Role of tachykinins in sephadex-induced airway hyperreactivity and inflammation in guinea pigs

Tramontana, Manuela; Santicioli, Paolo; Giuliani, Sandro; Catalioto, Rose‐Marie; Lecci, Alessandro; Carini, F; Maggi, Carlo Alberto

doi:10.1016/s0014-2999(02)01365-1

Cited by 14 publications

(9 citation statements)

References 50 publications

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“…The importance of endogenous neuropeptide release and action on tachykinin NK receptors for the recruitment of eosinophils in various models of inflammation has also been demonstrated. Thus, blockade of tachykinin receptors was associated with the inhibition of eosinophil influx after pulmonary administration of sephadex ( Tramontana et al , 2002 ) or in models of allergic pulmonary inflammation ( Schuiling et al , 1999a ,b; Nénan et al , 2001 ). Few of the studies above have evaluated the comparative effect of drugs that inhibit each of the tachykinin NK receptors.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms underlying the inhibitory effects of tachykinin receptor antagonists on eosinophil recruitment in an allergic pleurisy model in mice

Alessandri

Pinho

Souza

et al. 2003

British J Pharmacology

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1 The activation of tachykinin NK receptors by neuropeptides may induce the recruitment of eosinophils in vivo. The aim of the present study was to investigate the effects and underlying mechanism(s) of the action of tachykinin receptor antagonists on eosinophil recruitment in a model of allergic pleurisy in mice. 2 Pretreatment of immunized mice with capsaicin partially prevented the recruitment of eosinophils after antigen challenge, suggesting the potential contribution of sensory nerves for the recruitment of eosinophils 3 Local (10 -50 nmol per pleural cavity) or systemic (100 -300 nmol per animal) pretreatment with the tachykinin NK 1 receptor antagonist SR140333 prevented the recruitment of eosinophils induced by antigen challenge of immunized mice. Neither tachykinin NK 2 nor NK 3 receptor antagonists suppressed eosinophil recruitment. 4 Pretreatment with SR140333 failed to prevent the antigen-induced increase of interleukin-5 concentrations in the pleural cavity. Similarly, SR140333 failed to affect the bone marrow eosinophilia observed at 48 h after antigen challenge of immunized mice. 5 SR140333 induced a significant increase in the concentrations of antigen-induced eotaxin at 6 h after challenge. 6 Antigen challenge of immunized mice induced a significant increase of Leucotriene B 4 (LTB 4 ) concentrations at 6 h after challenge. Pretreatment with SR140333 prevented the antigen-induced increase of LTB 4 concentrations. 7 Our data suggest an important role for NK 1 receptor activation with consequent LTB 4 release and eosinophil recruitment in a model of allergic pleurisy in the mouse. Tachykinins appear to be released mainly from peripheral endings of capsaicin-sensitive sensory neurons and may act on mast cells to facilitate antigen-driven release of LTB 4 .

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Section: Introductionmentioning

confidence: 99%

Mechanisms underlying the inhibitory effects of tachykinin receptor antagonists on eosinophil recruitment in an allergic pleurisy model in mice

Alessandri

Pinho

Souza

et al. 2003

British J Pharmacology

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“…This suggests a differentiation of the role of the tachykinins of neurosensory origin to those of inflammatory cell origin. In contrast, Tramontana et al 38 showed an inhibitory effect of napedutant, an antagonist of NK 2 receptors, on the cell inflammation reported in their model.…”

Section: Discussionmentioning

confidence: 77%

“…Several pieces of evidence suggest that stimulation of tachykinin NK 2 receptors is also involved in the infiltration of neutrophils and lymphocytes in the airways of ovalbumin‐challenged guinea‐pigs 37 or macrophages and eosinophils in a non‐allergic model of sephadex‐induced airway inflammation in the same species 38 . Because NK 3 receptor antagonists, such as SR 142801, SR 146977 and SB 235375, reproduce some of the effects of both NK 1 and NK 2 antagonists, 11–14 we compared the effects of SR 142801 with those of the combination of SR 140333 and SR 48968.…”

Section: Discussionmentioning

confidence: 99%

“…These results emphasize the importance of the role of tachykinins in the cellular origin of the inflammatory process observed in airways under the influence of LPS. The role of the tachykinins contained in and/or synthesized by the inflammatory cells, distinct from that of the tachykinins released by sensory nerve endings (C‐fibres), was recently underlined in another model of non‐allergic inflammation of the airways induced in the guinea‐pig by the intravenous administration of sephadex beads 38 . In that study, pretreatment of animals with capsaicin abolished the bronchial hyperreactivity to acetylcholine, but neither the cellular mobilization nor the increase in the rates of tachykinin (neurokinin A and substance P) in BALF was modified.…”

Section: Discussionmentioning

confidence: 99%

“…or macrophages and eosinophils in a non-allergic model of sephadex-induced airway inflammation in the same species. 38 Because NK3 receptor antagonists, such as SR 142801, SR 146977 and SB 235375, reproduce some of the effects of both NK1 and NK2 antagonists, [11][12][13][14] we compared the effects of SR 142801 with those of the combination of SR 140333 and SR 48968. Aerosol administration of SR 142801 (10 -6 mol/L) was ineffective in inhibiting the increase in total cell number and neutrophils 2.5 or 20 h following LPS exposure.…”

Section: Figmentioning

confidence: 99%

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Interactions of tachykinin receptor antagonists with lipopolysaccharide‐induced airway inflammation in mice

Veron

Guénon

Nénan

et al. 2004

Clin Exp Pharma Physio

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1. Several observations suggest that tachykinins are involved in the pathogenesis of bronchopulmonary alterations. We have investigated the effect of antagonists for tachykinin NK1 (SR 140333), NK2 (SR 48968) or NK3 (SR 142801) receptors on inflammatory cell recruitment, tumour necrosis factor (TNF)-alpha and interleukin (IL)-6 release and matrix metalloproteinase (MMP)-9 activity in the bronchoalveolar lavage fluid (BALF) of mice exposed to lipopolysaccharide (LPS; 100 microg/mL aerosol for 30 min). 2. Treatment of mice with a combination of SR 140333 and SR 48968 (10(-6) mol/L, aerosol) significantly reduced the increase in the number of total cells and neutrophils and MMP-9 activity in the BALF of mice 2.5 h after LPS exposure. Treatment with the NK3 antagonist SR 142801 (10(-6) mol/L, aerosol) did not inhibit the influx of neutrophils, but markedly reduced the increase in TNF-alpha and IL-6 levels at 2.5 h and MMP-9 activity at 20 h. 3. These results show that the three tachykinin receptor antagonists may interfere with the development of airway inflammation, namely neutrophilia, TNF-alpha release or MMP-9 activity in the BALF of mice exposed to LPS and suggest that not only NK1 and NK2 receptors, but also NK3 receptors are involved in the modulation of the inflammatory response and airway remodelling.

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Tachykinin NK2 Receptor Antagonists

Emonds‐Alt

2004

Handbook of Experimental Pharmacology

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Role of tachykinins in sephadex-induced airway hyperreactivity and inflammation in guinea pigs

Cited by 14 publications

References 50 publications

Mechanisms underlying the inhibitory effects of tachykinin receptor antagonists on eosinophil recruitment in an allergic pleurisy model in mice

Mechanisms underlying the inhibitory effects of tachykinin receptor antagonists on eosinophil recruitment in an allergic pleurisy model in mice

Interactions of tachykinin receptor antagonists with lipopolysaccharide‐induced airway inflammation in mice

Tachykinin NK2 Receptor Antagonists

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