Early-life heterologous rhinovirus infections induce an exaggerated asthma-like phenotype
Early-life wheezing-associated respiratory tract infection by rhinovirus (RV) is a risk factor for asthma development. Infants are infected with many different RV strains per year. We previously showed that RV infection of 6-day-old BALB/c mice induces a mucous metaplasia phenotype that is dependent...
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| Veröffentlicht in: | Journal of allergy and clinical immunology 2020-09, Vol.146 (3), p.571-582.e3 |
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| creator | Rajput, Charu Han, Mingyuan Ishikawa, Tomoko Lei, Jing Jazaeri, Seyedehzarifeh Bentley, J. Kelley Hershenson, Marc B. |
| description | Early-life wheezing-associated respiratory tract infection by rhinovirus (RV) is a risk factor for asthma development. Infants are infected with many different RV strains per year.
We previously showed that RV infection of 6-day-old BALB/c mice induces a mucous metaplasia phenotype that is dependent on type 2 innate lymphoid cells (ILC2s). We hypothesized that early-life RV infection alters the response to subsequent heterologous infection, inducing an exaggerated asthma-like phenotype.
Wild-type BALB/c mice and Rorafl/flIl7rcre mice lacking ILC2s were treated as follows: (1) sham on day 6 of life plus sham on day 13 of life, (2) RV-A1B on day 6 plus sham on day 13, (3) sham on day 6 plus RV-A2 on day 13, and (4) RV-A1B on day 6 plus RV-A2 on day 13.
Mice infected with RV-A1B at day 6 and sham at day 13 showed an increased number of bronchoalveolar lavage eosinophils and increased expression of IL-13 mRNA but not expression of IFN-γ mRNA (which is indicative of a type 2 immune response), whereas mice infected with sham on day 6 and RV-A2 on day 13 of life demonstrated increased IFN-γ expression (which is a mature antiviral response). In contrast, mice infected with RV-A1B on day 6 before RV-A2 infection on day 13 showed increased expression of IL-13, IL-5, Gob5, Muc5b, and Muc5ac mRNA; increased numbers of eosinophils and IL-13–producing ILC2s; and exaggerated mucus metaplasia and airway hyperresponsiveness. Compared with Rorafl/fl mice, Rorafl/flIl7rcre mice showed complete suppression of bronchoalveolar lavage eosinophils and mucous metaplasia.
Early-life RV infection alters the response to subsequent heterologous infection, inducing an intensified asthma-like phenotype that is dependent on ILC2s.
[Display omitted] |
| doi_str_mv | 10.1016/j.jaci.2020.03.039 |
| format | Article |
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We previously showed that RV infection of 6-day-old BALB/c mice induces a mucous metaplasia phenotype that is dependent on type 2 innate lymphoid cells (ILC2s). We hypothesized that early-life RV infection alters the response to subsequent heterologous infection, inducing an exaggerated asthma-like phenotype.
Wild-type BALB/c mice and Rorafl/flIl7rcre mice lacking ILC2s were treated as follows: (1) sham on day 6 of life plus sham on day 13 of life, (2) RV-A1B on day 6 plus sham on day 13, (3) sham on day 6 plus RV-A2 on day 13, and (4) RV-A1B on day 6 plus RV-A2 on day 13.
Mice infected with RV-A1B at day 6 and sham at day 13 showed an increased number of bronchoalveolar lavage eosinophils and increased expression of IL-13 mRNA but not expression of IFN-γ mRNA (which is indicative of a type 2 immune response), whereas mice infected with sham on day 6 and RV-A2 on day 13 of life demonstrated increased IFN-γ expression (which is a mature antiviral response). In contrast, mice infected with RV-A1B on day 6 before RV-A2 infection on day 13 showed increased expression of IL-13, IL-5, Gob5, Muc5b, and Muc5ac mRNA; increased numbers of eosinophils and IL-13–producing ILC2s; and exaggerated mucus metaplasia and airway hyperresponsiveness. Compared with Rorafl/fl mice, Rorafl/flIl7rcre mice showed complete suppression of bronchoalveolar lavage eosinophils and mucous metaplasia.
Early-life RV infection alters the response to subsequent heterologous infection, inducing an intensified asthma-like phenotype that is dependent on ILC2s.
[Display omitted]</description><identifier>ISSN: 0091-6749</identifier><identifier>EISSN: 1097-6825</identifier><identifier>DOI: 10.1016/j.jaci.2020.03.039</identifier><identifier>PMID: 32344055</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adverse Childhood Experiences ; Animals ; Animals, Newborn ; Asthma ; Asthma - immunology ; childhood ; Disease Progression ; early-life ; Eosinophils - immunology ; Humans ; IL-13 ; ILC2 ; Immunity, Innate ; Infant, Newborn ; Interleukin-13 - genetics ; Interleukin-13 - metabolism ; Mice ; Mice, Inbred BALB C ; Phenotype ; Picornaviridae Infections - immunology ; Respiratory Sounds ; rhinovirus ; Rhinovirus - physiology ; RV-A1B ; RV-A2 ; Th2 Cells - immunology ; trained immunity ; type 2 innate lymphoid cell</subject><ispartof>Journal of allergy and clinical immunology, 2020-09, Vol.146 (3), p.571-582.e3</ispartof><rights>2020 American Academy of Allergy, Asthma & Immunology</rights><rights>Copyright © 2020 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c521t-26a5d3010c3747d026256df992850b5aa96781fe106d806b0bbe080bb66c5cdd3</citedby><cites>FETCH-LOGICAL-c521t-26a5d3010c3747d026256df992850b5aa96781fe106d806b0bbe080bb66c5cdd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jaci.2020.03.039$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32344055$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rajput, Charu</creatorcontrib><creatorcontrib>Han, Mingyuan</creatorcontrib><creatorcontrib>Ishikawa, Tomoko</creatorcontrib><creatorcontrib>Lei, Jing</creatorcontrib><creatorcontrib>Jazaeri, Seyedehzarifeh</creatorcontrib><creatorcontrib>Bentley, J. Kelley</creatorcontrib><creatorcontrib>Hershenson, Marc B.</creatorcontrib><title>Early-life heterologous rhinovirus infections induce an exaggerated asthma-like phenotype</title><title>Journal of allergy and clinical immunology</title><addtitle>J Allergy Clin Immunol</addtitle><description>Early-life wheezing-associated respiratory tract infection by rhinovirus (RV) is a risk factor for asthma development. Infants are infected with many different RV strains per year.
We previously showed that RV infection of 6-day-old BALB/c mice induces a mucous metaplasia phenotype that is dependent on type 2 innate lymphoid cells (ILC2s). We hypothesized that early-life RV infection alters the response to subsequent heterologous infection, inducing an exaggerated asthma-like phenotype.
Wild-type BALB/c mice and Rorafl/flIl7rcre mice lacking ILC2s were treated as follows: (1) sham on day 6 of life plus sham on day 13 of life, (2) RV-A1B on day 6 plus sham on day 13, (3) sham on day 6 plus RV-A2 on day 13, and (4) RV-A1B on day 6 plus RV-A2 on day 13.
Mice infected with RV-A1B at day 6 and sham at day 13 showed an increased number of bronchoalveolar lavage eosinophils and increased expression of IL-13 mRNA but not expression of IFN-γ mRNA (which is indicative of a type 2 immune response), whereas mice infected with sham on day 6 and RV-A2 on day 13 of life demonstrated increased IFN-γ expression (which is a mature antiviral response). In contrast, mice infected with RV-A1B on day 6 before RV-A2 infection on day 13 showed increased expression of IL-13, IL-5, Gob5, Muc5b, and Muc5ac mRNA; increased numbers of eosinophils and IL-13–producing ILC2s; and exaggerated mucus metaplasia and airway hyperresponsiveness. Compared with Rorafl/fl mice, Rorafl/flIl7rcre mice showed complete suppression of bronchoalveolar lavage eosinophils and mucous metaplasia.
Early-life RV infection alters the response to subsequent heterologous infection, inducing an intensified asthma-like phenotype that is dependent on ILC2s.
[Display omitted]</description><subject>Adverse Childhood Experiences</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Asthma</subject><subject>Asthma - immunology</subject><subject>childhood</subject><subject>Disease Progression</subject><subject>early-life</subject><subject>Eosinophils - immunology</subject><subject>Humans</subject><subject>IL-13</subject><subject>ILC2</subject><subject>Immunity, Innate</subject><subject>Infant, Newborn</subject><subject>Interleukin-13 - genetics</subject><subject>Interleukin-13 - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Phenotype</subject><subject>Picornaviridae Infections - immunology</subject><subject>Respiratory Sounds</subject><subject>rhinovirus</subject><subject>Rhinovirus - physiology</subject><subject>RV-A1B</subject><subject>RV-A2</subject><subject>Th2 Cells - immunology</subject><subject>trained immunity</subject><subject>type 2 innate lymphoid cell</subject><issn>0091-6749</issn><issn>1097-6825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU9rGzEQxUVpaNykX6CHssde1hlJlnYFpVBC-gcCvbSHnIRWmvXKXUuOtDb1t48WpyG5FAZphN78JN4j5D2FJQUqrzbLjbF-yYDBEngp9YosKKimli0Tr8kCQNFaNit1Tt7mvIFy5q16Q84546sVCLEgdzcmjcd69D1WA06Y4hjXcZ-rNPgQDz6V1oce7eRjmFu3t1iZUOFfs15jMhO6yuRp2JoC-YPVbsAQp-MOL8lZb8aM7x73C_L7682v6-_17c9vP66_3NZWMDrVTBrhOFCwvFk1DphkQrpeKdYK6IQxSjYt7ZGCdC3IDroOoS2rlFZY5_gF-Xzi7vbdFp3FMCUz6l3yW5OOOhqvX94EP-h1POi2OCW5KoCPj4AU7_eYJ7312eI4moDFCc24khwaELRI2UlqU8w5Yf_0DAU9Z6I3es5Ez5lo4KVm_ofnH3wa-RdCEXw6CbDYdPCYdLYeg0XnUzFeu-j_x38Az_Gf0A</recordid><startdate>20200901</startdate><enddate>20200901</enddate><creator>Rajput, Charu</creator><creator>Han, Mingyuan</creator><creator>Ishikawa, Tomoko</creator><creator>Lei, Jing</creator><creator>Jazaeri, Seyedehzarifeh</creator><creator>Bentley, J. 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Kelley ; Hershenson, Marc B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c521t-26a5d3010c3747d026256df992850b5aa96781fe106d806b0bbe080bb66c5cdd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adverse Childhood Experiences</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Asthma</topic><topic>Asthma - immunology</topic><topic>childhood</topic><topic>Disease Progression</topic><topic>early-life</topic><topic>Eosinophils - immunology</topic><topic>Humans</topic><topic>IL-13</topic><topic>ILC2</topic><topic>Immunity, Innate</topic><topic>Infant, Newborn</topic><topic>Interleukin-13 - genetics</topic><topic>Interleukin-13 - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Phenotype</topic><topic>Picornaviridae Infections - immunology</topic><topic>Respiratory Sounds</topic><topic>rhinovirus</topic><topic>Rhinovirus - physiology</topic><topic>RV-A1B</topic><topic>RV-A2</topic><topic>Th2 Cells - immunology</topic><topic>trained immunity</topic><topic>type 2 innate lymphoid cell</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rajput, Charu</creatorcontrib><creatorcontrib>Han, Mingyuan</creatorcontrib><creatorcontrib>Ishikawa, Tomoko</creatorcontrib><creatorcontrib>Lei, Jing</creatorcontrib><creatorcontrib>Jazaeri, Seyedehzarifeh</creatorcontrib><creatorcontrib>Bentley, J. Kelley</creatorcontrib><creatorcontrib>Hershenson, Marc B.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of allergy and clinical immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rajput, Charu</au><au>Han, Mingyuan</au><au>Ishikawa, Tomoko</au><au>Lei, Jing</au><au>Jazaeri, Seyedehzarifeh</au><au>Bentley, J. Kelley</au><au>Hershenson, Marc B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Early-life heterologous rhinovirus infections induce an exaggerated asthma-like phenotype</atitle><jtitle>Journal of allergy and clinical immunology</jtitle><addtitle>J Allergy Clin Immunol</addtitle><date>2020-09-01</date><risdate>2020</risdate><volume>146</volume><issue>3</issue><spage>571</spage><epage>582.e3</epage><pages>571-582.e3</pages><issn>0091-6749</issn><eissn>1097-6825</eissn><abstract>Early-life wheezing-associated respiratory tract infection by rhinovirus (RV) is a risk factor for asthma development. Infants are infected with many different RV strains per year.
We previously showed that RV infection of 6-day-old BALB/c mice induces a mucous metaplasia phenotype that is dependent on type 2 innate lymphoid cells (ILC2s). We hypothesized that early-life RV infection alters the response to subsequent heterologous infection, inducing an exaggerated asthma-like phenotype.
Wild-type BALB/c mice and Rorafl/flIl7rcre mice lacking ILC2s were treated as follows: (1) sham on day 6 of life plus sham on day 13 of life, (2) RV-A1B on day 6 plus sham on day 13, (3) sham on day 6 plus RV-A2 on day 13, and (4) RV-A1B on day 6 plus RV-A2 on day 13.
Mice infected with RV-A1B at day 6 and sham at day 13 showed an increased number of bronchoalveolar lavage eosinophils and increased expression of IL-13 mRNA but not expression of IFN-γ mRNA (which is indicative of a type 2 immune response), whereas mice infected with sham on day 6 and RV-A2 on day 13 of life demonstrated increased IFN-γ expression (which is a mature antiviral response). In contrast, mice infected with RV-A1B on day 6 before RV-A2 infection on day 13 showed increased expression of IL-13, IL-5, Gob5, Muc5b, and Muc5ac mRNA; increased numbers of eosinophils and IL-13–producing ILC2s; and exaggerated mucus metaplasia and airway hyperresponsiveness. Compared with Rorafl/fl mice, Rorafl/flIl7rcre mice showed complete suppression of bronchoalveolar lavage eosinophils and mucous metaplasia.
Early-life RV infection alters the response to subsequent heterologous infection, inducing an intensified asthma-like phenotype that is dependent on ILC2s.
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Adverse Childhood Experiences Animals Animals, Newborn Asthma Asthma - immunology childhood Disease Progression early-life Eosinophils - immunology Humans IL-13 ILC2 Immunity, Innate Infant, Newborn Interleukin-13 - genetics Interleukin-13 - metabolism Mice Mice, Inbred BALB C Phenotype Picornaviridae Infections - immunology Respiratory Sounds rhinovirus Rhinovirus - physiology RV-A1B RV-A2 Th2 Cells - immunology trained immunity type 2 innate lymphoid cell |
| title | Early-life heterologous rhinovirus infections induce an exaggerated asthma-like phenotype |
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