: 99%

Infection of lymphoid tissues in the macaque upper respiratory tract contributes to the emergence of transmissible measles virus

Ludlow

Vries

Lemon

et al. 2013

Journal of General Virology

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Measles virus (MV), a member of the family Paramyxoviridae, remains a major cause of morbidity and mortality in the developing world. MV is spread by aerosols but the mechanism(s) responsible for the high transmissibility of MV are largely unknown. We previously infected macaques with enhanced green fluorescent protein-expressing recombinant MV and euthanized them at a range of time points. In this study a comprehensive pathological analysis has been performed of tissues from the respiratory tract around the peak of virus replication. Isolation of virus from nose and throat swab samples showed that high levels of both cell-associated and cell-free virus were present in the upper respiratory tract. Analysis of tissue sections from lung and primary bronchus revealed localized infection of epithelial cells, concomitant infiltration of MV-infected immune cells into the epithelium and localized shedding of cells or cell debris into the lumen. While high numbers of MV-infected cells were present in the tongue, these were largely encapsulated by intact keratinocyte cell layers that likely limit virus transmission. In contrast, the integrity of tonsillar and adenoidal epithelia was disrupted with high numbers of MV-infected epithelial cells and infiltrating immune cells present throughout epithelial cell layers. Disruption was associated with large numbers of MV-infected cells or cell debris 'spilling' from epithelia into the respiratory tract. The coughing and sneezing response induced by disruption of the ciliated epithelium, leading to the expulsion of MV-infected cells, cell debris and cell-free virus, contributes to the highly infectious nature of MV.

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Section: Discussionmentioning

confidence: 99%

Infection of lymphoid tissues in the macaque upper respiratory tract contributes to the emergence of transmissible measles virus

Ludlow

Vries

Lemon

et al. 2013

Journal of General Virology

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“…They are particularly responsible for several biological effects in the airways, including: bronchospasm, increase in microvascular permeability, vasodilatation, stimulation of glandular secretions, facilitation of cholinergic neurotransmission, and the recruitment and activation of inflammatory cells. Moreover, sensory nerves also mediate respiratory defence reflexes, such as coughing and sneezing [13][14][15].…”

mentioning

confidence: 99%

Tachykinins and airway microvascular leakage induced by HCl intra-oesophageal instillation

Daoui

D’Agostino²,

Gallelli³

et al. 2002

Eur Respir J

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Gastro-oesophageal reflux is a common clinical disorder associated with a variety of respiratory symptoms, including chronic cough and exacerbation of asthma. In this study, the potential role of acid-induced tachykinin release was examined in guinea pigs and rabbits, by examining the effects of the tachykinin NK1and NK3receptors antagonists (SR 140333 and SR 142801, respectively) (1–10 mg·kg−1) on plasma protein extravasation induced in airways by hydrochloric acid (HCl) infusion in the oesophagus.Guinea pigs were anaesthetised with urethane, while rabbits were subject to neuroleptoanalgesia with hypnorm. Airway vascular leakage was evaluated by measuring extravasation of Evans blue dye. All animals were pretreated with atropine (1 mg·kg−1i.p.), propranolol (1 mg·kg−1i.p.), phosphoramidon (2.5 mg·kg−1i.v.) and saline or tachykinin receptor antagonists (1–10 mg·kg−1i.p.).Infusion of 1 N HCl into the oesophagus led to a three- and five-fold increase in plasma extravasation in the main bronchi and trachea, respectively. This increase was largely prevented by the tachykinin NK1and NK3receptor antagonists SR 140333 and SR 142801 (1–10 mg·kg−1).These results suggest that protein extravasation in the airways, as induced by intra-oesophageal HCl infusion, is mainly dependent on the release of tachykinins, and that both NK1and NK3tachykinin receptors are involved. The results suggest that HCl-induced sensory nerve stimulation may act in the periphery on intermediate neurons and/or ganglia where NK3receptors have been shown to play an important role.

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“…By activating the rapidly adapting stretch receptors (RAR's), also called irritant receptors, ammonia may elicit the cough reflex as demonstrated in rabbit at high concentration (Matsumoto 1988). These receptors induce coughing through a central reflex when activated by several other exogenous physical and chemical stimuli (Widdicombe 1995). However, by enhancing the electrophysiological activity of the afferent amyelinated C-fibers, ammonia could also modulate cough via an inhibitory control gating mechanism (Matsumoto 1989;Tatar et al 1994).…”

mentioning

confidence: 99%

Inhibiting Effect of Ammonia on Citric Acid‐Induced Cough in Pigs: A Possible Involvement of Substance P

Moreaux

Beerens

Gustin³

2000

Pharmacology & Toxicology

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The effect of ammonia on the cough response to citric acid and on substance P release from C-fibers involved in this reflex was assessed. For a period from one to four days, piglets were exposed, in an inhalation chamber, to ammonia at a concentration of 15 or 30 ppm. During exposure, cough induction tests were done every two days. Recovery of the cough reflex after ammonia exposure was also determined. In a separate group of piglets exposed for 2 days to 30 ppm ammonia, substance P content was determined in bronchial and tracheal lavage fluids and in the tracheal and bronchial mucosa. Ammonia (30 ppm) was found to inhibit coughing significantly (the cough frequency was reduced by 64%) after a two-day exposure. In animals exposed for 4 days to this ammonia concentration, the recovery ranged from 3 to 7 days (mean: 5 days). The same ammonia concentration also caused the substance P content to increase significantly in bronchoalveolar lavage fluid (to 432% of its initial value) and tracheal lavage fluid (to 149%) and to decrease significantly in the tracheal mucosa (-58%), however the content in bronchial mucosa was not significantly affected (ª43%). Exposure to 15 ppm ammonia had no effect on the frequency of citric acid-induced coughing. In conclusion, ammonia inhibits citric acid-induced coughing in pigs at concentrations that can be detected in piggeries. This inhibitory effect may be related to substance-P depletion in C-fiber endings.

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Neurophysiology of the cough reflex

Abstract: How these mechanisms apply to clinical cough in patients is at present poorly understood, but is beginning to be clarified.

Cited by 343 publications

References 82 publications

Infection of lymphoid tissues in the macaque upper respiratory tract contributes to the emergence of transmissible measles virus

Infection of lymphoid tissues in the macaque upper respiratory tract contributes to the emergence of transmissible measles virus

Tachykinins and airway microvascular leakage induced by HCl intra-oesophageal instillation

Inhibiting Effect of Ammonia on Citric Acid‐Induced Cough in Pigs: A Possible Involvement of Substance P

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