Bronchodilatation by tachykinins and capsaicin in the mouse main bronchus

Manzini, Stefano

doi:10.1111/j.1476-5381.1992.tb09086.x

Cited by 78 publications

(57 citation statements)

References 30 publications

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“…If airway generations within the respiratory tract serve different functional tasks, comparability through size may not be sufficient. Finally, the airway response of mouse and human preparations to different agonists is not always comparable [44][45][46]. For example, it has been shown that the cholinergic muscarinic subtype 3 receptor-mediated construction, as well as the adrenergic b 2 -adrenoreceptor-mediated relaxation, is comparable in both species.…”

Section: In Vitro Airway Responsivenessmentioning

confidence: 99%

Murine models of asthma

Kips¹,

Anderson²,

Fredberg³

et al. 2003

European Respiratory Journal

182

122

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In vivo animal models can offer valuable information on several aspects of asthma pathogenesis and treatment. The mouse is increasingly used in these models, mainly because this species allows for the application in vivo of a broad range of immunological tools, including gene deletion technology. Mice, therefore, seem particularly useful to further elucidate factors influencing the response to inhaled allergens. Examples include: the role of immunoregulatory mechanisms that protect against T-helper cell type 2 cell development; the trafficking of T-cells; and the contribution of the innate immunity. However, as for other animal species, murine models also have limitations. Mice do not spontaneously develop asthma and no model mimics the entire asthma phenotype. Instead, mice should be used to model specific traits of the human disease. The present task force report draws attention to specific aspects of lung structure and function that need to be borne in mind when developing such models and interpreting the results. In particular, efforts should be made to develop models that mimic the lung function changes characteristic of asthma as closely as possible. A large section of this report is therefore devoted to an overview of airway function and its measurement in mice.

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Section: In Vitro Airway Responsivenessmentioning

confidence: 99%

Murine models of asthma

Kips¹,

Anderson²,

Fredberg³

et al. 2003

European Respiratory Journal

182

122

View full text Add to dashboard Cite

show abstract

“…In contrast, TRPV1 is activated by heat (Ͼ42°C), protons, N-arachidonoyldopamine, anandamide, and lipoxygenase products and is involved in the detection of inflammatory thermal pain (Caterina et al, 1997;Tominaga et al, 1998;Hwang et al, 2000;Chuang et al, 2001;Julius and Basbaum, 2001;Huang et al, 2002). Distribution of TRPM8 and TRPV1 in areas that are not subjected to these temperature ranges suggests a role beyond that as temperature sensors (Manzini, 1992;Zygmunt et al, 1999;Mezey et al, 2000;Birder et al, 2002;Baccei et al, 2003;Tsuzuki et al, 2004). TRPM8 (previously identified as Trp-p8) is upregulated in prostate cancer and is involved in urinary bladder function, which broadens the horizon of TRPM8 in other pathophysiological conditions (Tsavaler et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Downregulation of Transient Receptor Potential Melastatin 8 by Protein Kinase C-Mediated Dephosphorylation

Premkumar¹,

Raisinghani²,

Pingle³

et al. 2005

J. Neurosci.

146

155

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Transient receptor potential melastatin 8 (TRPM8) and transient receptor potential vanilloid 1 (TRPV1) are ion channels that detect cold and hot sensations, respectively. Their activation depolarizes the peripheral nerve terminals resulting in action potentials that propagate to brain via the spinal cord. These receptors also play a significant role in synaptic transmission between dorsal root ganglion (DRG) and dorsal horn (DH) neurons. Here, we show that TRPM8 is functionally downregulated by activation of protein kinase C (PKC) resulting in inhibition of membrane currents and increases in intracellular Ca 2ϩ compared with upregulation of TRPV1 in cloned and native receptors. Bradykinin significantly downregulates TRPM8 via activation of PKC in DRG neurons. Activation of TRPM8 or TRPV1 at first sensory synapse between DRG and DH neurons leads to a robust increase in frequency of spontaneous/miniature EPSCs. PKC activation blunts TRPM8-and facilitates TRPV1-mediated synaptic transmission. Significantly, downregulation is attributable to PKC-mediated dephosphorylation of TRPM8 that could be reversed by phosphatase inhibitors. These findings suggest that inflammatory thermal hyperalgesia mediated by TRPV1 may be further aggravated by downregulation of TRPM8, because the latter could mediate the much needed cool/soothing sensation.

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“…Accumulating and compelling evidence indicates this sensory function is mediated primarily by members of the transient receptor potential (TRP) family of ion channels, which are highly expressed on sensory nerve endings. For example, TRP vanilloid type 1 (TRPV1) is a calcium ion channel, which is activated by high temperature (Ͼ40°C), low pH, and exogenous vanilloids such as the chili plant extract capsaicin (Manzini, 1992;Bevan and Geppetti, 1994;Caterina et al, 1997;Szallasi and Blumberg, 1999).…”

Section: Introductionmentioning

confidence: 99%

Influence of Influenza A Infection on Capsaicin-Induced Responses in Murine Airways

Taylor

Mann²,

Henry³

2011

J Pharmacol Exp Ther

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The principal aim of the study was to determine the influence of influenza A virus infection on capsaicin-induced relaxation responses in mouse isolated tracheal segments and clarify the underlying mechanisms. Anesthetized mice were intranasally inoculated with influenza A/PR-8/34 virus (VIRUS) or vehicle (SHAM), and 4 days later tracheal segments were harvested for isometric tension recording and biochemical and histologic analyses. Capsaicin induced dose-dependent relaxation responses in carbachol-contracted SHAM trachea (e.g., 10 M capsaicin produced 66 Ϯ 4% relaxation; n ϭ 11), which were significantly inhibited by capsazepine prostanoid (EP) 2 and EP 4 receptor antagonists, respectively], indicating that capsaicin-induced relaxation involved the TRPV1-mediated release of substance P (SP), activation of epithelial NK 1 receptors, and production of COX products capable of activating relaxant EP 2 /EP 4 receptors. Consistent with this postulate, capsaicin-induced relaxation was associated with the significant release of SP and prostaglandin E 2 (PGE 2 ) from mouse tracheal segments. As expected, influenza A virus infection was associated with widespread disruption of the tracheal epithelium. Tracheal segments from VIRUS mice responded weakly to capsaicin (7 Ϯ 3% relaxation) and were 25-fold less responsive to SP than tracheas from SHAM mice. In contrast, relaxation responses to exogenous PGE 2 and the ␤-adrenoceptor agonist isoprenaline were not inhibited in VIRUS trachea. Virus infection was associated with impaired capsaicin-induced release of PGE 2 , but the release of SP was not affected. In summary, influenza A virus infection profoundly inhibits capsaicin-and SP-induced relaxation responses, most likely by inhibiting the production of PGE 2 .

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Bronchodilatation by tachykinins and capsaicin in the mouse main bronchus

Cited by 78 publications

References 30 publications

Murine models of asthma

Murine models of asthma

Downregulation of Transient Receptor Potential Melastatin 8 by Protein Kinase C-Mediated Dephosphorylation

Influence of Influenza A Infection on Capsaicin-Induced Responses in Murine Airways

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