Pulmonary neuroendocrine cells amplify allergic asthma responses

Pulmonary neuroendocrine cells (PNECs) are rare airway epithelial cells whose function is poorly understood. Here we show that -mutant mice that have no PNECs exhibit severely blunted mucosal type 2 response in models of allergic asthma. PNECs reside in close proximity to group 2 innate lymphoid cel...

Full description

Saved in:
Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 2018-06, Vol.360 (6393)
Main Authors: Sui, Pengfei, Wiesner, Darin L, Xu, Jinhao, Zhang, Yan, Lee, Jinwoo, Van Dyken, Steven, Lashua, Amber, Yu, Chuyue, Klein, Bruce S, Locksley, Richard M, Deutsch, Gail, Sun, Xin
Format: Article
Language:English
Subjects:
Acids
Allergens
Allergies
Allergy
Alveoli
Amines
Amphibians
Amplification
Animal models
Animals
ASCL1 protein
Asthma
Asthma - immunology
Asthma - pathology
Basic Helix-Loop-Helix Transcription Factors - deficiency
Basic Helix-Loop-Helix Transcription Factors - genetics
Calcitonin
Calcitonin gene-related peptide
Calcitonin Gene-Related Peptide - metabolism
Cell culture
Chemical sensors
Chemoreceptors
Clustering
Cytokines
Cytokines - biosynthesis
Deactivation
Dense core vesicles
Disease Models, Animal
Effectors
Epithelial cells
Epithelial Cells - immunology
Epithelial Cells - pathology
Epithelium
Feedback (Response)
Female
gamma-Aminobutyric Acid - biosynthesis
gamma-Aminobutyric Acid - metabolism
Goblet Cells - pathology
House dust
Humans
Hyperplasia
Hypersensitivity
Immune response
Immune system
In vivo methods and tests
Inactivation
Interleukin 5
Lung - pathology
Lungs
Mice
Modules
Molecular chains
Mucosa
Mucous membrane
Mucus
Mutants
Neuroendocrine Cells - immunology
Neuroendocrine Cells - pathology
Neuropeptides
Neurotransmitters
Numbers
Patients
Peptides
Physiological responses
Proximity
Reptiles
Respiratory tract
Rodents
Scientific Concepts
Sensory neurons
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c487t-8663927d48f2e772f71a447e05e1b488d81ea757ecb10dce4f10f7a36f5bd8863
cites cdi_FETCH-LOGICAL-c487t-8663927d48f2e772f71a447e05e1b488d81ea757ecb10dce4f10f7a36f5bd8863
container_end_page
container_issue 6393
container_start_page
container_title Science (American Association for the Advancement of Science)
container_volume 360
creator Sui, Pengfei
Wiesner, Darin L
Xu, Jinhao
Zhang, Yan
Lee, Jinwoo
Van Dyken, Steven
Lashua, Amber
Yu, Chuyue
Klein, Bruce S
Locksley, Richard M
Deutsch, Gail
Sun, Xin
description Pulmonary neuroendocrine cells (PNECs) are rare airway epithelial cells whose function is poorly understood. Here we show that -mutant mice that have no PNECs exhibit severely blunted mucosal type 2 response in models of allergic asthma. PNECs reside in close proximity to group 2 innate lymphoid cells (ILC2s) near airway branch points. PNECs act through calcitonin gene-related peptide (CGRP) to stimulate ILC2s and elicit downstream immune responses. In addition, PNECs act through the neurotransmitter γ-aminobutyric acid (GABA) to induce goblet cell hyperplasia. The instillation of a mixture of CGRP and GABA in -mutant airways restores both immune and goblet cell responses. In accordance, lungs from human asthmatics show increased PNECs. These findings demonstrate that the PNEC-ILC2 neuroimmunological modules function at airway branch points to amplify allergic asthma responses.
doi_str_mv 10.1126/science.aan8546
format article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6387886</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2020494274</sourcerecordid><originalsourceid>FETCH-LOGICAL-c487t-8663927d48f2e772f71a447e05e1b488d81ea757ecb10dce4f10f7a36f5bd8863</originalsourceid><addsrcrecordid>eNpdkb1PwzAUxC0EoqUws6FILCxp_ZXYWRCo4kuqBAPMluu8tKkSu9gJUv97XLVUwHTD_d7pnQ6hS4LHhNB8EkwN1sBYaysznh-hIcFFlhYUs2M0xJjlqcQiG6CzEFYYR69gp2hAoxakYEN099Y3rbPabxILvXdgS2d8bSEx0DQh0e26qatNopsG_KI2iQ7dstWJh7B2NkA4RyeVbgJc7HWEPh4f3qfP6ez16WV6P0sNl6JLZZ6zgoqSy4qCELQSRHMuAGdA5lzKUhLQIhNg5gSXBnhFcCU0y6tsXkqZsxG63eWu-3kLkbCd141a-7qNzyuna_XXsfVSLdyXypkUu4CbfYB3nz2ETrV12JbUFlwfFMUU84JTwSN6_Q9dud7bWC9SGRGZlIxGarKjjHcheKgOzxCstuuo_Tpqv068uPrd4cD_zMG-AbHxjtk</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2051758832</pqid></control><display><type>article</type><title>Pulmonary neuroendocrine cells amplify allergic asthma responses</title><source>American Association for the Advancement of Science</source><source>JSTOR Archival Journals and Primary Sources Collection</source><source>Alma/SFX Local Collection</source><creator>Sui, Pengfei ; Wiesner, Darin L ; Xu, Jinhao ; Zhang, Yan ; Lee, Jinwoo ; Van Dyken, Steven ; Lashua, Amber ; Yu, Chuyue ; Klein, Bruce S ; Locksley, Richard M ; Deutsch, Gail ; Sun, Xin</creator><creatorcontrib>Sui, Pengfei ; Wiesner, Darin L ; Xu, Jinhao ; Zhang, Yan ; Lee, Jinwoo ; Van Dyken, Steven ; Lashua, Amber ; Yu, Chuyue ; Klein, Bruce S ; Locksley, Richard M ; Deutsch, Gail ; Sun, Xin</creatorcontrib><description>Pulmonary neuroendocrine cells (PNECs) are rare airway epithelial cells whose function is poorly understood. Here we show that -mutant mice that have no PNECs exhibit severely blunted mucosal type 2 response in models of allergic asthma. PNECs reside in close proximity to group 2 innate lymphoid cells (ILC2s) near airway branch points. PNECs act through calcitonin gene-related peptide (CGRP) to stimulate ILC2s and elicit downstream immune responses. In addition, PNECs act through the neurotransmitter γ-aminobutyric acid (GABA) to induce goblet cell hyperplasia. The instillation of a mixture of CGRP and GABA in -mutant airways restores both immune and goblet cell responses. In accordance, lungs from human asthmatics show increased PNECs. These findings demonstrate that the PNEC-ILC2 neuroimmunological modules function at airway branch points to amplify allergic asthma responses.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.aan8546</identifier><identifier>PMID: 29599193</identifier><language>eng</language><publisher>United States: The American Association for the Advancement of Science</publisher><subject>Acids ; Allergens ; Allergies ; Allergy ; Alveoli ; Amines ; Amphibians ; Amplification ; Animal models ; Animals ; ASCL1 protein ; Asthma ; Asthma - immunology ; Asthma - pathology ; Basic Helix-Loop-Helix Transcription Factors - deficiency ; Basic Helix-Loop-Helix Transcription Factors - genetics ; Calcitonin ; Calcitonin gene-related peptide ; Calcitonin Gene-Related Peptide - metabolism ; Cell culture ; Chemical sensors ; Chemoreceptors ; Clustering ; Cytokines ; Cytokines - biosynthesis ; Deactivation ; Dense core vesicles ; Disease Models, Animal ; Effectors ; Epithelial cells ; Epithelial Cells - immunology ; Epithelial Cells - pathology ; Epithelium ; Feedback (Response) ; Female ; gamma-Aminobutyric Acid - biosynthesis ; gamma-Aminobutyric Acid - metabolism ; Goblet Cells - pathology ; House dust ; Humans ; Hyperplasia ; Hypersensitivity ; Immune response ; Immune system ; In vivo methods and tests ; Inactivation ; Interleukin 5 ; Lung - pathology ; Lungs ; Mice ; Modules ; Molecular chains ; Mucosa ; Mucous membrane ; Mucus ; Mutants ; Neuroendocrine Cells - immunology ; Neuroendocrine Cells - pathology ; Neuropeptides ; Neurotransmitters ; Numbers ; Patients ; Peptides ; Physiological responses ; Proximity ; Reptiles ; Respiratory tract ; Rodents ; Scientific Concepts ; Sensory neurons</subject><ispartof>Science (American Association for the Advancement of Science), 2018-06, Vol.360 (6393)</ispartof><rights>Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.</rights><rights>Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c487t-8663927d48f2e772f71a447e05e1b488d81ea757ecb10dce4f10f7a36f5bd8863</citedby><cites>FETCH-LOGICAL-c487t-8663927d48f2e772f71a447e05e1b488d81ea757ecb10dce4f10f7a36f5bd8863</cites><orcidid>0000-0003-4018-2825 ; 0000-0003-1233-3219 ; 0000-0002-5468-6867 ; 0000-0003-4771-6172 ; 0000-0003-2991-4183 ; 0000-0002-9787-0883 ; 0000-0002-0571-0285 ; 0000-0002-3286-3199 ; 0000-0003-3212-1539 ; 0000-0002-8140-7050 ; 0000-0001-8387-4966</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,2884,2885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29599193$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sui, Pengfei</creatorcontrib><creatorcontrib>Wiesner, Darin L</creatorcontrib><creatorcontrib>Xu, Jinhao</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Lee, Jinwoo</creatorcontrib><creatorcontrib>Van Dyken, Steven</creatorcontrib><creatorcontrib>Lashua, Amber</creatorcontrib><creatorcontrib>Yu, Chuyue</creatorcontrib><creatorcontrib>Klein, Bruce S</creatorcontrib><creatorcontrib>Locksley, Richard M</creatorcontrib><creatorcontrib>Deutsch, Gail</creatorcontrib><creatorcontrib>Sun, Xin</creatorcontrib><title>Pulmonary neuroendocrine cells amplify allergic asthma responses</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>Pulmonary neuroendocrine cells (PNECs) are rare airway epithelial cells whose function is poorly understood. Here we show that -mutant mice that have no PNECs exhibit severely blunted mucosal type 2 response in models of allergic asthma. PNECs reside in close proximity to group 2 innate lymphoid cells (ILC2s) near airway branch points. PNECs act through calcitonin gene-related peptide (CGRP) to stimulate ILC2s and elicit downstream immune responses. In addition, PNECs act through the neurotransmitter γ-aminobutyric acid (GABA) to induce goblet cell hyperplasia. The instillation of a mixture of CGRP and GABA in -mutant airways restores both immune and goblet cell responses. In accordance, lungs from human asthmatics show increased PNECs. These findings demonstrate that the PNEC-ILC2 neuroimmunological modules function at airway branch points to amplify allergic asthma responses.</description><subject>Acids</subject><subject>Allergens</subject><subject>Allergies</subject><subject>Allergy</subject><subject>Alveoli</subject><subject>Amines</subject><subject>Amphibians</subject><subject>Amplification</subject><subject>Animal models</subject><subject>Animals</subject><subject>ASCL1 protein</subject><subject>Asthma</subject><subject>Asthma - immunology</subject><subject>Asthma - pathology</subject><subject>Basic Helix-Loop-Helix Transcription Factors - deficiency</subject><subject>Basic Helix-Loop-Helix Transcription Factors - genetics</subject><subject>Calcitonin</subject><subject>Calcitonin gene-related peptide</subject><subject>Calcitonin Gene-Related Peptide - metabolism</subject><subject>Cell culture</subject><subject>Chemical sensors</subject><subject>Chemoreceptors</subject><subject>Clustering</subject><subject>Cytokines</subject><subject>Cytokines - biosynthesis</subject><subject>Deactivation</subject><subject>Dense core vesicles</subject><subject>Disease Models, Animal</subject><subject>Effectors</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - immunology</subject><subject>Epithelial Cells - pathology</subject><subject>Epithelium</subject><subject>Feedback (Response)</subject><subject>Female</subject><subject>gamma-Aminobutyric Acid - biosynthesis</subject><subject>gamma-Aminobutyric Acid - metabolism</subject><subject>Goblet Cells - pathology</subject><subject>House dust</subject><subject>Humans</subject><subject>Hyperplasia</subject><subject>Hypersensitivity</subject><subject>Immune response</subject><subject>Immune system</subject><subject>In vivo methods and tests</subject><subject>Inactivation</subject><subject>Interleukin 5</subject><subject>Lung - pathology</subject><subject>Lungs</subject><subject>Mice</subject><subject>Modules</subject><subject>Molecular chains</subject><subject>Mucosa</subject><subject>Mucous membrane</subject><subject>Mucus</subject><subject>Mutants</subject><subject>Neuroendocrine Cells - immunology</subject><subject>Neuroendocrine Cells - pathology</subject><subject>Neuropeptides</subject><subject>Neurotransmitters</subject><subject>Numbers</subject><subject>Patients</subject><subject>Peptides</subject><subject>Physiological responses</subject><subject>Proximity</subject><subject>Reptiles</subject><subject>Respiratory tract</subject><subject>Rodents</subject><subject>Scientific Concepts</subject><subject>Sensory neurons</subject><issn>0036-8075</issn><issn>1095-9203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNpdkb1PwzAUxC0EoqUws6FILCxp_ZXYWRCo4kuqBAPMluu8tKkSu9gJUv97XLVUwHTD_d7pnQ6hS4LHhNB8EkwN1sBYaysznh-hIcFFlhYUs2M0xJjlqcQiG6CzEFYYR69gp2hAoxakYEN099Y3rbPabxILvXdgS2d8bSEx0DQh0e26qatNopsG_KI2iQ7dstWJh7B2NkA4RyeVbgJc7HWEPh4f3qfP6ez16WV6P0sNl6JLZZ6zgoqSy4qCELQSRHMuAGdA5lzKUhLQIhNg5gSXBnhFcCU0y6tsXkqZsxG63eWu-3kLkbCd141a-7qNzyuna_XXsfVSLdyXypkUu4CbfYB3nz2ETrV12JbUFlwfFMUU84JTwSN6_Q9dud7bWC9SGRGZlIxGarKjjHcheKgOzxCstuuo_Tpqv068uPrd4cD_zMG-AbHxjtk</recordid><startdate>20180608</startdate><enddate>20180608</enddate><creator>Sui, Pengfei</creator><creator>Wiesner, Darin L</creator><creator>Xu, Jinhao</creator><creator>Zhang, Yan</creator><creator>Lee, Jinwoo</creator><creator>Van Dyken, Steven</creator><creator>Lashua, Amber</creator><creator>Yu, Chuyue</creator><creator>Klein, Bruce S</creator><creator>Locksley, Richard M</creator><creator>Deutsch, Gail</creator><creator>Sun, Xin</creator><general>The American Association for the Advancement of Science</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QF</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QQ</scope><scope>7QR</scope><scope>7SC</scope><scope>7SE</scope><scope>7SN</scope><scope>7SP</scope><scope>7SR</scope><scope>7SS</scope><scope>7T7</scope><scope>7TA</scope><scope>7TB</scope><scope>7TK</scope><scope>7TM</scope><scope>7U5</scope><scope>7U9</scope><scope>8BQ</scope><scope>8FD</scope><scope>C1K</scope><scope>F28</scope><scope>FR3</scope><scope>H8D</scope><scope>H8G</scope><scope>H94</scope><scope>JG9</scope><scope>JQ2</scope><scope>K9.</scope><scope>KR7</scope><scope>L7M</scope><scope>L~C</scope><scope>L~D</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-4018-2825</orcidid><orcidid>https://orcid.org/0000-0003-1233-3219</orcidid><orcidid>https://orcid.org/0000-0002-5468-6867</orcidid><orcidid>https://orcid.org/0000-0003-4771-6172</orcidid><orcidid>https://orcid.org/0000-0003-2991-4183</orcidid><orcidid>https://orcid.org/0000-0002-9787-0883</orcidid><orcidid>https://orcid.org/0000-0002-0571-0285</orcidid><orcidid>https://orcid.org/0000-0002-3286-3199</orcidid><orcidid>https://orcid.org/0000-0003-3212-1539</orcidid><orcidid>https://orcid.org/0000-0002-8140-7050</orcidid><orcidid>https://orcid.org/0000-0001-8387-4966</orcidid></search><sort><creationdate>20180608</creationdate><title>Pulmonary neuroendocrine cells amplify allergic asthma responses</title><author>Sui, Pengfei ; Wiesner, Darin L ; Xu, Jinhao ; Zhang, Yan ; Lee, Jinwoo ; Van Dyken, Steven ; Lashua, Amber ; Yu, Chuyue ; Klein, Bruce S ; Locksley, Richard M ; Deutsch, Gail ; Sun, Xin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c487t-8663927d48f2e772f71a447e05e1b488d81ea757ecb10dce4f10f7a36f5bd8863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acids</topic><topic>Allergens</topic><topic>Allergies</topic><topic>Allergy</topic><topic>Alveoli</topic><topic>Amines</topic><topic>Amphibians</topic><topic>Amplification</topic><topic>Animal models</topic><topic>Animals</topic><topic>ASCL1 protein</topic><topic>Asthma</topic><topic>Asthma - immunology</topic><topic>Asthma - pathology</topic><topic>Basic Helix-Loop-Helix Transcription Factors - deficiency</topic><topic>Basic Helix-Loop-Helix Transcription Factors - genetics</topic><topic>Calcitonin</topic><topic>Calcitonin gene-related peptide</topic><topic>Calcitonin Gene-Related Peptide - metabolism</topic><topic>Cell culture</topic><topic>Chemical sensors</topic><topic>Chemoreceptors</topic><topic>Clustering</topic><topic>Cytokines</topic><topic>Cytokines - biosynthesis</topic><topic>Deactivation</topic><topic>Dense core vesicles</topic><topic>Disease Models, Animal</topic><topic>Effectors</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - immunology</topic><topic>Epithelial Cells - pathology</topic><topic>Epithelium</topic><topic>Feedback (Response)</topic><topic>Female</topic><topic>gamma-Aminobutyric Acid - biosynthesis</topic><topic>gamma-Aminobutyric Acid - metabolism</topic><topic>Goblet Cells - pathology</topic><topic>House dust</topic><topic>Humans</topic><topic>Hyperplasia</topic><topic>Hypersensitivity</topic><topic>Immune response</topic><topic>Immune system</topic><topic>In vivo methods and tests</topic><topic>Inactivation</topic><topic>Interleukin 5</topic><topic>Lung - pathology</topic><topic>Lungs</topic><topic>Mice</topic><topic>Modules</topic><topic>Molecular chains</topic><topic>Mucosa</topic><topic>Mucous membrane</topic><topic>Mucus</topic><topic>Mutants</topic><topic>Neuroendocrine Cells - immunology</topic><topic>Neuroendocrine Cells - pathology</topic><topic>Neuropeptides</topic><topic>Neurotransmitters</topic><topic>Numbers</topic><topic>Patients</topic><topic>Peptides</topic><topic>Physiological responses</topic><topic>Proximity</topic><topic>Reptiles</topic><topic>Respiratory tract</topic><topic>Rodents</topic><topic>Scientific Concepts</topic><topic>Sensory neurons</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sui, Pengfei</creatorcontrib><creatorcontrib>Wiesner, Darin L</creatorcontrib><creatorcontrib>Xu, Jinhao</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Lee, Jinwoo</creatorcontrib><creatorcontrib>Van Dyken, Steven</creatorcontrib><creatorcontrib>Lashua, Amber</creatorcontrib><creatorcontrib>Yu, Chuyue</creatorcontrib><creatorcontrib>Klein, Bruce S</creatorcontrib><creatorcontrib>Locksley, Richard M</creatorcontrib><creatorcontrib>Deutsch, Gail</creatorcontrib><creatorcontrib>Sun, Xin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Aluminium Industry Abstracts</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Ceramic Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Computer and Information Systems Abstracts</collection><collection>Corrosion Abstracts</collection><collection>Ecology Abstracts</collection><collection>Electronics &amp; Communications Abstracts</collection><collection>Engineered Materials Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Materials Business File</collection><collection>Mechanical &amp; Transportation Engineering Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>METADEX</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ANTE: Abstracts in New Technology &amp; Engineering</collection><collection>Engineering Research Database</collection><collection>Aerospace Database</collection><collection>Copper Technical Reference Library</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Materials Research Database</collection><collection>ProQuest Computer Science Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Civil Engineering Abstracts</collection><collection>Advanced Technologies Database with Aerospace</collection><collection>Computer and Information Systems Abstracts – Academic</collection><collection>Computer and Information Systems Abstracts Professional</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Science (American Association for the Advancement of Science)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sui, Pengfei</au><au>Wiesner, Darin L</au><au>Xu, Jinhao</au><au>Zhang, Yan</au><au>Lee, Jinwoo</au><au>Van Dyken, Steven</au><au>Lashua, Amber</au><au>Yu, Chuyue</au><au>Klein, Bruce S</au><au>Locksley, Richard M</au><au>Deutsch, Gail</au><au>Sun, Xin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pulmonary neuroendocrine cells amplify allergic asthma responses</atitle><jtitle>Science (American Association for the Advancement of Science)</jtitle><addtitle>Science</addtitle><date>2018-06-08</date><risdate>2018</risdate><volume>360</volume><issue>6393</issue><issn>0036-8075</issn><eissn>1095-9203</eissn><abstract>Pulmonary neuroendocrine cells (PNECs) are rare airway epithelial cells whose function is poorly understood. Here we show that -mutant mice that have no PNECs exhibit severely blunted mucosal type 2 response in models of allergic asthma. PNECs reside in close proximity to group 2 innate lymphoid cells (ILC2s) near airway branch points. PNECs act through calcitonin gene-related peptide (CGRP) to stimulate ILC2s and elicit downstream immune responses. In addition, PNECs act through the neurotransmitter γ-aminobutyric acid (GABA) to induce goblet cell hyperplasia. The instillation of a mixture of CGRP and GABA in -mutant airways restores both immune and goblet cell responses. In accordance, lungs from human asthmatics show increased PNECs. These findings demonstrate that the PNEC-ILC2 neuroimmunological modules function at airway branch points to amplify allergic asthma responses.</abstract><cop>United States</cop><pub>The American Association for the Advancement of Science</pub><pmid>29599193</pmid><doi>10.1126/science.aan8546</doi><orcidid>https://orcid.org/0000-0003-4018-2825</orcidid><orcidid>https://orcid.org/0000-0003-1233-3219</orcidid><orcidid>https://orcid.org/0000-0002-5468-6867</orcidid><orcidid>https://orcid.org/0000-0003-4771-6172</orcidid><orcidid>https://orcid.org/0000-0003-2991-4183</orcidid><orcidid>https://orcid.org/0000-0002-9787-0883</orcidid><orcidid>https://orcid.org/0000-0002-0571-0285</orcidid><orcidid>https://orcid.org/0000-0002-3286-3199</orcidid><orcidid>https://orcid.org/0000-0003-3212-1539</orcidid><orcidid>https://orcid.org/0000-0002-8140-7050</orcidid><orcidid>https://orcid.org/0000-0001-8387-4966</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0036-8075
ispartof Science (American Association for the Advancement of Science), 2018-06, Vol.360 (6393)
issn 0036-8075
1095-9203
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6387886
source American Association for the Advancement of Science; JSTOR Archival Journals and Primary Sources Collection; Alma/SFX Local Collection
subjects Acids
Allergens
Allergies
Allergy
Alveoli
Amines
Amphibians
Amplification
Animal models
Animals
ASCL1 protein
Asthma
Asthma - immunology
Asthma - pathology
Basic Helix-Loop-Helix Transcription Factors - deficiency
Basic Helix-Loop-Helix Transcription Factors - genetics
Calcitonin
Calcitonin gene-related peptide
Calcitonin Gene-Related Peptide - metabolism
Cell culture
Chemical sensors
Chemoreceptors
Clustering
Cytokines
Cytokines - biosynthesis
Deactivation
Dense core vesicles
Disease Models, Animal
Effectors
Epithelial cells
Epithelial Cells - immunology
Epithelial Cells - pathology
Epithelium
Feedback (Response)
Female
gamma-Aminobutyric Acid - biosynthesis
gamma-Aminobutyric Acid - metabolism
Goblet Cells - pathology
House dust
Humans
Hyperplasia
Hypersensitivity
Immune response
Immune system
In vivo methods and tests
Inactivation
Interleukin 5
Lung - pathology
Lungs
Mice
Modules
Molecular chains
Mucosa
Mucous membrane
Mucus
Mutants
Neuroendocrine Cells - immunology
Neuroendocrine Cells - pathology
Neuropeptides
Neurotransmitters
Numbers
Patients
Peptides
Physiological responses
Proximity
Reptiles
Respiratory tract
Rodents
Scientific Concepts
Sensory neurons
title Pulmonary neuroendocrine cells amplify allergic asthma responses
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-29T09%3A04%3A10IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Pulmonary%20neuroendocrine%20cells%20amplify%20allergic%20asthma%20responses&rft.jtitle=Science%20(American%20Association%20for%20the%20Advancement%20of%20Science)&rft.au=Sui,%20Pengfei&rft.date=2018-06-08&rft.volume=360&rft.issue=6393&rft.issn=0036-8075&rft.eissn=1095-9203&rft_id=info:doi/10.1126/science.aan8546&rft_dat=%3Cproquest_pubme%3E2020494274%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c487t-8663927d48f2e772f71a447e05e1b488d81ea757ecb10dce4f10f7a36f5bd8863%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2051758832&rft_id=info:pmid/29599193&rfr_iscdi=true