Interleukin-1 is responsible for acute lung immunopathology but increases survival of respiratory influenza virus infection.
Interleukin-1alpha (IL-1alpha) and IL-1beta are proinflammatory cytokines, which induce a plethora of genes and activities by binding to the type 1 IL-1 receptor (IL-1R1). We have investigated the role of IL-1 during pulmonary antiviral immune responses in IL-1R1(-/-) mice infected with influenza vi...
| Main Authors: | , , , |
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| Format: | Journal article |
| Language: | English |
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2005
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| _version_ | 1826271166631772160 |
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| author | Schmitz, N Kurrer, M Bachmann, M Kopf, M |
| author_facet | Schmitz, N Kurrer, M Bachmann, M Kopf, M |
| author_sort | Schmitz, N |
| collection | OXFORD |
| description | Interleukin-1alpha (IL-1alpha) and IL-1beta are proinflammatory cytokines, which induce a plethora of genes and activities by binding to the type 1 IL-1 receptor (IL-1R1). We have investigated the role of IL-1 during pulmonary antiviral immune responses in IL-1R1(-/-) mice infected with influenza virus. IL-1R1(-/-) mice showed markedly reduced inflammatory pathology in the lung, primarily due to impaired neutrophil recruitment. Activation of CD4(+) T cells in secondary lymphoid organs and subsequent migration to the lung were impaired in the absence of IL-1R1. In contrast, activation of virus-specific cytotoxic T lymphocytes and killing of virus-infected cells in the lung were intact. Influenza virus-specific immunoglobulin G (IgG) and IgA antibody responses were intact, while the IgM response was markedly reduced in both serum and mucosal sites in IL-1R1(-/-) mice. We found significantly increased mortality in the absence of IL-1R1; however, lung viral titers were only moderately increased. Our results demonstrate that IL-1alpha/beta mediate acute pulmonary inflammatory pathology while enhancing survival during influenza virus infection. IL-1alpha/beta appear not to influence killing of virus-infected cells but to enhance IgM antibody responses and recruitment of CD4(+) T cells to the site of infection. |
| first_indexed | 2024-03-06T21:52:23Z |
| format | Journal article |
| id | oxford-uuid:4bbea47a-297f-48af-95c1-84146675f3ef |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T21:52:23Z |
| publishDate | 2005 |
| record_format | dspace |
| spelling | oxford-uuid:4bbea47a-297f-48af-95c1-84146675f3ef2022-03-26T15:45:21ZInterleukin-1 is responsible for acute lung immunopathology but increases survival of respiratory influenza virus infection.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:4bbea47a-297f-48af-95c1-84146675f3efEnglishSymplectic Elements at Oxford2005Schmitz, NKurrer, MBachmann, MKopf, MInterleukin-1alpha (IL-1alpha) and IL-1beta are proinflammatory cytokines, which induce a plethora of genes and activities by binding to the type 1 IL-1 receptor (IL-1R1). We have investigated the role of IL-1 during pulmonary antiviral immune responses in IL-1R1(-/-) mice infected with influenza virus. IL-1R1(-/-) mice showed markedly reduced inflammatory pathology in the lung, primarily due to impaired neutrophil recruitment. Activation of CD4(+) T cells in secondary lymphoid organs and subsequent migration to the lung were impaired in the absence of IL-1R1. In contrast, activation of virus-specific cytotoxic T lymphocytes and killing of virus-infected cells in the lung were intact. Influenza virus-specific immunoglobulin G (IgG) and IgA antibody responses were intact, while the IgM response was markedly reduced in both serum and mucosal sites in IL-1R1(-/-) mice. We found significantly increased mortality in the absence of IL-1R1; however, lung viral titers were only moderately increased. Our results demonstrate that IL-1alpha/beta mediate acute pulmonary inflammatory pathology while enhancing survival during influenza virus infection. IL-1alpha/beta appear not to influence killing of virus-infected cells but to enhance IgM antibody responses and recruitment of CD4(+) T cells to the site of infection. |
| spellingShingle | Schmitz, N Kurrer, M Bachmann, M Kopf, M Interleukin-1 is responsible for acute lung immunopathology but increases survival of respiratory influenza virus infection. |
| title | Interleukin-1 is responsible for acute lung immunopathology but increases survival of respiratory influenza virus infection. |
| title_full | Interleukin-1 is responsible for acute lung immunopathology but increases survival of respiratory influenza virus infection. |
| title_fullStr | Interleukin-1 is responsible for acute lung immunopathology but increases survival of respiratory influenza virus infection. |
| title_full_unstemmed | Interleukin-1 is responsible for acute lung immunopathology but increases survival of respiratory influenza virus infection. |
| title_short | Interleukin-1 is responsible for acute lung immunopathology but increases survival of respiratory influenza virus infection. |
| title_sort | interleukin 1 is responsible for acute lung immunopathology but increases survival of respiratory influenza virus infection |
| work_keys_str_mv | AT schmitzn interleukin1isresponsibleforacutelungimmunopathologybutincreasessurvivalofrespiratoryinfluenzavirusinfection AT kurrerm interleukin1isresponsibleforacutelungimmunopathologybutincreasessurvivalofrespiratoryinfluenzavirusinfection AT bachmannm interleukin1isresponsibleforacutelungimmunopathologybutincreasessurvivalofrespiratoryinfluenzavirusinfection AT kopfm interleukin1isresponsibleforacutelungimmunopathologybutincreasessurvivalofrespiratoryinfluenzavirusinfection |