Budesonide and formoterol inhibit inflammatory mediator production by bronchial epithelial cells infected with rhinovirus

Skevaki, Chrysanthi; Christodoulou, Ioannis; Spyridaki, Irini; Tiniakou, Ioanna; Georgiou, Vassiliki; Xepapadaki, Paraskevi; Kafetzis, Dimitrios; Papadopoulos, Nikolaos G.

doi:10.1111/j.1365-2222.2009.03307.x

Cited by 62 publications

(66 citation statements)

References 35 publications

(42 reference statements)

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“…2006; Skevaki et al. 2009). We found evidence that low‐dose CHF6001 (10 −8 mol/L), when used together with FP (10 −9 mol/L), gave a greater suppressive effect than FP 10 −9 mol/L or high‐dose CHF6001 10 −6 mol/L.…”

Section: Discussionmentioning

confidence: 99%

Anti‐inflammatory effects of the novel inhaled phosphodiesterase type 4 inhibitor CHF6001 on virus‐inducible cytokines

Edwards

Facchinetti

Civelli

et al. 2016

Pharmacology Res & Perspec

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Respiratory virus infections precipitate asthma and chronic obstructive pulmonary disease (COPD) exacerbations, with most exacerbations due to rhinovirus infection. Both asthma and COPD exacerbations are not well controlled by steroid therapies, and there is a much research interest in finding improved therapies or combinations of therapies for controlling exacerbations. CHF6001 is a new, inhaled highly potent and selective phosphodiesterase type 4 (PDE4) inhibitor. Using in vitro human bronchial epithelial cells (BEAS‐2B), we investigated the potential anti‐inflammatory effects of CHF6001 on rhinovirus (RV1B)‐induced cytokines. Cytokine mRNA was measured by real‐time PCR, while protein release was measured by ELISA. CHF6001 was used in a 7‐point dose–response curve (1000–0.001 nmol/L) as a 1.5‐h pretreatment prior to infection in comparison with roflumilast. Both roflumilast and CHF6001 reduced RV1B‐induced IL‐8, IL‐29, IP‐10, and RANTES mRNA and protein in a concentration‐dependent manner. Generally, CHF6001 was 13‐ to 16‐fold more potent (subnanomolar EC 50 values) than roflumilast at reducing IL‐8, IL‐29, IP‐10, and RANTES mRNA and protein release, but had similar efficacies. In combination with the steroid fluticasone propionate (1 nmol/L), CHF6001 had additive effects, significantly reducing RV‐induced cytokines when compared with steroid or CHF6001 alone. Combined low‐dose steroid and low‐dose CHF6001 had a similar efficacy as high‐dose steroid or CHF6001 alone, indicating the combination had steroid and PDE4 inhibitor sparing effects. Overall results indicate that PDE4 inhibitors have anti‐inflammatory activity against virus‐induced inflammatory mediators and that CHF6001 is more potent than roflumilast.

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Section: Discussionmentioning

confidence: 99%

Anti‐inflammatory effects of the novel inhaled phosphodiesterase type 4 inhibitor CHF6001 on virus‐inducible cytokines

Edwards

Facchinetti

Civelli

et al. 2016

Pharmacology Res & Perspec

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“…Interestingly, data from in vitro studies have suggested that the timing of administration of steroids has profound effects upon their ability to inhibit virus-induced cytokines. For example, in bronchial epithelial cells, rhinovirus-induced CXCL-10 was inhibited by budesonide when the drug was given at the start of the infection period [50], but not when applied 24 h prior to infection [51]. Quite how these in vitro results translate into clinical practice is uncertain.…”

Section: Are Corticosteroids Effective or Ineffective During Virus-rementioning

confidence: 99%

Viral infections and asthma: an inflammatory interface?

et al. 2014

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Asthma is a chronic inflammatory disease of the airways in which the majority of patients respond to treatment with corticosteroids and b 2 -adrenoceptor agonists. Acute exacerbations of asthma substantially contribute to disease morbidity, mortality and healthcare costs, and are not restricted to patients who are not compliant with their treatment regimens. Given that respiratory viral infections are the principal cause of asthma exacerbations, this review article will explore the relationship between viral infections and asthma, and will put forward hypotheses as to why virus-induced exacerbations occur. Potential mechanisms that may explain why current therapeutics do not fully inhibit virus-induced exacerbations, for example, b 2 -adrenergic desensitisation and corticosteroid insensitivity, are explored, as well as which aspects of virus-induced inflammation are likely to be attenuated by current therapy. @ERSpublications Why do virus-induced asthma exacerbations occur? Mechanisms and interventions

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“…These effects are additive to, or even synergise with the anti-inflammatory effects of glucocorticosteroids [35][36][37][38] and include suppression of inflammatory responses induced by viral exposure [39][40][41] and anti-remodelling effects. Airway remodelling is an inherent component of asthma and includes increased numbers of airway smooth muscle cells, goblet cell hyperplasia and fibrotic rearrangement of the airway extracellular matrix.…”

Section: Airway Inflammation and Remodellingmentioning

confidence: 99%

Why use long acting bronchodilators in chronic obstructive lung diseases? An extensive review on formoterol and salmeterol

Santus

Radovanovic

Paggiaro

et al. 2015

European Journal of Internal Medicine

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Budesonide and formoterol inhibit inflammatory mediator production by bronchial epithelial cells infected with rhinovirus

Cited by 62 publications

References 35 publications

Anti‐inflammatory effects of the novel inhaled phosphodiesterase type 4 inhibitor CHF6001 on virus‐inducible cytokines

Anti‐inflammatory effects of the novel inhaled phosphodiesterase type 4 inhibitor CHF6001 on virus‐inducible cytokines

Viral infections and asthma: an inflammatory interface?

Why use long acting bronchodilators in chronic obstructive lung diseases? An extensive review on formoterol and salmeterol

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