Adrenergic Signaling at the Interface of Allergic Asthma and Viral Infections
Upper respiratory viral infections are a major etiologic instigator of allergic asthma, and they drive severe exacerbations of allergic inflammation in the lower airways of asthma sufferers. Rhinovirus (RV), in particular, is the main viral instigator of these pathologies. Asthma exacerbations due t...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2018-04-01
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| Series: | Frontiers in Immunology |
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| Online Access: | http://journal.frontiersin.org/article/10.3389/fimmu.2018.00736/full |
| _version_ | 1818275121073225728 |
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| author | Didem Ağaç Michelle A. Gill Michelle A. Gill J. David Farrar |
| author_facet | Didem Ağaç Michelle A. Gill Michelle A. Gill J. David Farrar |
| author_sort | Didem Ağaç |
| collection | DOAJ |
| description | Upper respiratory viral infections are a major etiologic instigator of allergic asthma, and they drive severe exacerbations of allergic inflammation in the lower airways of asthma sufferers. Rhinovirus (RV), in particular, is the main viral instigator of these pathologies. Asthma exacerbations due to RV infections are the most frequent reasons for hospitalization and account for the majority of morbidity and mortality in asthma patients. In both critical care and disease control, long- and short-acting β2-agonists are the first line of therapeutic intervention, which are used to restore airway function by promoting smooth muscle cell relaxation in bronchioles. While prophylactic use of β2-agonists reduces the frequency and pathology of exacerbations, their role in modulating the inflammatory response is only now being appreciated. Adrenergic signaling is a component of the sympathetic nervous system, and the natural ligands, epinephrine and norepinephrine (NE), regulate a multitude of autonomic functions including regulation of both the innate and adaptive immune response. NE is the primary neurotransmitter released by post-ganglionic sympathetic neurons that innervate most all peripheral tissues including lung and secondary lymphoid organs. Thus, the adrenergic signaling pathways are in direct contact with both the central and peripheral immune compartments. We present a perspective on how the adrenergic signaling pathway controls immune function and how β2-agonists may influence inflammation in the context of virus-induced asthma exacerbations. |
| first_indexed | 2024-12-12T22:24:43Z |
| format | Article |
| id | doaj.art-fd8695dde4844a00a3fa98705d0a6ea4 |
| institution | Directory Open Access Journal |
| issn | 1664-3224 |
| language | English |
| last_indexed | 2024-12-12T22:24:43Z |
| publishDate | 2018-04-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj.art-fd8695dde4844a00a3fa98705d0a6ea42022-12-22T00:09:48ZengFrontiers Media S.A.Frontiers in Immunology1664-32242018-04-01910.3389/fimmu.2018.00736359788Adrenergic Signaling at the Interface of Allergic Asthma and Viral InfectionsDidem Ağaç0Michelle A. Gill1Michelle A. Gill2J. David Farrar3Department of Immunology, The University of Texas Southwestern Medical Center, Dallas, TX, United StatesDepartment of Immunology, The University of Texas Southwestern Medical Center, Dallas, TX, United StatesDepartment of Pediatrics, The University of Texas Southwestern Medical Center, Dallas, TX, United StatesDepartment of Immunology, The University of Texas Southwestern Medical Center, Dallas, TX, United StatesUpper respiratory viral infections are a major etiologic instigator of allergic asthma, and they drive severe exacerbations of allergic inflammation in the lower airways of asthma sufferers. Rhinovirus (RV), in particular, is the main viral instigator of these pathologies. Asthma exacerbations due to RV infections are the most frequent reasons for hospitalization and account for the majority of morbidity and mortality in asthma patients. In both critical care and disease control, long- and short-acting β2-agonists are the first line of therapeutic intervention, which are used to restore airway function by promoting smooth muscle cell relaxation in bronchioles. While prophylactic use of β2-agonists reduces the frequency and pathology of exacerbations, their role in modulating the inflammatory response is only now being appreciated. Adrenergic signaling is a component of the sympathetic nervous system, and the natural ligands, epinephrine and norepinephrine (NE), regulate a multitude of autonomic functions including regulation of both the innate and adaptive immune response. NE is the primary neurotransmitter released by post-ganglionic sympathetic neurons that innervate most all peripheral tissues including lung and secondary lymphoid organs. Thus, the adrenergic signaling pathways are in direct contact with both the central and peripheral immune compartments. We present a perspective on how the adrenergic signaling pathway controls immune function and how β2-agonists may influence inflammation in the context of virus-induced asthma exacerbations.http://journal.frontiersin.org/article/10.3389/fimmu.2018.00736/fulladrenergic receptorasthmarhinovirusinflammationcytokine |
| spellingShingle | Didem Ağaç Michelle A. Gill Michelle A. Gill J. David Farrar Adrenergic Signaling at the Interface of Allergic Asthma and Viral Infections Frontiers in Immunology adrenergic receptor asthma rhinovirus inflammation cytokine |
| title | Adrenergic Signaling at the Interface of Allergic Asthma and Viral Infections |
| title_full | Adrenergic Signaling at the Interface of Allergic Asthma and Viral Infections |
| title_fullStr | Adrenergic Signaling at the Interface of Allergic Asthma and Viral Infections |
| title_full_unstemmed | Adrenergic Signaling at the Interface of Allergic Asthma and Viral Infections |
| title_short | Adrenergic Signaling at the Interface of Allergic Asthma and Viral Infections |
| title_sort | adrenergic signaling at the interface of allergic asthma and viral infections |
| topic | adrenergic receptor asthma rhinovirus inflammation cytokine |
| url | http://journal.frontiersin.org/article/10.3389/fimmu.2018.00736/full |
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