α7 nicotinic acetylcholine receptor agonist attenuates allergen-induced immediate nasal response in murine model of allergic rhinitis

The expression of nicotinic acetylcholine receptor (nAChR) subunits on various immune cells suggests their involvement in allergic rhinitis. However, how exactly they contribute to this pathogenesis is not yet confirmed. Our present study examined the therapeutic potential of GTS-21, an α7 nAChR ago...

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Published inJournal of Veterinary Medical Science Vol. 86; no. 7; pp. 824 - 827
Main Authors OGATA, Sawako, MIURA, Kento, MATSUURA, Anna, HOSOMI, Naohisa, MORI, Akio, YAMASHITA, Shuhei, YAMASAKI, Norimasa, KITAMURA, Noriko, UDA, Naoto, GOTOH, Minoru, NAKAJIMA, Shotaro, KAMINUMA, Osamu
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LanguageEnglish
Published Japan JAPANESE SOCIETY OF VETERINARY SCIENCE 2024
Japan Science and Technology Agency
The Japanese Society of Veterinary Science
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ISSN0916-7250
1347-7439
1347-7439
DOI10.1292/jvms.24-0033

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Abstract The expression of nicotinic acetylcholine receptor (nAChR) subunits on various immune cells suggests their involvement in allergic rhinitis. However, how exactly they contribute to this pathogenesis is not yet confirmed. Our present study examined the therapeutic potential of GTS-21, an α7 nAChR agonist, for treating allergic rhinitis by employing its mouse models. GTS-21 treatment reduced allergen-induced immediate nasal response in ovalbumin (OVA)-sensitized model. However, nasal hyperresponsiveness or eosinophil infiltration elicited in either the OVA-sensitized or T helper 2 cell-transplanted model was not affected by GTS-21. GTS-21 did not alter allergen-induced passive cutaneous anaphylaxis response in anti-dinitrophenyl IgE-sensitized mice. This evidence implies GTS-21’s potential to alleviate allergic rhinitis without perturbing T cells or mast cells.
AbstractList The expression of nicotinic acetylcholine receptor (nAChR) subunits on various immune cells suggests their involvement in allergic rhinitis. However, how exactly they contribute to this pathogenesis is not yet confirmed. Our present study examined the therapeutic potential of GTS-21, an α7 nAChR agonist, for treating allergic rhinitis by employing its mouse models. GTS-21 treatment reduced allergen-induced immediate nasal response in ovalbumin (OVA)-sensitized model. However, nasal hyperresponsiveness or eosinophil infiltration elicited in either the OVA-sensitized or T helper 2 cell-transplanted model was not affected by GTS-21. GTS-21 did not alter allergen-induced passive cutaneous anaphylaxis response in anti-dinitrophenyl IgE-sensitized mice. This evidence implies GTS-21’s potential to alleviate allergic rhinitis without perturbing T cells or mast cells.
The expression of nicotinic acetylcholine receptor (nAChR) subunits on various immune cells suggests their involvement in allergic rhinitis. However, how exactly they contribute to this pathogenesis is not yet confirmed. Our present study examined the therapeutic potential of GTS-21, an α7 nAChR agonist, for treating allergic rhinitis by employing its mouse models. GTS-21 treatment reduced allergen-induced immediate nasal response in ovalbumin (OVA)-sensitized model. However, nasal hyperresponsiveness or eosinophil infiltration elicited in either the OVA-sensitized or T helper 2 cell-transplanted model was not affected by GTS-21. GTS-21 did not alter allergen-induced passive cutaneous anaphylaxis response in anti-dinitrophenyl IgE-sensitized mice. This evidence implies GTS-21's potential to alleviate allergic rhinitis without perturbing T cells or mast cells.The expression of nicotinic acetylcholine receptor (nAChR) subunits on various immune cells suggests their involvement in allergic rhinitis. However, how exactly they contribute to this pathogenesis is not yet confirmed. Our present study examined the therapeutic potential of GTS-21, an α7 nAChR agonist, for treating allergic rhinitis by employing its mouse models. GTS-21 treatment reduced allergen-induced immediate nasal response in ovalbumin (OVA)-sensitized model. However, nasal hyperresponsiveness or eosinophil infiltration elicited in either the OVA-sensitized or T helper 2 cell-transplanted model was not affected by GTS-21. GTS-21 did not alter allergen-induced passive cutaneous anaphylaxis response in anti-dinitrophenyl IgE-sensitized mice. This evidence implies GTS-21's potential to alleviate allergic rhinitis without perturbing T cells or mast cells.
The expression of nicotinic acetylcholine receptor (nAChR) subunits on various immune cells suggests their involvement in allergic rhinitis. However, how exactly they contribute to this pathogenesis is not yet confirmed. Our present study examined the therapeutic potential of GTS-21, an α7 nAChR agonist, for treating allergic rhinitis by employing its mouse models. GTS-21 treatment reduced allergen-induced immediate nasal response in ovalbumin (OVA)-sensitized model. However, nasal hyperresponsiveness or eosinophil infiltration elicited in either the OVA-sensitized or T helper 2 cell-transplanted model was not affected by GTS-21. GTS-21 did not alter allergen-induced passive cutaneous anaphylaxis response in anti-dinitrophenyl IgE-sensitized mice. This evidence implies GTS-21’s potential to alleviate allergic rhinitis without perturbing T cells or mast cells.
ArticleNumber 24-0033
Author KITAMURA, Noriko
GOTOH, Minoru
YAMASHITA, Shuhei
UDA, Naoto
MATSUURA, Anna
NAKAJIMA, Shotaro
HOSOMI, Naohisa
YAMASAKI, Norimasa
OGATA, Sawako
KAMINUMA, Osamu
MIURA, Kento
MORI, Akio
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  fullname: OGATA, Sawako
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  fullname: MATSUURA, Anna
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Keywords allergic rhinitis
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α7 nicotinic acetylcholine receptor
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– reference: 8. Keever KR, Yakubenko VP, Hoover DB. 2023. Neuroimmune nexus in the pathophysiology and therapy of inflammatory disorders: Role of α7 nicotinic acetylcholine receptors. Pharmacol Res 191: 106758.
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– reference: 7. Kageyama-Yahara N, Suehiro Y, Yamamoto T, Kadowaki M. 2008. IgE-induced degranulation of mucosal mast cells is negatively regulated via nicotinic acetylcholine receptors. Biochem Biophys Res Commun 377: 321–325.
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– reference: 20. Yang T, Xiao T, Sun Q, Wang K. 2017. The current agonists and positive allosteric modulators of α7 nAChR for CNS indications in clinical trials. Acta Pharm Sin B 7: 611–622.
– reference: 6. Gharpure A, Noviello CM, Hibbs RE. 2020. Progress in nicotinic receptor structural biology. Neuropharmacology 171: 108086.
– reference: 3. Broide RS, Winzer-Serhan UH, Chen Y, Leslie FM. 2019. Distribution of α7 nicotinic acetylcholine receptor subunit mRNA in the developing mouse. Front Neuroanat 13: 76.
– reference: 9. Manetti D, Bellucci C, Chiaramonte N, Dei S, Teodori E, Romanelli MN. 2018. Designing selective modulators for the nicotinic receptor subtypes: challenges and opportunities. Future Med Chem 10: 433–459.
– reference: 16. Nishimura T, Kaminuma O, Saeki M, Kitamura N, Matsuoka K, Yonekawa H, Mori A, Hiroi T. 2016. Essential contribution of CD4+ T cells to antigen-induced nasal hyperresponsiveness in experimental allergic rhinitis. PLoS One 11: e0146686.
– reference: 15. Nishimura T, Kaminuma O, Saeki M, Kitamura N, Mori A, Hiroi T. 2020. Suppressive effect of environmental tobacco smoke on murine Th2 cell-mediated nasal eosinophilic inflammation. Asia Pac Allergy 10: e18.
– reference: 4. Dani JA. 2001. Overview of nicotinic receptors and their roles in the central nervous system. Biol Psychiatry 49: 166–174.
– reference: 5. Fujii T, Mashimo M, Moriwaki Y, Misawa H, Ono S, Horiguchi K, Kawashima K. 2017. Expression and function of the cholinergic system in immune cells. Front Immunol 8: 1085.
– reference: 17. Turner RR, Testa MA, Hayes JF, Su M. 2013. Validation of the allergic rhinitis treatment satisfaction and preference scale. Allergy Asthma Proc 34: 551–557.
– reference: 2. Benedé S, Cody E, Agashe C, Berin MC. 2018. Immune characterization of bone marrow-derived models of mucosal and connective tissue mast cells. Allergy Asthma Immunol Res 10: 268–277.
– reference: 12. Meyer EM, Tay ET, Papke RL, Meyers C, Huang GL, de Fiebre CM. 1997. 3-[2,4-Dimethoxybenzylidene]anabaseine (DMXB) selectively activates rat alpha7 receptors and improves memory-related behaviors in a mecamylamine-sensitive manner. Brain Res 768: 49–56.
– reference: 19. Wang H, Yu M, Ochani M, Amella CA, Tanovic M, Susarla S, Li JH, Wang H, Yang H, Ulloa L, Al-Abed Y, Czura CJ, Tracey KJ. 2003. Nicotinic acetylcholine receptor alpha7 subunit is an essential regulator of inflammation. Nature 421: 384–388.
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– reference: 10. Mashimo M, Komori M, Matsui YY, Murase MX, Fujii T, Takeshima S, Okuyama H, Ono S, Moriwaki Y, Misawa H, Kawashima K. 2019. Distinct roles of α7 nAChRs in antigen-presenting cells and CD4+ T cells in the regulation of t cell differentiation. Front Immunol 10: 1102.
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Snippet The expression of nicotinic acetylcholine receptor (nAChR) subunits on various immune cells suggests their involvement in allergic rhinitis. However, how...
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SubjectTerms Acetylcholine receptors (nicotinic)
Agonists
Allergens
Allergic rhinitis
Allergies
alpha7 Nicotinic Acetylcholine Receptor - agonists
Anaphylaxis
Animal models
Animals
Benzylidene Compounds - pharmacology
Benzylidene Compounds - therapeutic use
Disease Models, Animal
Female
Leukocytes (eosinophilic)
Lymphocytes T
Mast cells
Mice
Mice, Inbred BALB C
murine model
Nicotinic Agonists - pharmacology
Nicotinic Agonists - therapeutic use
Ovalbumin
Passive cutaneous anaphylaxis
Pharmacology
Pyridines - pharmacology
Pyridines - therapeutic use
Rhinitis, Allergic - drug therapy
α7 nicotinic acetylcholine receptor
Title α7 nicotinic acetylcholine receptor agonist attenuates allergen-induced immediate nasal response in murine model of allergic rhinitis
URI https://www.jstage.jst.go.jp/article/jvms/86/7/86_24-0033/_article/-char/en
https://www.ncbi.nlm.nih.gov/pubmed/38839347
https://www.proquest.com/docview/3093062231
https://www.proquest.com/docview/3065276719
https://pubmed.ncbi.nlm.nih.gov/PMC11251814
Volume 86
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