IFN-γ Attenuates Eosinophilic Inflammation but Is Not Essential for Protection against RSV-Enhanced Asthmatic Comorbidity in Adult Mice
The susceptibility to respiratory syncytial virus (RSV) infection in early life has been associated with a deficient T-helper cell type 1 (Th1) response. Conversely, healthy adults generally do not exhibit severe illness from RSV infection. In the current study, we investigated whether Th1 cytokine...
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2022-01-01
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Online Access: | https://www.mdpi.com/1999-4915/14/1/147 |
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author | Abenaya Muralidharan Md Bashir Uddin Christopher Bauer Wenzhe Wu Xiaoyong Bao Keer Sun |
author_facet | Abenaya Muralidharan Md Bashir Uddin Christopher Bauer Wenzhe Wu Xiaoyong Bao Keer Sun |
author_sort | Abenaya Muralidharan |
collection | DOAJ |
description | The susceptibility to respiratory syncytial virus (RSV) infection in early life has been associated with a deficient T-helper cell type 1 (Th1) response. Conversely, healthy adults generally do not exhibit severe illness from RSV infection. In the current study, we investigated whether Th1 cytokine IFN-γ is essential for protection against RSV and RSV-associated comorbidities in adult mice. We found that, distinct from influenza virus, prior RSV infection does not induce significant IFN-γ production and susceptibility to secondary <i>Streptococcus pneumoniae</i> infection in adult wild-type (WT) mice. In ovalbumin (OVA)-induced asthmatic mice, RSV super-infection increases airway neutrophil recruitment and inflammatory lung damage but has no significant effect on OVA-induced eosinophilia. Compared with WT controls, RSV infection of asthmatic <i>Ifng<sup>−/−</sup></i> mice results in increased airway eosinophil accumulation. However, a comparable increase in eosinophilia was detected in house dust mite (HDM)-induced asthmatic <i>Ifng<sup>−/−</sup></i> mice in the absence of RSV infection. Furthermore, neither WT nor <i>Ifng<sup>−/−</sup></i> mice exhibit apparent eosinophil infiltration during RSV infection alone. Together, these findings indicate that, despite its critical role in limiting eosinophilic inflammation during asthma, IFN-γ is not essential for protection against RSV-induced exacerbation of asthmatic inflammation in adult mice. |
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institution | Directory Open Access Journal |
issn | 1999-4915 |
language | English |
last_indexed | 2024-03-10T00:21:04Z |
publishDate | 2022-01-01 |
publisher | MDPI AG |
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series | Viruses |
spelling | doaj.art-a56ced5a5dfc480fbcada91e78594df12023-11-23T15:43:04ZengMDPI AGViruses1999-49152022-01-0114114710.3390/v14010147IFN-γ Attenuates Eosinophilic Inflammation but Is Not Essential for Protection against RSV-Enhanced Asthmatic Comorbidity in Adult MiceAbenaya Muralidharan0Md Bashir Uddin1Christopher Bauer2Wenzhe Wu3Xiaoyong Bao4Keer Sun5Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198-5900, USADepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1017, USADepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198-5900, USADepartment of Pediatrics, The University of Texas Medical Branch, Galveston, TX 77555-0372, USADepartment of Pediatrics, The University of Texas Medical Branch, Galveston, TX 77555-0372, USADepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198-5900, USAThe susceptibility to respiratory syncytial virus (RSV) infection in early life has been associated with a deficient T-helper cell type 1 (Th1) response. Conversely, healthy adults generally do not exhibit severe illness from RSV infection. In the current study, we investigated whether Th1 cytokine IFN-γ is essential for protection against RSV and RSV-associated comorbidities in adult mice. We found that, distinct from influenza virus, prior RSV infection does not induce significant IFN-γ production and susceptibility to secondary <i>Streptococcus pneumoniae</i> infection in adult wild-type (WT) mice. In ovalbumin (OVA)-induced asthmatic mice, RSV super-infection increases airway neutrophil recruitment and inflammatory lung damage but has no significant effect on OVA-induced eosinophilia. Compared with WT controls, RSV infection of asthmatic <i>Ifng<sup>−/−</sup></i> mice results in increased airway eosinophil accumulation. However, a comparable increase in eosinophilia was detected in house dust mite (HDM)-induced asthmatic <i>Ifng<sup>−/−</sup></i> mice in the absence of RSV infection. Furthermore, neither WT nor <i>Ifng<sup>−/−</sup></i> mice exhibit apparent eosinophil infiltration during RSV infection alone. Together, these findings indicate that, despite its critical role in limiting eosinophilic inflammation during asthma, IFN-γ is not essential for protection against RSV-induced exacerbation of asthmatic inflammation in adult mice.https://www.mdpi.com/1999-4915/14/1/147RSVasthmacomorbidity |
spellingShingle | Abenaya Muralidharan Md Bashir Uddin Christopher Bauer Wenzhe Wu Xiaoyong Bao Keer Sun IFN-γ Attenuates Eosinophilic Inflammation but Is Not Essential for Protection against RSV-Enhanced Asthmatic Comorbidity in Adult Mice Viruses RSV asthma comorbidity |
title | IFN-γ Attenuates Eosinophilic Inflammation but Is Not Essential for Protection against RSV-Enhanced Asthmatic Comorbidity in Adult Mice |
title_full | IFN-γ Attenuates Eosinophilic Inflammation but Is Not Essential for Protection against RSV-Enhanced Asthmatic Comorbidity in Adult Mice |
title_fullStr | IFN-γ Attenuates Eosinophilic Inflammation but Is Not Essential for Protection against RSV-Enhanced Asthmatic Comorbidity in Adult Mice |
title_full_unstemmed | IFN-γ Attenuates Eosinophilic Inflammation but Is Not Essential for Protection against RSV-Enhanced Asthmatic Comorbidity in Adult Mice |
title_short | IFN-γ Attenuates Eosinophilic Inflammation but Is Not Essential for Protection against RSV-Enhanced Asthmatic Comorbidity in Adult Mice |
title_sort | ifn γ attenuates eosinophilic inflammation but is not essential for protection against rsv enhanced asthmatic comorbidity in adult mice |
topic | RSV asthma comorbidity |
url | https://www.mdpi.com/1999-4915/14/1/147 |
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