Continued inhalation of lidocaine suppresses antigen-induced airway hyperreactivity and airway inflammation in ovalbumin-sensitized guinea pigs

Muraki, Masato; Iwanaga, Takashi; Haraguchi, Ryuta; Kubo, Hirokazu; Tohda, Yuji

doi:10.1016/j.intimp.2008.01.021

Cited by 19 publications

(15 citation statements)

References 32 publications

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“…As expected, assuming a causative association between eosinophilic inflammatory infiltrates and airway hyper‐reactivity, treatment with JMF2‐1 and dexamethasone also inhibited the methacholine‐evoked increases in lung resistance and elastance noted after OVA challenge, reinforcing the idea of beneficial effects of JMF2‐1 on airways. A recent study conducted in guinea‐pigs raised the possibility that local anaesthesia with lidocaine in the airways improved airway hyper‐reactivity by inhibiting neurogenic inflammation [21]. The evidence from the current study, however, is that the protective effect of lidocaine on airway hyper‐reactivity is probably unrelated to its ability to cause local anaesthesia because the analogue JMF2‐1, despite the lack of anaesthetic activity [13], remained active against allergen‐evoked airway hyper‐reactivity in mice.…”

Section: Discussionmentioning

confidence: 99%

Lidocaine‐derivative JMF2‐1 prevents ovalbumin‐induced airway inflammation by regulating the function and survival of T cells

Olsen

Ferreira

Serra

et al. 2010

Clin Experimental Allergy

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Section: Discussionmentioning

confidence: 99%

Lidocaine‐derivative JMF2‐1 prevents ovalbumin‐induced airway inflammation by regulating the function and survival of T cells

Olsen

Ferreira

Serra

et al. 2010

Clin Experimental Allergy

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“…The antidromic release of neuropeptides from nociceptors in the airways causes vasodilatation and oedema, which are associated with nasal obstruction in the upper airways and bronchoconstriction in the lower airways, as well as plasma protein exudation, mucus secretion and inflammatory cell recruitment. As a proof of neurogenic inflammation in the airways, it was shown that local anaesthesia with lidocaine improved airway hyperreactivity and reduced capsaicin-induced cough (Muraki et al, 2008). …”

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confidence: 99%

The role of histamine in neurogenic inflammation

Rosa

Fantozzi

2013

British J Pharmacology

167

140

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The term 'neurogenic inflammation' has been adopted to describe the local release of inflammatory mediators, such as substance P and calcitonin gene-related peptide, from neurons. Once released, these neuropeptides induce the release of histamine from adjacent mast cells. In turn, histamine evokes the release of substance P and calcitonin gene-related peptide; thus, a bidirectional link between histamine and neuropeptides in neurogenic inflammation is established. The aim of this review is to summarize the most recent findings on the role of histamine in neurogenic inflammation, with particular regard to nociceptive pain, as well as neurogenic inflammation in the skin, airways and bladder. LINKED ARTICLESThis article is part of a themed issue on Histamine Pharmacology Update. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2013.170.issue-1 Abbreviations CGRP, calcitonin gene-related peptide; ERs, oestrogen receptors; GERD, gastro-oesophageal reflux disease; HDC, histidine decarboxylase; IC, interstitial cystitis; PBS, painful bladder syndrome; SP, substance P; VIP, vasoactive intestinal peptide IntroductionThe term 'neurogenic inflammation' describes the local release of inflammatory mediators, such as substance P (SP) and calcitonin gene-related peptide (CGRP), from afferent neurons. The initial evidence for neurogenic vasodilatation in response to noxious stimuli was obtained in the skin of humans and other mammals (Schmelz and Petersen, 2001), but now it is recognized that neurogenic inflammation also occurs in visceral organs. The inflammatory response evoked by the activation of the sensory nerve fibres, which includes local vasodilatation, plasma extravasation, leukocyte and platelet adhesion, and mast cell degranulation, is brought about by neuropeptides released from the peripheral endings of sensory neurons upon stimulation of the primary sensory terminals. Both SP in neurons and histamine in mast cells have a dual mediator role in neurogenic inflammation (Figure 1). In fact, as demonstrated by Foreman and Jordan (1984), injury causes activation of sensory nerve endings either directly or through the release of histamine from the adjacent mast cells. The action potential generated travels orthodromically to the dorsal horn of the spinal cord and spreads to other branches of the same neurons, which will then release SP from their terminals or varicosities. The released SP, as well as contributing itself to local vasodilatation, induces histamine release from the adjacent mast cells, which produces flare and further activates other sensory nerve endings (Foreman et al., 1983).Neutrophils, whose responsiveness to SP has been repeatedly demonstrated, contribute to the inflammatory soup following neurogenic inflammation. In fact, neutrophils express the SP receptors NK 1, NK2 and NK3, and when stimulated with SP induce the expression of COX-2 and PGE2 release in the nanomolar range (Gallicchio et al., 2008;. Furthermore, SP at micromolar concentrations primes neutrophils, thus en...

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“…Although the duration of montelukast effects can be predicted from blood concentration, concentration was not measured in the present study. Judged from other experiments on inhaled theophyllin (unpublished) and inhaled lidocaine used in OVA-sensitized guinea-pigs [17], we predicted that the blood concentration of montelukast may be lower in animals that received inhaled montelukast than in animals that received oral montelukast at a clinical dose. The present study tested only the efficacy of the drug to inhibit the initiation of the response induced by LT; the efficacy of the drug to inhibit an ongoing response (e.g., by prechallenged LT or allergen) was not tested.…”

Section: Discussionmentioning

confidence: 99%

“…For tracheotomy and intubation, guinea-pigs were first anesthetized with 40 mg/kg of intraperitoneal pentobarbital sodium (Abbot Laboratories, Abbot Park, IL). Pao was measured using a differential pressure transducer (TP-603 T, Nihon Kohden, Tokyo, Japan) [14,17,18], and the peak Pao was calculated.…”

Section: Airway Reactivitymentioning

confidence: 99%

Inhaled montelukast inhibits cysteinyl-leukotriene-induced bronchoconstriction in ovalbumin-sensitized guinea-pigs: The potential as a new asthma medication

Muraki

Imbe

Sakakibara

et al. 2009

International Immunopharmacology

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Continued inhalation of lidocaine suppresses antigen-induced airway hyperreactivity and airway inflammation in ovalbumin-sensitized guinea pigs

Cited by 19 publications

References 32 publications

Lidocaine‐derivative JMF2‐1 prevents ovalbumin‐induced airway inflammation by regulating the function and survival of T cells

Lidocaine‐derivative JMF2‐1 prevents ovalbumin‐induced airway inflammation by regulating the function and survival of T cells

The role of histamine in neurogenic inflammation

Inhaled montelukast inhibits cysteinyl-leukotriene-induced bronchoconstriction in ovalbumin-sensitized guinea-pigs: The potential as a new asthma medication

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