Airway neuropeptides and asthma

Barnes, P. J.

doi:10.1016/0167-0115(88)90124-3

Cited by 22 publications

(23 citation statements)

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“…and produce potent local effects such as bronchoconstriction, extravasation of macromolecules, and edema of airway mucosa. Prolonged stimulation leads to neurogenic inflammation in the airways (8,10). Further, increasing evidence suggests that endogenous tachykinins are involved in the AHR associated with airway mucosal inflammation (9,10).…”

Section: Discussionmentioning

confidence: 97%

“…Tachykinins and CGRP are synthesized in the cell bodies of small-size (predominantly C) sensory neurons in the nodose, jugular, and dorsal root ganglia, then transported to and stored in the peripheral nerve terminals. When bronchopulmonary C-fiber endings are activated, the impulses trigger the release of these neuropeptides, which can induce neurogenic inflammation in the airways (8)(9)(10). A recent study by Wu and Lee (11) reported that chronic exposure to CS induced airway mucosal inflammation accompanied by bronchial hyperreactivity in guinea pigs, and that the tachykininergic mechanism is involved.…”

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confidence: 97%

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Chronic Smoking Enhances Tachykinin Synthesis and Airway Responsiveness in Guinea Pigs

Kwong

Kashon

et al. 2001

Am J Respir Cell Mol Biol

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This study tests the hypothesis that the bronchial hyperreactivity induced by chronic cigarette smoke (CS) exposure involves the increased expression and release of tachykinins and calcitonin gene-related peptide (CGRP) from afferent nerve fibers innervating the airways. In guinea pigs chronically exposed to CS (20 min twice daily for 14-17 d), peak response in total lung resistance to capsaicin (1.68 microg/kg, intravenously) was significantly greater than that evoked by the same dose of capsaicin in control (air-exposed) animals. This augmented response in CS-exposed animals was abolished after treatment with CP-99994 and SR-48968, the neurokinin (NK)-1 and NK-2 receptor antagonists, suggesting the involvement of tachykinins in chronic CS-induced airway hyperresponsiveness (AHR). Further, substance P (SP)-like immunoreactivity (LI) and CGRP-LI in the airway tissue were significantly greater in the CS animals than in the control animals. Finally, beta-preprotachykinin (PPT, a splice variant from the PPT A gene encoding tachykinins including SP and NKA) messenger RNA levels as measured by in situ hybridization histochemistry displayed a significant increase in jugular ganglion neurons but not in dorsal root or nodose ganglion neurons. These data suggest that chronic CS-induced AHR is related to an increase in SP synthesis and release in jugular ganglion neurons innervating the lungs and airways.

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Section: Discussionmentioning

confidence: 97%

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confidence: 97%

Chronic Smoking Enhances Tachykinin Synthesis and Airway Responsiveness in Guinea Pigs

Kwong

Kashon

et al. 2001

Am J Respir Cell Mol Biol

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“…For experiments, the modified version of the Ussing apparatus was used [6,29]. This apparatus consists of two symmetric chambers enabling for electric isolation of both surfaces of mounted epithelial sample.…”

Section: Methodsmentioning

confidence: 99%

“…The released neuropeptides regulate the tension of smooth muscles, blood flow, various epithelial functions and particularly electric transepithelial potential difference [28,29].…”

Section: Introductionmentioning

confidence: 99%

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Postmortem examination of transepithelial ion currents in rabbit colon and trachea in relation to temperature of storage and its importance for interlethal reactions

Wolska

Danielewicz

Kaczorowski

et al. 2005

Forensic Science International

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Airway inflammation and hypersensitivity induced by chronic smoking

Kou¹,

Kwong

Lee

2011

Respiratory Physiology & Neurobiology

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Airway hypersensitivity, characterized by enhanced excitability of airway sensory nerves, is a prominent pathophysiological feature in patients with airway inflammatory diseases. Although the underlying pathogenic mechanism is not fully understood, chronic airway inflammation is believed to be primarily responsible. Cigarette smoking is known to cause chronic airway inflammation, accompanied by airway hyperresponsiveness. Experimental evidence indicates that enhanced excitability of vagal bronchopulmonary sensory nerves and increased tachykinin synthesis in these nerves resulting from chronic inflammation are important contributing factors to the airway hyperresponsiveness. Multiple inflammatory mediators released from various types of structural and inflammatory cells are involved in the smoking-induced airway inflammation, which is mainly regulated by redox-sensitive signaling pathways and transcription factors. Furthermore, recent studies have reported potent sensitizing and stimulatory effects of these inflammatory mediators such as prostanoids and reactive oxygen species on these sensory nerves. In summary, these studies using cigarette smoking as an experimental approach have identified certain potentially important cell signaling pathways and underlying mechanisms of the airway hypersensitivity induced by chronic airway inflammation.

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Airway neuropeptides and asthma

Cited by 22 publications

References 0 publications

Chronic Smoking Enhances Tachykinin Synthesis and Airway Responsiveness in Guinea Pigs

Chronic Smoking Enhances Tachykinin Synthesis and Airway Responsiveness in Guinea Pigs

Postmortem examination of transepithelial ion currents in rabbit colon and trachea in relation to temperature of storage and its importance for interlethal reactions

Airway inflammation and hypersensitivity induced by chronic smoking

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