Potentiation by viral respiratory infection of ovalbumin‐induced guinea‐pig tracheal hyperresponsiveness: role for tachykinins

Ladenius, A. R. C.; Folkerts, Gert; Linde, Henk J. van der; Nijkamp, Frans P.

doi:10.1111/j.1476-5381.1995.tb15917.x

Cited by 29 publications

(15 citation statements)

References 26 publications

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“…A possible explanation would be that SP is a common downstream mediator in the sequence of events leading to airway hyperreactivity. In agreement with this, it has been shown that depletion of sensory neuropeptides, including SP, by capsaicin treatment prevents not only ovalbumin-induced hyperreactivity [7,8] but also hyperreactivity after platelet-activating factor [29], toluene diisocyante [30], delayed type hypersensitivity reactions [31], or respiratory viral infection [32].…”

Section: Discussionmentioning

confidence: 61%

Role of interleukin-5 and substance P in development of airway hyperreactivity to histamine in guinea-pigs

Oosterhout

Ark²,

Hofman³

et al. 1996

Eur Respir J

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In this study, we examined the mechanism by which bronchoalveolar lavage (BAL) cells induced hyperreactivity of the trachea in vitro. As both interleukin-5 (IL-5) and substance P (SP) appeared to be involved, the effect of these mediators was examined in vivo.Tracheae were incubated with BAL cells from ovalbumin or saline challenged animals, and from naive animals, in the absence or presence of either IL-5, SP, or both. In addition, the effect of intra-airway application of IL-5, SP, both, or vehicle on tracheal hyperreactivity was examined.Incubation These data suggest that IL-5 is important in the recruitment of eosinophils, whereas both IL-5 and substance P are involved in the induction of airway hyperreactivity. Eur Respir J., 1996, 9, 493-499 Airway hyperreactivity to bronchoconstrictor mediators is a main characteristic in a majority of asthmatic patients and correlates well with the severity of the disease [1]. Airway hyperreactivity often coincides with the infiltration of inflammatory cells, in particular eosinophilic granulocytes [2]. The mechanistic relationship between hyperreactivity and cell infiltration is currently unknown.Recently, we and others demonstrated that antibodies to interleukin-5 (IL-5) inhibit the airway hyperreactivity and eosinophil infiltration in a guinea-pig model of allergic asthma [3,4]. Conversely, administration of IL-5 has been demonstrated to induce airway eosinophilia and hyperreactivity in guinea-pigs and mice [3,5,6]. These data underline the putative role of the eosinophil in airway hyperreactivity. On the other hand, in guinea-pigs depleted of sensory neuropeptides by capsaicin treatment, ovalbumin challenge does not induce airway hyperreactivity despite the infiltration of eosinophils [7,8]. A possible explanation is that as well as other factors IL-5 is involved in the recruitment of eosinophils, whereas sensory neuropeptides seem to be involved in the process by which eosinophils induce hyperreactivity. In agreement with this, IL-5 enhances adhesion of eosinophils to endothelial cells and is an eosinophil chemoattractant [9,10]. Furthermore, it is well-known that IL-5 primes eosinophils for enhanced effector function to activators [11][12][13][14][15]. Although substance P (SP) may also act as a priming substance for eosinophil chemoattractants [16], little is known about the effect on eosinophil activation.To investigate the role of inflammatory cells in the induction of airway hyperreactivity, BAL cells from ovalbumin-challenged guinea-pigs were incubated with isolated tracheal rings from naive animals. Furthermore, the effect of IL-5 or SP, or the combination of these factors, on the responsiveness of guinea-pig trachea was examined after incubation in vitro or after intra-airway application in vivo.

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Section: Discussionmentioning

confidence: 61%

Role of interleukin-5 and substance P in development of airway hyperreactivity to histamine in guinea-pigs

Oosterhout

Ark²,

Hofman³

et al. 1996

Eur Respir J

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“…In addition, capsaicin affects airway responsiveness to cholinergic agonists in guinea pigs (120). Pretreatment with capsaicin also blocks airway hyperresponsiveness induced by viruses in guinea pigs (121). This points to a role of capsaicin-sensitive sensory airway nerves in the regulation of airway responsiveness.…”

Section: Neuropeptide Depletion Studiesmentioning

confidence: 85%

Neurogenic mechanisms in bronchial inflammatory diseases

Groneberg

Quarcoo

Frossard

et al. 2004

Allergy

153

103

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Neurogenic inflammation encompasses the release of neuropeptides from airway nerves leading to inflammatory effects. This neurogenic inflammatory response of the airways can be initiated by exogenous irritants such as cigarette smoke or gases and is characterized by a bi‐directional linkage between airway nerves and airway inflammation. The event of neurogenic inflammation may participate in the development and progression of chronic inflammatory airway diseases such as allergic asthma or chronic obstructive pulmonary disease (COPD). The molecular mechanisms underlying neurogenic inflammation are orchestrated by a large number of neuropeptides including tachykinins such as substance P and neurokinin A, or calcitonin gene‐related peptide. Also, other biologically active peptides such as neuropeptide tyrosine, vasoactive intestinal polypeptide or endogenous opioids may modulate the inflammatory response and recently, novel tachykinins such as virokinin and hemokinins were identified. Whereas the different aspects of neurogenic inflammation have been studied in detail in laboratory animal models, only little is known about the role of airway neurogenic inflammation in human diseases. However, different functional properties of airway nerves may be used as targets for future therapeutic strategies and recent clinical data indicates that novel dual receptor antagonists may be relevant new drugs for bronchial asthma or COPD.

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“…of capsaicin, which depletes tachykinins from NANC nerves, eliminated airway hyperresponsiveness induced by acute capsaicin [48], citric acid [53], ovalbumin [54,55] toluene diisocyanate [56], endotoxin [57], plateletactivating factor (PAF) [58], respiratory viral infection [59], and ozone [60] in guinea-pigs, dinitro-fluorobenzene [61] and toluene diisocyanate [62] in mice, and Altenaria tenuis aerosol in rabbits [63].…”

Section: Involvement Of Tachykinins In Airway Hyperresponsivenessmentioning

confidence: 99%

The role of tachykinin receptor antagonists in the prevention of bronchial hyperresponsiveness, airway inflammation and cough

Advenier¹,

Lagente²,

Boichot³

1997

Eur Respir J

113

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The excitatory nonadrenergic noncholinergic (NANC) system, involving various neuropeptides of the tachykinin family, such as substance P (SP), neurokinin A (NKA), neurokinin B (NKB) and calcitonin gene-related peptide (CGRP), as transmitters, has now been well characterized. In airways, SP, NKA and CGRP are co-localized in the sensory unmyelinated C-fibres, which innervate all compartments of the airway wall from the trachea down to the bronchioles. C-fibre endings are found within the epithelium. They form a dense plexus in the subepithelial lamina propria, supply the glands, ramify within the smooth muscle layer and make direct contacts with postganglionic parasympathetic neurons, located in the local ganglion. In the trachea, this sensory innervation is almost exclusively derived from sensory vagal neurons, supplied by the jugular ganglion, whilst that of the lung is of mixed origin with a predominating vagal and a smaller spinal contribution [1][2][3][4][5]. The NANC system can be activated by different stimuli, which affect the chemosensitive C-fibre afferents in airways and lead to a local release of tachykinins that are responsible for several biological effects in the bronchopulmonary system: bronchospasm; increase in vascular permeability from postcapillary venules; stimulation of glandular secretion; facilitation of cholinergic neurotransmission; and recruitment and activation of some types of inflammatory cells. Sensory nerves also mediate respiratory defence reflexes, such as coughing, sneezing and secretion of mucus ( fig. 1).From these data, it has been hypothesized that abnormal stimulation of the sensory nerve terminals, e.g. induced by epithelial shedding as seen in asthma, results in enhanced release of tachykinins in the airway wall with subsequent exaggeration of inflammation. This concept of "neurogenic inflammation" introduces sensory nerve fibres as important components in the pathogenesis of asthma.The biological actions of tachykinins are mediated via three types of receptors, denoted neurokinins 1-3 (NK 1 , NK 2 and NK 3 ), which have the highest affinity for SP, NKA and NKB, respectively. This receptor classification has been established from receptor-binding and functional studies. It has now been recognized that the expression of tachykinin NK 3 receptors is confined mainly to the central and peripheral nervous system, whilst tachykinin NK 1 and tachykinin NK 2 receptors are expressed both in the central and peripheral nervous system and in target organs, including airways [5][6][7][8][9][10]. According Taken together, the results obtained with the various selective receptor antagonists provide pharmacological evidence that tachykinins play a role in delayed bronchopulmonary alterations and suggest that tachykinin receptor antagonists may be useful for investigating mechanisms and possibly reducing airway functional alterations in asthmatic patients. PHARMACOLOGICAL REVIEW

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Potentiation by viral respiratory infection of ovalbumin‐induced guinea‐pig tracheal hyperresponsiveness: role for tachykinins

Cited by 29 publications

References 26 publications

Role of interleukin-5 and substance P in development of airway hyperreactivity to histamine in guinea-pigs

Role of interleukin-5 and substance P in development of airway hyperreactivity to histamine in guinea-pigs

Neurogenic mechanisms in bronchial inflammatory diseases

The role of tachykinin receptor antagonists in the prevention of bronchial hyperresponsiveness, airway inflammation and cough

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