Adenovirus expressing interleukin-1 receptor antagonist alleviates allergic airway inflammation in a murine model of asthma

Cc, Wang; Cl, Fu; Yh, Yang; Yc, Lo; Wang, Li‐Chieh; Chuang, Ya Hui; Dm, Chang; Chiang, Bor‐Luen

doi:10.1038/sj.gt.3302798

Cited by 49 publications

(34 citation statements)

References 46 publications

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“…Ovalbumin-challenged mice displayed significantly increased activation of caspase-1 in BAL cells (the majority of which are macrophages), which correlated with a significant increase in lung IL-1β secretion and Itgb8 mRNA (Supplemental Figure 8). These data support other reports that IL-1β is important for the ovalbumin-induced asthma phenotype (13).…”

Section: Figuresupporting

confidence: 82%

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Mouse and human lung fibroblasts regulate dendritic cell trafficking, airway inflammation, and fibrosis through integrin αvβ8–mediated activation of TGF-β

Kitamura

Cambier²,

Somanath³

et al. 2011

J. Clin. Invest.

160

201

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The airway is a primary portal of entry for noxious environmental stimuli that can trigger airway remodeling, which contributes significantly to airway obstruction in chronic obstructive pulmonary disease (COPD) and chronic asthma. Important pathologic components of airway remodeling include fibrosis and abnormal innate and adaptive immune responses. The positioning of fibroblasts in interstitial spaces suggests that they could participate in both fibrosis and chemokine regulation of the trafficking of immune cells such as dendritic cells, which are crucial antigen-presenting cells. However, physiological evidence for this dual role for fibroblasts is lacking. Here, in two physiologically relevant models -conditional deletion in mouse fibroblasts of the TGF-β-activating integrin αvβ8 and neutralization of αvβ8 in human COPD fibroblasts -we have elucidated a mechanism whereby lung fibroblast chemokine secretion directs dendritic cell trafficking, in a manner that is critically dependent on αvβ8-mediated activation of TGF-β by fibroblasts. Our data therefore indicate that fibroblasts have a crucial role in regulating both fibrotic and immune responses in the lung.

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Section: Figuresupporting

confidence: 82%

“…Lung innate immune responses are initiated and enhanced through increased function of proinflammatory cytokines, such as IL-1β (6)(7)(8)(9)(10)(11)(12)(13). Airway delivery of an adenoviral vector expressing IL-1β (Ad-IL-1β) and transgenic overexpression of IL-1β are associated with airway inflammation and remodeling in mice (14,15).…”

Section: Introductionmentioning

confidence: 99%

Mouse and human lung fibroblasts regulate dendritic cell trafficking, airway inflammation, and fibrosis through integrin αvβ8–mediated activation of TGF-β

Kitamura

Cambier²,

Somanath³

et al. 2011

J. Clin. Invest.

160

201

View full text Add to dashboard Cite

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“…Thus, an adenovirus expressing IL-1RA was observed to attenuate allergic airways inflammation in a mouse model of asthma. 19 The ability of IL-1RA to reduce allergeninduced airway inflammation and mucus secretion in mice has also been reported by Gurusamy et al 20 IL-1RA has also been shown to prevent experimentally induced allergic eye disease in mice by downregulation of the recruitment of eosinophils and other inflammatory cells. 21 There is ample evidence that allergic disorders such as asthma, rhinitis and atopic dermatitis may be mediated by oxidative stress.…”

Section: 13mentioning

confidence: 83%

Phage therapy in allergic disorders?

Górski

Jończyk‐Matysiak

Łusiak-Szelachowska

et al. 2018

Exp Biol Med (Maywood)

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Allergic disorders pose a growing challenge to medicine and our society. Therefore, novel approaches to prevention and therapy are needed. Recent progress in studies on bacterial viruses (phages) has provided new data indicating that they have significant immunomodulating activities. We show how those activities could be translated into beneficial effects in allergic disorders and present initial clinical data that support this hope.

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“…An IL-1 cytokine-mediated increase or decrease in inflammation ensues after imbalances between the IL-1RI agonist and antagonist cytokines (4). The proinflammatory role of IL-1 and the anti-inflammatory role of IL-1Ra in chronic inflammatory lung diseases such as asthma are widely documented (5)(6)(7).…”

mentioning

confidence: 99%

Interleukin-1 Family Member 9 Stimulates Chemokine Production and Neutrophil Influx in Mouse Lungs

Ramadas¹,

Ewart²,

Medoff³

et al. 2011

Am J Respir Cell Mol Biol

100

105

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Interleukin-1 (IL-1) is a proinflammatory cytokine that signals through the Type I IL-1 receptor (IL-1RI). Novel IL-1-like cytokines were recently identified. Their functions in lung disease remain unclear. Interleukin-1 family member-9 (IL-1F9) is one such IL-1-like cytokine, expressed in the lungs of humans and mice. IL-1F9 signals through IL-1 receptor-related protein 2 (IL-1Rrp2/IL-1RL2), which is distinct from IL-1RI. We sought to determine if IL-1F9 acts as a proinflammatory cytokine in lung disease. IL-1F9 protein was increased in lung homogenates of house dust mite-challenged A/J mice compared with controls, and expression was seen in airway epithelial cells. The intratracheal administration of recombinant mouse IL-1F9 increased airway hyperresponsiveness and induced neutrophil influx and mucus production, but not eosinophilic infiltration in the lungs of mice. In addition, IL-1a protein levels in bronchoalveolar lavage fluid, chemokines, and chemokine-receptor mRNA expression in the lungs were increased after the instillation of intratracheal IL-1F9. Consistent with these changes, NF-kB transcription factor activity was increased in the lungs of mice challenged with IL-1F9 and in a macrophage cell line treated with IL-1F9. These data suggest that IL-1F9 is upregulated during inflammation, and acts as a proinflammatory cytokine in the lungs.

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Adenovirus expressing interleukin-1 receptor antagonist alleviates allergic airway inflammation in a murine model of asthma

Cited by 49 publications

References 46 publications

Mouse and human lung fibroblasts regulate dendritic cell trafficking, airway inflammation, and fibrosis through integrin αvβ8–mediated activation of TGF-β

Mouse and human lung fibroblasts regulate dendritic cell trafficking, airway inflammation, and fibrosis through integrin αvβ8–mediated activation of TGF-β

Phage therapy in allergic disorders?

Interleukin-1 Family Member 9 Stimulates Chemokine Production and Neutrophil Influx in Mouse Lungs

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