Interleukin‐1β and interleukin‐1ra levels in nasal lavages during experimental rhinovirus infection in asthmatic and non‐asthmatic subjects

Kluijver, Josephine de; Grünberg, Katrien; Pons, Douwe; Klerk, E. P. A. De; Dick, Claire R.; Sterk, Peter J.; Hiemstra, Pieter S.

doi:10.1046/j.1365-2222.2003.01770.x

Cited by 52 publications

(53 citation statements)

References 14 publications

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“…For example, after inoculation with the virus, nasal lavage levels of IL-8 and the proinflammatory mediator IL-1b were increased in asthmatic patients. 27 In this study, a small increase in the anti-inflammatory marker IL-1 receptor antagonist (IL-1ra), a competitive inhibitor of IL-1, also occurred in asthmatic subjects treated with budesonide, whereas lower levels were found in these patients at baseline. These findings suggest that RV might be able to alter the proinflammatory/antiinflammatory balance of IL-1b/IL-1ra toward inflammation more markedly in people with existing and active asthma.…”

Section: How Does Rv Modulate Inflammatory Mediators Of Epithelial Cementioning

confidence: 68%

The role of rhinovirus in asthma exacerbations

Friedlander

Busse

2005

Journal of Allergy and Clinical Immunology

166

104

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Section: How Does Rv Modulate Inflammatory Mediators Of Epithelial Cementioning

confidence: 68%

The role of rhinovirus in asthma exacerbations

Friedlander

Busse

2005

Journal of Allergy and Clinical Immunology

166

104

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“…The sample size was estimated based on cytokine production in previous studies with RV16,26 showing variation of 20% after RV16 infection in patients with allergic asthma. Fourteen individuals per group were needed to detect an effect of 25% with two-sided significance of p=0.05 and a power of 90%.…”

Section: Methodsmentioning

confidence: 99%

Systemic tryptophan and kynurenine catabolite levels relate to severity of rhinovirus-induced asthma exacerbation: a prospective study with a parallel-group design

Sluijs

Pol

Kulik

et al. 2013

Thorax

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Background Patients with allergic asthma have exacerbations which are frequently caused by rhinovirus infection. The antiviral tryptophan-catabolising enzyme indoleamine 2,3-dioxygenase (IDO) is induced by interferon-γ and suppressed by Th2 mediators interleukin (IL)-4 and IL-13. We hypothesised that local IDO activity after viral airway infection is lower in patients with allergic asthma than in healthy controls. Objective To determine whether IDO activity differs between patients with allergic asthma and healthy individuals before and after rhinovirus infection. Methods Healthy individuals and patients with allergic asthma were experimentally infected with low-dose (10 TCID 50 ) rhinovirus 16. Blood, bronchoalveolar lavage fluid and exhaled breath condensate (for mass spectrometry by UPLC-MS/MS) were obtained before and after rhinovirus challenge. Results IDO activity was not induced by rhinovirus infection in either group, despite increases in cold scores. However, baseline pulmonary IDO activity was lower in patients with allergic asthma than in healthy individuals. In contrast, systemic tryptophan and its catabolites were markedly higher in patients with allergic asthma. Moreover, systemic quinolinic acid and tryptophan were associated with eosinophil cationic protein (r=0.43 and r=0.78, respectively) and eosinophils (r=0.38 and r=0.58, respectively) in bronchoalveolar lavage fluid and peak asthma symptom scores after rhinovirus challenge (r=0.53 and r=0.64, respectively). Conclusions Rhinovirus infection by itself induces no IDO activity, but the reduced pulmonary IDO activity in patients with allergic asthma at baseline may underlie a reduced control of viral infections. Notably, the enhanced systemic catabolism of tryptophan in patients with allergic asthma was strongly related to the outcome of rhinovirus challenge in asthma and may serve as a prognostic factor.

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“…There is a wealth of data to suggest that IL-1␤ levels are enhanced within the airways of patients with COPD or asthma, with further increases detected during acute exacerbations (7,10,59). Furthermore, epithelial and monocytic cells (PBMCs and alveolar macrophages) taken from such patients respond to inflammatory stimuli with greater IL-1␤ production (21,48,68).…”

mentioning

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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Interleukin‐1β and interleukin‐1ra levels in nasal lavages during experimental rhinovirus infection in asthmatic and non‐asthmatic subjects

Cited by 52 publications

References 14 publications

The role of rhinovirus in asthma exacerbations

The role of rhinovirus in asthma exacerbations

Systemic tryptophan and kynurenine catabolite levels relate to severity of rhinovirus-induced asthma exacerbation: a prospective study with a parallel-group design

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

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