Pulmonary actions of the neurokinin1-specific agonist [Sar9, Met(O2)11]-substance P

Yiamouyiannis, Carmen A.; Stengel, Peter W.; Silbaugh, Steven A.

doi:10.1016/0143-4179(95)90072-1

Cited by 4 publications

(4 citation statements)

References 31 publications

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“…as indicated in a maximum volume of 20µL. To locally stimulate NK1R+ sinonasal cells, mice received 500ng of [Sar 9 ,Met(O 2 ) 11 ]-Substance P (Sar-SP, Tocris Bioscience, cat# 1178), which has been previously used as a potent synthetic SP analog and NK1R agonist 74,75 . Mice were treated 3 times on days 0 (D0), 2 (D2), and 4 (D4) with PBS, Sar-SP alone, or in combination with a single i.n.…”

Section: Sinonasal Tractmentioning

confidence: 99%

WITHDRAWN: Neuron-dependent tuft cell expansion initiates sinonasal allergic Type 2 inflammation

Ortiz-Carpena

Inclan-Rico

Weiner

et al. 2023

Preprint

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It is unknown whether interactions between tuft cells and trigeminal sinonasal neurons contribute to allergic disease. Intranasal administration of house dust mite or fungal allergens induced tuft cell expansion, eosinophilia, sneezing, Type 2 responses, and neuropeptide release. Mice lacking tuft cells lost these responses but retained eosinophilia and elevated neuropeptides. Ablation of Transient Receptor Potential Channel Vanilloid 1 (TRPV1)+ neurons prevented allergen-evoked tuft cell expansion and eosinophilia without affecting ILC2 and TH2 cell recruitment. Exposure of naive TG neurons to allergen evoked calcium influx and neuropeptide release, but only Substance P (SP) adaptively increased upon repetitive allergen exposure. SP instructed tuft cell lineage commitment and initiated allergic inflammation. Ablation or inhibition of the SP receptor, neurokinin 1, reversed allergen-induced sneezing, tuft cell expansion, and eosinophilia. We propose that sinonasal nociceptors detect protease-containing allergens and adaptively secrete SP to drive tuft cell expansion and early features of Type 2 immunity.

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Section: Sinonasal Tractmentioning

confidence: 99%

WITHDRAWN: Neuron-dependent tuft cell expansion initiates sinonasal allergic Type 2 inflammation

Ortiz-Carpena

Inclan-Rico

Weiner

et al. 2023

Preprint

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“…Millard and colleagues demonstrated that NKA interacts with both NK-1 and NK-2 binding sites in the rabbit lung [ 36] . [ Sar 9 Met O 2 11 ] -SP, a NK-1-speci c agonist, exhibits pulmonary actions such as airway obstruction and plasma extravasation [ 37] . Recently obtained results by Kaltreider and coworkers suggest that tachykinins may be secreted locally during pulmonary immune responses, and are recognized by leukocytes in ltrating lung tissue [ 26] .…”

Section: Discussionmentioning

confidence: 99%

Influence of Neuropeptides on Neutrophil Adhesion and Transmigration Through a Lung Fibroblast Barrier in Vitro

Kähler¹

2001

Experimental Lung Research

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The lu n g is richly su pplied with peptidergic n erv es that store an d secrete su bstan ce P (SP), v asoactiv e in testin al peptide (VIP), an d other n eu ropeptides kn own to poten tly mod u late leu kocyte fu n ction in v itro an d airway in ammation in v iv o. We examin ed the effect of SP, VIP an d the n ov el sen sory n eu ropeptide secreton eu rin (SN), as well as of in terleu kin (IL)-8, IL-6, IL-1 , tran sformin g g rowth factor (TGF)-, an d tu mor n ecrosis factor (TNF), all associated with acu te lu n g in ju ry, on hu man n eu trophil mig ration across a 5-m pore polycarbon ate lter system cov ered by hu man lu n g broblast mon olayers. Addition ally, we tested the ability of these n eu ropeptides to elicit n eu trophil adhesion to broblast mon olayers. SP, bu t n ot VIP an d SN, may be importan t in directly in u en cin g n eu trophil adhesion to an d su bsequ en t migration across a su ben dothelial barrier of broblasts an d extracellu lar matrix towards lu n g in ammatory sites. The effect was main ly mediated by n eu rokin in (NK)-1 receptors, as ev alu ated by a speci c NK-1 an tag on ist, [[(S,S)Pro-Leu (spiro-y-lactam)] 9 10 , Trp 11 ]su bstan ce P (1 -11), whereas a speci c NK-2 receptor an tagon ist, [Tyr 5 , D-Trp 6 8 9 , Lys 10 ]n eu rokin in A (4-10), was in effectiv e. The SP an alog septide an d the NK-1 receptor agon ist ([Sar 9 Met(O 2 11 )SP were comparably effectiv e. Fu rthermore, the SP effect was con cen tration an d time depen den t. Howev er, the other tested n eu ropeptides might also affect n eu trophil recru itmen t in in ammatory lu n g by mod u latin g other lu n g cell fu n ction s. Addition ally, all tested cytokin es stimu lated n eu trophil tran s broblast migration in v itro, except IL-6. In con clu sion , SP in con cert with proin ammatory cytokin es may reg u late n eu trophil in terstitial accu mu lation an d their traf c to the alv eolar space in lu n g in ammation .Keywords adhesion , broblast, n eu trophil, secreton eu rin , su bstan ce P, tran sm ig ration , v asoactiv e in testin al peptide A characteristic feature of several lung in ammatory conditions is the accumulation of polymorphonuclear leukocytes ( PMNL) and monocytes in

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“…Because of the limited number of samples available for the tracheal perfusion studies, doses for the peptide agonists and SR-48968 were chosen from published studies examining human and animal model airway responses. Doses used in the tracheal perfusion assays were those that caused bronchoconstriction in adult guinea pig samples studied with tracheal perfusion assay (31,32) and those demonstrated to be effective bronchoconstricting doses in other models (13,48,63). At the completion of the assays, the intact capacity of the pulmonary smooth muscle to respond to agonists was demonstrated by administering 6.1 mg (0.025 mol) of the nonspecific smooth muscle agonist BaCl 2.…”

Section: L1349mentioning

confidence: 99%

Developmental expression of neurokinin A and functional neurokinin-2 receptors in lung

Haley¹,

Sunday²,

Osathanondh

et al. 2001

American Journal of Physiology-Lung Cellular and Molecular Phys

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Peribronchial smooth muscle constriction causes airway stretch, an important mechanical force in developing lung. Little is known about factors influencing these spontaneously active muscle elements. We measured contractile activity of neurokinin (NK) receptors on fetal intrapulmonary smooth muscle by tracheal perfusion assay (n = 11). Injecting either capsaicin or the NK(2) receptor agonist [NLE(10)]NKA resulted in significant (P < 0.05) bronchoconstriction. A specific NK(2) receptor antagonist inhibited constriction caused by endogenous tachykinins released by capsaicin. We then examined NK(2) receptor (n = 44) and NKA (n = 23) ontogeny in human lung. NKA immunostaining was identified in peribronchial nerves in samples with gestational age >12 wk. NK(2) receptor protein was identified in peribronchial and perivascular smooth muscle. These results indicate that endogenous tachykinins released by the developing lung act via NK(2) receptors to cause smooth muscle constriction. We speculate that tachykinins could modulate lung development.

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Pulmonary actions of the neurokinin1-specific agonist [Sar9, Met(O2)11]-substance P

Cited by 4 publications

References 31 publications

WITHDRAWN: Neuron-dependent tuft cell expansion initiates sinonasal allergic Type 2 inflammation

WITHDRAWN: Neuron-dependent tuft cell expansion initiates sinonasal allergic Type 2 inflammation

Influence of Neuropeptides on Neutrophil Adhesion and Transmigration Through a Lung Fibroblast Barrier in Vitro

Developmental expression of neurokinin A and functional neurokinin-2 receptors in lung

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