Rhinovirus-mediated changes in airway smooth muscle responsiveness: induced autocrine role of interleukin-1β

Hákonarson, Hákon; Carter, Carrie; Maskeri, Neil; Hodinka, Richard L.; Grunstein, Michael

doi:10.1152/ajplung.1999.277.1.l13

Cited by 39 publications

(44 citation statements)

References 33 publications

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“…First, the flu virus infection may directly induce AHR by increasing airway smooth muscle contraction through the production of IL-1␤. Rhinovirus-induced IL-1␤-dependent increase in airway smooth-muscle contraction has been shown to occur in vitro (44), and it has been shown that flu virus infection leads to the production of IL-1␤ in the lung (45). A second possibility is that the flu virus infection induced the production of IL-13 in the airways.…”

Section: Discussionmentioning

confidence: 99%

Influenza A Virus Infection Inhibits the Efficient Recruitment of Th2 Cells into the Airways and the Development of Airway Eosinophilia

Wohlleben

Müller

Tatsch

et al. 2003

The Journal of Immunology

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Most infections with respiratory viruses induce Th1 responses characterized by the generation of Th1 and CD8+ T cells secreting IFN-γ, which in turn have been shown to inhibit the development of Th2 cells. Therefore, it could be expected that respiratory viral infections mediate protection against asthma. However, the opposite seems to be true, because viral infections are often associated with the exacerbation of asthma. For this reason, we investigated what effect an influenza A (flu) virus infection has on the development of asthma. We found that flu infection 1, 3, 6, or 9 wk before allergen airway challenge resulted in a strong suppression of allergen-induced airway eosinophilia. This effect was associated with strongly reduced numbers of Th2 cells in the airways and was not observed in IFN-γ- or IL-12 p35-deficient mice. Mice infected with flu virus and immunized with OVA showed decreased IL-5 and increased IFN-γ, eotaxin/CC chemokine ligand (CCL)11, RANTES/CCL5, and monocyte chemoattractant protein-1/CCL2 levels in the bronchoalveolar lavage fluid, and increased airway hyperreactivity compared with OVA-immunized mice. These results suggest that the flu virus infection reduced airway eosinophilia by inducing Th1 responses, which lead to the inefficient recruitment of Th2 cells into the airways. However, OVA-specific IgE and IgG1 serum levels, blood eosinophilia, and goblet cell metaplasia in the lung were not reduced by the flu infection. Flu virus infection also directly induced AHR and goblet cell metaplasia. Taken together, our results show that flu virus infections can induce, exacerbate, and suppress features of asthmatic disease in mice.

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Section: Discussionmentioning

confidence: 99%

Influenza A Virus Infection Inhibits the Efficient Recruitment of Th2 Cells into the Airways and the Development of Airway Eosinophilia

Wohlleben

Müller

Tatsch

et al. 2003

The Journal of Immunology

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“…One potential mechanism of the amplification of responses in our coinfection model is IL-1␤-induced upregulation of the receptors responsible for viral infection or detection. Indeed, major-group RVs cause the endogenous release of IL-1␤, which then acts in an autocrine manner to further potentiate inflammatory responses, for example, through upregulation of the RV major group receptor ICAM-1 (18,19,58). However, we found that while IL-1␤ enhanced CXCL8 release from virally infected epithelial cells, it did not augment virally induced ISGs, having no impact on CXCL10 production and in fact modestly reducing CCL5 release, implying that the cooperation of stimuli exerts selective actions on specific pathways.…”

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confidence: 99%

Role of Interleukin-1 and MyD88-Dependent Signaling in Rhinovirus Infection

Stokes

Ismail

Dick

et al. 2011

J Virol

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Rhinoviral infection is an important trigger of acute inflammatory exacerbations in patients with underlying airway disease. We have previously established that interleukin-1␤ (IL-1␤) is central in the communication between epithelial cells and monocytes during the initiation of inflammation. In this study we explored the roles of IL-1␤ and its signaling pathways in the responses of airway cells to rhinovirus-1B (RV-1B) and further determined how responses to RV-1B were modified in a model of bacterial coinfection. Our results revealed that IL-1␤ dramatically potentiated RV-1B-induced proinflammatory responses, and while monocytes did not directly amplify responses to RV-1B alone, they played an important role in the responses observed with our coinfection model. MyD88 is the essential signaling adapter for IL-1␤ and most Toll-like receptors. To examine the role of MyD88 in more detail, we created stable MyD88 knockdown epithelial cells using short hairpin RNA (shRNA) targeted to MyD88. We determined that IL-1␤/MyD88 plays a role in regulating RV-1B replication and the inflammatory response to viral infection of airway cells. These results identify central roles for IL-1␤ and its signaling pathways in the production of CXCL8, a potent neutrophil chemoattractant, in viral infection. Thus, IL-1␤ is a viable target for controlling the neutrophilia that is often found in inflammatory airway disease and is exacerbated by viral infection of the airways.

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“…Inhibiting IL-1b or blocking IL-1 receptors prevents virus-induced, toluene diisocyanate-induced, and antigen challenge-induced hyperreactivity in animals (24)(25)(26)(27). In humans with asthma, IL-1b is present in lavage, epithelial cells, and alveolar macrophages (28)(29)(30)(31).…”

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confidence: 99%

IL-1 Receptors Mediate Persistent, but Not Acute, Airway Hyperreactivity to Ozone in Guinea Pigs

Verhein¹,

Jacoby

Fryer

2008

Am J Respir Cell Mol Biol

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Ozone exposure in the lab and environment causes airway hyperreactivity lasting at least 3 days in humans and animals. In guinea pigs 1 day after ozone exposure, airway hyperreactivity is mediated by eosinophils that block neuronal M 2 muscarinic receptor function, thus increasing acetylcholine release from airway parasympathetic nerves. However, mechanisms of ozone-induced airway hyperreactivity change over time, so that depleting eosinophils 3 days after ozone makes airway hyperreactivity worse rather than better. Ozone exposure increases IL-1b in bone marrow, which may contribute to acute and chronic airway hyperreactivity. To test whether IL-1b mediates ozone-induced airway hyperreactivity 1 and 3 days after ozone exposure, guinea pigs were pretreated with an IL-1 receptor antagonist (anakinra, 30 mg/kg, intraperitoneally) 30 minutes before exposure to filtered air or to ozone (2 ppm, 4 h). One or three days after exposure, airway reactivity was measured in anesthetized guinea pigs. The IL-1 receptor antagonist prevented ozoneinduced airway hyperreactivity 3 days, but not 1 day, after ozone exposure. Ozone-induced airway hyperreactivity was vagally mediated, since bronchoconstriction induced by intravenous acetylcholine was not changed by ozone. The IL-1 receptor antagonist selectively prevented ozone-induced reduction of eosinophils around nerves and prevented ozone-induced deposition of extracellular eosinophil major basic protein in airways. These data demonstrate that IL-1 mediates ozone-induced airway hyperreactivity at 3 days, but not 1 day, after ozone exposure. Furthermore, preventing hyperreactivity was accompanied by decreased eosinophil major basic protein deposition within the lung, suggesting that IL-1 affects eosinophil activation 3 days after ozone exposure.

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Rhinovirus-mediated changes in airway smooth muscle responsiveness: induced autocrine role of interleukin-1β

Cited by 39 publications

References 33 publications

Influenza A Virus Infection Inhibits the Efficient Recruitment of Th2 Cells into the Airways and the Development of Airway Eosinophilia

Influenza A Virus Infection Inhibits the Efficient Recruitment of Th2 Cells into the Airways and the Development of Airway Eosinophilia

Role of Interleukin-1 and MyD88-Dependent Signaling in Rhinovirus Infection

IL-1 Receptors Mediate Persistent, but Not Acute, Airway Hyperreactivity to Ozone in Guinea Pigs

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