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 in | Journal of Veterinary Medical Science Vol. 86; no. 7; pp. 824 - 827 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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JAPANESE SOCIETY OF VETERINARY SCIENCE
2024
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ISSN | 0916-7250 1347-7439 1347-7439 |
DOI | 10.1292/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. |
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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 |
Author_xml | – sequence: 1 fullname: OGATA, Sawako organization: Department of Disease Model, Research Institute of Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan – sequence: 1 fullname: MIURA, Kento organization: Department of Disease Model, Research Institute of Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan – sequence: 1 fullname: MATSUURA, Anna organization: Department of Disease Model, Research Institute of Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan – sequence: 1 fullname: HOSOMI, Naohisa organization: Department of Disease Model, Research Institute of Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan – sequence: 1 fullname: MORI, Akio organization: Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Kanagawa, Japan – sequence: 1 fullname: YAMASHITA, Shuhei organization: Department of Disease Model, Research Institute of Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan – sequence: 1 fullname: YAMASAKI, Norimasa organization: Department of Disease Model, Research Institute of Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan – sequence: 1 fullname: KITAMURA, Noriko organization: Department of Otorhinolaryngology, Nippon Medical School, Tokyo, Japan – sequence: 1 fullname: UDA, Naoto organization: Department of Disease Model, Research Institute of Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan – sequence: 1 fullname: GOTOH, Minoru organization: Department of Otorhinolaryngology, Nippon Medical School, Tokyo, Japan – sequence: 1 fullname: NAKAJIMA, Shotaro organization: Departments of Multidisciplinary Treatment of Cancer and Regional Medical Support, Fukushima Medical University School of Medicine, Fukushima, Japan – sequence: 1 fullname: KAMINUMA, Osamu organization: Department of Disease Model, Research Institute of Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan |
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Cites_doi | 10.1371/journal.pone.0146686 10.4168/aair.2018.10.3.268 10.1093/intimm/11.6.987 10.1016/j.jphs.2022.10.004 10.5415/apallergy.2020.10.e18 10.1038/nature01339 10.3389/fimmu.2019.01102 10.3390/ijms23031779 10.4049/jimmunol.180.11.7655 10.3389/fimmu.2017.01085 10.1016/S0006-8993(97)00536-2 10.1016/j.phrs.2023.106758 10.1016/j.apsb.2017.09.001 10.1016/j.bbrc.2008.10.004 10.2500/aap.2013.34.3715 10.1371/journal.pone.0190453 10.3389/fnana.2019.00076 10.1016/j.neuropharm.2020.108086 10.1016/S0006-3223(00)01011-8 10.4155/fmc-2017-0169 |
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References | 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. 13. Mishra NC, Rir-Sima-Ah J, Langley RJ, Singh SP, Peña-Philippides JC, Koga T, Razani-Boroujerdi S, Hutt J, Campen M, Kim KC, Tesfaigzi Y, Sopori ML. 2008. Nicotine primarily suppresses lung Th2 but not goblet cell and muscle cell responses to allergens. J Immunol 180: 7655–7663. 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. 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. 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. 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. 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. 1. Benedé S, Berin MC. 2018. Mast cell heterogeneity underlies different manifestations of food allergy in mice. PLoS One 13: e0190453. 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. 11. Matsuoka K, Taya C, Kubo S, Toyama-Sorimachi N, Kitamura F, Ra C, Yonekawa H, Karasuyama H. 1999. Establishment of antigen-specific IgE transgenic mice to study pathological and immunobiological roles of IgE in vivo. Int Immunol 11: 987–994. 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. 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. 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. 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. 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. 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. 14. Nakata Y, Miura K, Yamasaki N, Ogata S, Miura S, Hosomi N, Kaminuma O. 2022. Expression and function of nicotinic acetylcholine receptors in induced regulatory T cells. Int J Mol Sci 23: 23. 4. Dani JA. 2001. Overview of nicotinic receptors and their roles in the central nervous system. Biol Psychiatry 49: 166–174. 18. Uda N, Ogata S, Yamasaki N, Miura S, Hosomi N, Mori A, Gotoh M, Miura K, Kaminuma O. 2022. Re-evaluation of over-the-counter histamine H1-receptor antagonists based on their effects on murine models of allergen-induced nasal hyperresponsiveness. J Pharmacol Sci 150: 275–278. 6. Gharpure A, Noviello CM, Hibbs RE. 2020. Progress in nicotinic receptor structural biology. Neuropharmacology 171: 108086. 11 12 13 14 15 16 17 18 19 1 2 3 4 5 6 7 8 9 20 10 |
References_xml | – reference: 11. Matsuoka K, Taya C, Kubo S, Toyama-Sorimachi N, Kitamura F, Ra C, Yonekawa H, Karasuyama H. 1999. Establishment of antigen-specific IgE transgenic mice to study pathological and immunobiological roles of IgE in vivo. Int Immunol 11: 987–994. – reference: 14. Nakata Y, Miura K, Yamasaki N, Ogata S, Miura S, Hosomi N, Kaminuma O. 2022. Expression and function of nicotinic acetylcholine receptors in induced regulatory T cells. Int J Mol Sci 23: 23. – 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. – reference: 1. Benedé S, Berin MC. 2018. Mast cell heterogeneity underlies different manifestations of food allergy in mice. PLoS One 13: e0190453. – 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. – reference: 18. Uda N, Ogata S, Yamasaki N, Miura S, Hosomi N, Mori A, Gotoh M, Miura K, Kaminuma O. 2022. Re-evaluation of over-the-counter histamine H1-receptor antagonists based on their effects on murine models of allergen-induced nasal hyperresponsiveness. J Pharmacol Sci 150: 275–278. – 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. – reference: 13. Mishra NC, Rir-Sima-Ah J, Langley RJ, Singh SP, Peña-Philippides JC, Koga T, Razani-Boroujerdi S, Hutt J, Campen M, Kim KC, Tesfaigzi Y, Sopori ML. 2008. Nicotine primarily suppresses lung Th2 but not goblet cell and muscle cell responses to allergens. J Immunol 180: 7655–7663. – 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. – ident: 16 doi: 10.1371/journal.pone.0146686 – ident: 2 doi: 10.4168/aair.2018.10.3.268 – ident: 11 doi: 10.1093/intimm/11.6.987 – ident: 18 doi: 10.1016/j.jphs.2022.10.004 – ident: 15 doi: 10.5415/apallergy.2020.10.e18 – ident: 19 doi: 10.1038/nature01339 – ident: 10 doi: 10.3389/fimmu.2019.01102 – ident: 14 doi: 10.3390/ijms23031779 – ident: 13 doi: 10.4049/jimmunol.180.11.7655 – ident: 5 doi: 10.3389/fimmu.2017.01085 – ident: 12 doi: 10.1016/S0006-8993(97)00536-2 – ident: 8 doi: 10.1016/j.phrs.2023.106758 – ident: 20 doi: 10.1016/j.apsb.2017.09.001 – ident: 7 doi: 10.1016/j.bbrc.2008.10.004 – ident: 17 doi: 10.2500/aap.2013.34.3715 – ident: 1 doi: 10.1371/journal.pone.0190453 – ident: 3 doi: 10.3389/fnana.2019.00076 – ident: 6 doi: 10.1016/j.neuropharm.2020.108086 – ident: 4 doi: 10.1016/S0006-3223(00)01011-8 – ident: 9 doi: 10.4155/fmc-2017-0169 |
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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 |
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ispartofPNX | Journal of Veterinary Medical Science, 2024, Vol.86(7), pp.824-827 |
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