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Article ; Online: Modeling Asthma in Mice Using Rhinovirus Infection.

Bentley, J Kelley

Methods in molecular biology (Clifton, N.J.)

2022 Volume 2506, Page(s) 43–56

Abstract: Rhinovirus (RV) infection is linked to early life wheezing and exacerbation of adult asthma. RV infection can be modeled in adult and neonatal mice. This chapter outlines methods for the production of standardized human rhinovirus A1B and mouse infection. ...

Abstract	Rhinovirus (RV) infection is linked to early life wheezing and exacerbation of adult asthma. RV infection can be modeled in adult and neonatal mice. This chapter outlines methods for the production of standardized human rhinovirus A1B and mouse infection. The chapter also describes methods to couple infections with allergen (ovalbumin and house dust mite) administrations. The production of the virus involves its amplification, purification, and concentration. In order to standardize the concentrated RV stock, a plaque assay on HeLa cells is outlined as a method of calibrating infectivity. Once the number of plaque-forming units is determined, the standardized virus is used for mouse infection.
MeSH term(s)	Animals ; Asthma ; Enterovirus Infections ; HeLa Cells ; Humans ; Mice ; Picornaviridae Infections ; Pyroglyphidae ; Rhinovirus
Language	English
Publishing date	2022-06-30
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2364-0_3
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Article ; Online: Tuft cells are required for a rhinovirus-induced asthma phenotype in immature mice.

Li, Yiran / Han, Mingyuan / Singh, Shilpi / Breckenridge, Haley A / Kreger, Jordan E / Stroupe, Claudia C / Sawicky, Daniel A / Kuo, Shiuhyang / Goldsmith, Adam M / Ke, Fang / Shenoy, Anukul T / Bentley, J Kelley / Matsumoto, Ichiro / Hershenson, Marc B

JCI insight

2024 Volume 9, Issue 2

Abstract: Infection of immature mice with rhinovirus (RV) induces an asthma-like phenotype consisting of type 2 inflammation, mucous metaplasia, eosinophilic inflammation, and airway hyperresponsiveness that is dependent on IL-25 and type 2 innate lymphoid cells ( ... ...

Abstract	Infection of immature mice with rhinovirus (RV) induces an asthma-like phenotype consisting of type 2 inflammation, mucous metaplasia, eosinophilic inflammation, and airway hyperresponsiveness that is dependent on IL-25 and type 2 innate lymphoid cells (ILC2s). Doublecortin-like kinase 1-positive (DCLK1+) tuft cells are a major source of IL-25. We sought to determine the requirement of tuft cells for the RV-induced asthma phenotype in wild-type mice and mice deficient in Pou2f3, a transcription factor required for tuft cell development. C57BL/6J mice infected with RV-A1B on day 6 of life and RV-A2 on day 13 of life showed increased DCLK1+ tuft cells in the large airways. Compared with wild-type mice, RV-infected Pou2f3-/- mice showed reductions in IL-25 mRNA and protein expression, ILC2 expansion, type 2 cytokine expression, mucous metaplasia, lung eosinophils, and airway methacholine responsiveness. We conclude that airway tuft cells are required for the asthma phenotype observed in immature mice undergoing repeated RV infections. Furthermore, RV-induced tuft cell development provides a mechanism by which early-life viral infections could potentiate type 2 inflammatory responses to future infections.
MeSH term(s)	Animals ; Mice ; Immunity, Innate ; Rhinovirus ; Tuft Cells ; Lymphocytes/metabolism ; Mice, Inbred C57BL ; Asthma/metabolism ; Enterovirus Infections ; Inflammation ; Phenotype ; Metaplasia
Language	English
Publishing date	2024-01-23
Publishing country	United States
Document type	Journal Article
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.166136
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Article ; Online: Deficient inflammasome activation permits an exaggerated asthma phenotype in rhinovirus C-infected immature mice.

Han, Mingyuan / Ishikawa, Tomoko / Stroupe, Claudia C / Breckenridge, Haley A / Bentley, J Kelley / Hershenson, Marc B

Mucosal immunology

2021 Volume 14, Issue 6, Page(s) 1369–1380

Abstract: Compared to other RV species, RV-C has been associated with more severe respiratory illness and is more likely to occur in children with a history of asthma or who develop asthma. We therefore inoculated 6-day-old mice with sham, RV-A1B, or RV-C15. ... ...

Abstract	Compared to other RV species, RV-C has been associated with more severe respiratory illness and is more likely to occur in children with a history of asthma or who develop asthma. We therefore inoculated 6-day-old mice with sham, RV-A1B, or RV-C15. Inflammasome priming and activation were assessed, and selected mice treated with recombinant IL-1β. Compared to RV-A1B infection, RV-C15 infection induced an exaggerated asthma phenotype, with increased mRNA expression of Il5, Il13, Il25, Il33, Muc5ac, Muc5b, and Clca1; increased lung lineage-negative CD25+CD127+ST2+ ILC2s; increased mucous metaplasia; and increased airway responsiveness. Lung vRNA, induction of pro-inflammatory type 1 cytokines, and inflammasome priming (pro-IL-1β and NLRP3) were not different between the two viruses. However, inflammasome activation (mature IL-1β and caspase-1 p12) was reduced in RV-C15-infected mice compared to RV-A1B-infected mice. A similar deficiency was found in cultured macrophages. Finally, IL-1β treatment decreased RV-C-induced type 2 cytokine and mucus-related gene expression, ILC2s, mucous metaplasia, and airway responsiveness but not lung vRNA level. We conclude that RV-C induces an enhanced asthma phenotype in immature mice. Compared to RV-A, RV-C-induced macrophage inflammasome activation and IL-1β are deficient, permitting exaggerated type 2 inflammation and mucous metaplasia.
MeSH term(s)	Animals ; Asthma/diagnosis ; Asthma/etiology ; Asthma/metabolism ; Biomarkers ; Cell Line ; Coxsackievirus Infections/complications ; Coxsackievirus Infections/virology ; Cytokines/metabolism ; Disease Models, Animal ; Disease Progression ; Disease Susceptibility ; Enterovirus/physiology ; Humans ; Immunity, Innate ; Immunophenotyping ; Inflammasomes/metabolism ; Lymphocyte Activation/genetics ; Lymphocyte Activation/immunology ; Lymphocyte Subsets/immunology ; Lymphocyte Subsets/metabolism ; Macrophages/immunology ; Macrophages/metabolism ; Mice ; Phenotype
Chemical Substances	Biomarkers ; Cytokines ; Inflammasomes
Language	English
Publishing date	2021-08-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2411370-0
ISSN	1935-3456 ; 1933-0219
ISSN (online)	1935-3456
ISSN	1933-0219
DOI	10.1038/s41385-021-00436-0
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Article ; Online: Rhinovirus C Infection Induces Type 2 Innate Lymphoid Cell Expansion and Eosinophilic Airway Inflammation.

Rajput, Charu / Han, Mingyuan / Ishikawa, Tomoko / Lei, Jing / Goldsmith, Adam M / Jazaeri, Seyedehzarifeh / Stroupe, Claudia C / Bentley, J Kelley / Hershenson, Marc B

Frontiers in immunology

2021 Volume 12, Page(s) 649520

Abstract: Rhinovirus C (RV-C) infection is associated with severe asthma exacerbations. Since type 2 inflammation is an important disease mechanism in asthma, we hypothesized that RV-C infection, in contrast to RV-A, preferentially stimulates type 2 inflammation, ... ...

Abstract	Rhinovirus C (RV-C) infection is associated with severe asthma exacerbations. Since type 2 inflammation is an important disease mechanism in asthma, we hypothesized that RV-C infection, in contrast to RV-A, preferentially stimulates type 2 inflammation, leading to exacerbated eosinophilic inflammation. To test this, we developed a mouse model of RV-C15 airways disease. RV-C15 was generated from the full-length cDNA clone and grown in HeLa-E8 cells expressing human CDHR3. BALB/c mice were inoculated intranasally with 5 x 10
MeSH term(s)	Animals ; Asthma/blood ; Asthma/diagnosis ; Asthma/immunology ; Asthma/virology ; Bronchoalveolar Lavage Fluid/cytology ; Bronchoalveolar Lavage Fluid/immunology ; Cadherin Related Proteins ; Cadherins/genetics ; Cadherins/metabolism ; Coxsackievirus Infections/blood ; Coxsackievirus Infections/complications ; Coxsackievirus Infections/immunology ; Coxsackievirus Infections/virology ; Disease Models, Animal ; Enterovirus/immunology ; Enterovirus/metabolism ; Eosinophilia/blood ; Eosinophilia/immunology ; Eosinophilia/virology ; Eosinophils/immunology ; Female ; HeLa Cells ; Humans ; Immunity, Innate ; Lymphocytes/immunology ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Transgenic ; Nuclear Receptor Subfamily 1, Group F, Member 1/genetics ; Symptom Flare Up
Chemical Substances	CDHR3 protein, human ; Cadherin Related Proteins ; Cadherins ; Membrane Proteins ; Nuclear Receptor Subfamily 1, Group F, Member 1 ; Rora protein, mouse
Language	English
Publishing date	2021-04-22
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.649520
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Article ; Online: M2 Macrophages promote IL-33 expression, ILC2 expansion and mucous metaplasia in response to early life rhinovirus infections.

Han, Mingyuan / Breckenridge, Haley A / Kuo, Shiuhyang / Singh, Shilpi / Goldsmith, Adam G / Li, Yiran / Kreger, Jordan E / Bentley, J Kelley / Hershenson, Marc B

Frontiers in immunology

2022 Volume 13, Page(s) 952509

Abstract: Wheezing-associated rhinovirus (RV) infections are associated with asthma development. We have shown that infection of immature mice with RV induces type 2 cytokine production and mucous metaplasia which is dependent on IL-33 and type 2 innate lymphoid ... ...

Abstract	Wheezing-associated rhinovirus (RV) infections are associated with asthma development. We have shown that infection of immature mice with RV induces type 2 cytokine production and mucous metaplasia which is dependent on IL-33 and type 2 innate lymphoid cells (ILC2s) and intensified by a second heterologous RV infection. We hypothesize that M2a macrophages are required for the exaggerated inflammation and mucous metaplasia in response to heterologous RV infection. Wild-type C57Bl/6J mice and LysM Conclusion: Early-life RV infection alters the macrophage response to subsequent heterologous infection, permitting enhanced IL-33 expression, ILC2 expansion and intensified airway inflammation and mucous metaplasia.
MeSH term(s)	Animals ; Immunity, Innate ; Inflammation ; Interleukin-33 ; Lymphocytes ; Macrophages ; Metaplasia ; Mice ; RNA, Messenger ; Rhinovirus
Chemical Substances	Interleukin-33 ; RNA, Messenger
Language	English
Publishing date	2022-08-12
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.952509
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Article ; Online: Early-life heterologous rhinovirus infections induce an exaggerated asthma-like phenotype.

Rajput, Charu / Han, Mingyuan / Ishikawa, Tomoko / Lei, Jing / Jazaeri, Seyedehzarifeh / Bentley, J Kelley / Hershenson, Marc B

The Journal of allergy and clinical immunology

2020 Volume 146, Issue 3, Page(s) 571–582.e3

Abstract: Background: 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.: Objective: We previously showed that RV infection of 6- ... ...

Abstract	Background: 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. Objective: 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. Methods: Wild-type BALB/c mice and Rora Results: 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 Rora Conclusion: Early-life RV infection alters the response to subsequent heterologous infection, inducing an intensified asthma-like phenotype that is dependent on ILC2s.
MeSH term(s)	Adverse Childhood Experiences ; Animals ; Animals, Newborn ; Asthma/immunology ; Disease Progression ; Eosinophils/immunology ; Humans ; Immunity, Innate ; Infant, Newborn ; Interleukin-13/genetics ; Interleukin-13/metabolism ; Mice ; Mice, Inbred BALB C ; Phenotype ; Picornaviridae Infections/immunology ; Respiratory Sounds ; Rhinovirus/physiology ; Th2 Cells/immunology
Chemical Substances	Interleukin-13
Language	English
Publishing date	2020-04-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2020.03.039
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Article: Immunoprecipitation of PDE2 phosphorylated and inactivated by an associated protein kinase.

Bentley, J Kelley

Methods in molecular biology (Clifton, N.J.)

2005 Volume 307, Page(s) 211–223

Abstract: A PDE2A2-associated protein kinase phosphorylates PDE2A2 in vivo and in vitro to inhibit its catalytic activity. Rat brain PDE2A2 may be solubilized using nona (ethylene glycol) mono dodecyl ether (Lubrol 12A9). PDE2A2 exists in a complex with a protein ... ...

Abstract	A PDE2A2-associated protein kinase phosphorylates PDE2A2 in vivo and in vitro to inhibit its catalytic activity. Rat brain PDE2A2 may be solubilized using nona (ethylene glycol) mono dodecyl ether (Lubrol 12A9). PDE2A2 exists in a complex with a protein kinase regulating its activity in an adenosine triphosphate-dependent manner. When native or recombinant PDE2 is immunoprecipitated from PC12 cells using an antibody to the amino terminus in a buffer containing Lubrol 12A9, protease inhibitors, and phosphatase inhibitors, a coimmunoprecipitating nerve growth factor-stimulated protein kinase acts to phosphorylate it. PDE2A2 phosphoryla-tion occurs optimally at pH 6.5 in a sodium 2-(4-morpholino)-ethane sulfonate buffer with 5 mM MgCl2 and 1 mM Na3VO4. I describe protocols for producing an antibody to an amino-terminal bacterial fusion protein encoding amino acids 1-251 of PDE2A2 as well as the use of this antibody in immunoprecipitating a PDE2: tyrosine protein-kinase complex from rat brain or PC12 cells.
MeSH term(s)	Animals ; Cyclic Nucleotide Phosphodiesterases, Type 2 ; Gene Expression ; Humans ; Immunoprecipitation/methods ; Multienzyme Complexes/chemistry ; Multienzyme Complexes/genetics ; Multienzyme Complexes/immunology ; PC12 Cells ; Phosphoric Diester Hydrolases/chemistry ; Phosphoric Diester Hydrolases/genetics ; Phosphoric Diester Hydrolases/immunology ; Phosphorylation ; Protein Kinases/chemistry ; Protein Kinases/immunology ; Rats ; Transfection
Chemical Substances	Multienzyme Complexes ; Protein Kinases (EC 2.7.-) ; Phosphoric Diester Hydrolases (EC 3.1.4.-) ; Cyclic Nucleotide Phosphodiesterases, Type 2 (EC 3.1.4.17) ; PDE2A protein, human (EC 3.1.4.17) ; Pde2a protein, rat (EC 3.1.4.17)
Language	English
Publishing date	2005-06-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ISSN	1064-3745
ISSN	1064-3745
DOI	10.1385/1-59259-839-0:211
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Article ; Online: Initiation of fatty acid biosynthesis in Pseudomonas putida KT2440.

McNaught, Kevin J / Kuatsjah, Eugene / Zahn, Michael / Prates, Érica T / Shao, Huiling / Bentley, Gayle J / Pickford, Andrew R / Gruber, Josephine N / Hestmark, Kelley V / Jacobson, Daniel A / Poirier, Brenton C / Ling, Chen / San Marchi, Myrsini / Michener, William E / Nicora, Carrie D / Sanders, Jacob N / Szostkiewicz, Caralyn J / Veličković, Dušan / Zhou, Mowei /

Munoz, Nathalie / Kim, Young-Mo / Magnuson, Jon K / Burnum-Johnson, Kristin E / Houk, K N / McGeehan, John E / Johnson, Christopher W / Beckham, Gregg T

Metabolic engineering

2023 Volume 76, Page(s) 193–203

Abstract: Deciphering the mechanisms of bacterial fatty acid biosynthesis is crucial for both the engineering of bacterial hosts to produce fatty acid-derived molecules and the development of new antibiotics. However, gaps in our understanding of the initiation of ...

Abstract	Deciphering the mechanisms of bacterial fatty acid biosynthesis is crucial for both the engineering of bacterial hosts to produce fatty acid-derived molecules and the development of new antibiotics. However, gaps in our understanding of the initiation of fatty acid biosynthesis remain. Here, we demonstrate that the industrially relevant microbe Pseudomonas putida KT2440 contains three distinct pathways to initiate fatty acid biosynthesis. The first two routes employ conventional β-ketoacyl-ACP synthase III enzymes, FabH1 and FabH2, that accept short- and medium-chain-length acyl-CoAs, respectively. The third route utilizes a malonyl-ACP decarboxylase enzyme, MadB. A combination of exhaustive in vivo alanine-scanning mutagenesis, in vitro biochemical characterization, X-ray crystallography, and computational modeling elucidate the presumptive mechanism of malonyl-ACP decarboxylation via MadB. Given that functional homologs of MadB are widespread throughout domain Bacteria, this ubiquitous alternative fatty acid initiation pathway provides new opportunities to target a range of biotechnology and biomedical applications.
MeSH term(s)	Pseudomonas putida/genetics ; Pseudomonas putida/metabolism ; 3-Oxoacyl-(Acyl-Carrier-Protein) Synthase/genetics ; Mutagenesis ; Fatty Acids
Chemical Substances	monoaminocarboxydihydroborane (98169-69-8) ; 3-Oxoacyl-(Acyl-Carrier-Protein) Synthase (EC 2.3.1.41) ; Fatty Acids
Language	English
Publishing date	2023-02-15
Publishing country	Belgium
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1470383-x
ISSN	1096-7184 ; 1096-7176
ISSN (online)	1096-7184
ISSN	1096-7176
DOI	10.1016/j.ymben.2023.02.006
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Article ; Online: Myristoylated rhinovirus VP4 protein activates TLR2-dependent proinflammatory gene expression.

Bentley, J Kelley / Han, Mingyuan / Jaipalli, Suraj / Hinde, Joanna L / Lei, Jing / Ishikawa, Tomoko / Goldsmith, Adam M / Rajput, Charu / Hershenson, Marc B

American journal of physiology. Lung cellular and molecular physiology

2019 Volume 317, Issue 1, Page(s) L57–L70

Abstract: Asthma exacerbations are often caused by rhinovirus (RV). We and others have shown that Toll-like receptor 2 (TLR2), a membrane surface receptor that recognizes bacterial lipopeptides and lipoteichoic acid, is required and sufficient for RV-induced ... ...

Abstract	Asthma exacerbations are often caused by rhinovirus (RV). We and others have shown that Toll-like receptor 2 (TLR2), a membrane surface receptor that recognizes bacterial lipopeptides and lipoteichoic acid, is required and sufficient for RV-induced proinflammatory responses in vitro and in vivo. We hypothesized that viral protein-4 (VP4), an internal capsid protein that is myristoylated upon viral replication and externalized upon viral binding, is a ligand for TLR2. Recombinant VP4 and myristoylated VP4 (MyrVP4) were purified by Ni-affinity chromatography. MyrVP4 was also purified from RV-A1B-infected HeLa cells by urea solubilization and anti-VP4 affinity chromatography. Finally, synthetic MyrVP4 was produced by chemical peptide synthesis. MyrVP4-TLR2 interactions were assessed by confocal fluorescence microscopy, fluorescence resonance energy transfer (FRET), and monitoring VP4-induced cytokine mRNA expression in the presence of anti-TLR2 and anti-VP4. MyrVP4 and TLR2 colocalized in TLR2-expressing HEK-293 cells, mouse bone marrow-derived macrophages, human bronchoalveolar macrophages, and human airway epithelial cells. Colocalization was absent in TLR2-null HEK-293 cells and blocked by anti-TLR2 and anti-VP4. Cy3-labeled MyrVP4 and Cy5-labeled anti-TLR2 showed an average fractional FRET efficiency of 0.24 ± 0.05, and Cy5-labeled anti-TLR2 increased and unlabeled MyrVP4 decreased FRET efficiency. MyrVP4-induced chemokine mRNA expression was higher than that elicited by VP4 alone and was attenuated by anti-TLR2 and anti-VP4. Cytokine expression was similarly increased by MyrVP4 purified from RV-infected HeLa cells and synthetic MyrVP4. We conclude that, during RV infection, MyrVP4 and TLR2 interact to generate a proinflammatory response.
MeSH term(s)	Adolescent ; Amino Acid Sequence ; Animals ; Asthma/genetics ; Asthma/immunology ; Asthma/pathology ; Asthma/virology ; Capsid Proteins/genetics ; Capsid Proteins/immunology ; Child ; Eosinophilia/genetics ; Eosinophilia/immunology ; Eosinophilia/pathology ; Eosinophilia/virology ; Epithelial Cells/immunology ; Epithelial Cells/virology ; Female ; HEK293 Cells ; HeLa Cells ; Host-Pathogen Interactions/genetics ; Host-Pathogen Interactions/immunology ; Humans ; Macrophages/immunology ; Macrophages/virology ; Male ; Mice ; Mice, Inbred C57BL ; Myristic Acids/immunology ; Myristic Acids/metabolism ; Picornaviridae Infections/genetics ; Picornaviridae Infections/immunology ; Picornaviridae Infections/pathology ; Picornaviridae Infections/virology ; Protein Binding ; Protein Processing, Post-Translational ; Rhinovirus/immunology ; Rhinovirus/pathogenicity ; Signal Transduction ; Toll-Like Receptor 2/genetics ; Toll-Like Receptor 2/immunology ; Viral Proteins/genetics ; Viral Proteins/immunology ; Virus Replication
Chemical Substances	Capsid Proteins ; Myristic Acids ; TLR2 protein, human ; Toll-Like Receptor 2 ; Viral Proteins
Language	English
Publishing date	2019-03-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00365.2018
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Article ; Online: IL-1β prevents ILC2 expansion, type 2 cytokine secretion, and mucus metaplasia in response to early-life rhinovirus infection in mice.

Han, Mingyuan / Ishikawa, Tomoko / Bermick, Jennifer R / Rajput, Charu / Lei, Jing / Goldsmith, Adam M / Jarman, Caitlin R / Lee, Julie / Bentley, J Kelley / Hershenson, Marc B

Allergy

2020 Volume 75, Issue 8, Page(s) 2005–2019

Abstract: Background: Early-life wheezing-associated respiratory infection with human rhinovirus (RV) is associated with asthma development. RV infection of 6-day-old immature mice causes mucous metaplasia and airway hyperresponsiveness which is associated with ... ...

Abstract	Background: Early-life wheezing-associated respiratory infection with human rhinovirus (RV) is associated with asthma development. RV infection of 6-day-old immature mice causes mucous metaplasia and airway hyperresponsiveness which is associated with the expansion of IL-13-producing type 2 innate lymphoid cells (ILC2s) and dependent on IL-25 and IL-33. We examined regulation of this asthma-like phenotype by IL-1β. Methods: Six-day-old wild-type or NRLP3-/- mice were inoculated with sham or RV-A1B. Selected mice were treated with IL-1 receptor antagonist (IL-1RA), anti-IL-1β, or recombinant IL-1β. Results: Rhinovirus infection induced Il25, Il33, Il4, Il5, Il13, muc5ac, and gob5 mRNA expression, ILC2 expansion, mucus metaplasia, and airway hyperresponsiveness. RV also induced lung mRNA and protein expression of pro-IL-1β and NLRP3 as well as cleavage of caspase-1 and pro-IL-1β, indicating inflammasome priming and activation. Lung macrophages were a major source of IL-1β. Inhibition of IL-1β signaling with IL-1RA, anti-IL-1β, or NLRP3 KO increased RV-induced type 2 cytokine immune responses, ILC2 number, and mucus metaplasia, while decreasing IL-17 mRNA expression. Treatment with IL-1β had the opposite effect, decreasing IL-25, IL-33, and mucous metaplasia while increasing IL-17 expression. IL-1β and IL-17 each suppressed Il25, Il33, and muc5ac mRNA expression in cultured airway epithelial cells. Finally, RV-infected 6-day-old mice showed reduced IL-1β mRNA and protein expression compared to mature mice. Conclusion: Macrophage IL-1β limits type 2 inflammation and mucous metaplasia following RV infection by suppressing epithelial cell innate cytokine expression. Reduced IL-1β production in immature animals provides a mechanism permitting asthma development after early-life viral infection.
MeSH term(s)	Animals ; Cytokines ; Immunity, Innate ; Lymphocytes ; Metaplasia ; Mice ; Mucus ; Picornaviridae Infections ; Rhinovirus
Chemical Substances	Cytokines
Language	English
Publishing date	2020-03-10
Publishing country	Denmark
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	391933-x
ISSN	1398-9995 ; 0105-4538
ISSN (online)	1398-9995
ISSN	0105-4538
DOI	10.1111/all.14241
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