Smoke and viruses-a hindrance to relaxing the airways?

[tetano]

Clin Sci (Lond). 2016 May 1;130(10):839-41. doi: 10.1042/CS20160139.
[h=1]Smoke and viruses-a hindrance to relaxing the airways?[/h] Singanayagam A[SUP]1[/SUP], Johnston SL[SUP]2[/SUP].
[h=3]Author information[/h]

[h=3]Abstract[/h] Inhaled β2-adrenoceptor agonists are a mainstay of therapy for airways diseases and are almost universally prescribed for patients with asthma or chronic obstructive pulmonary disease (COPD). Very few studies have evaluated the efficacy of these commonly used therapies during acute disease exacerbations which are frequently triggered by viral infection. In this edition of Clinical Science, Donovan et al. assess the ex vivo effects of the most commonly used short-acting β2-agonist salbutamol on small airway reactivity using precision cut lung slices (PCLS) from a mouse model of virus-induced exacerbation of COPD. They demonstrate that combined challenge with cigarette smoke and influenza infection in mice markedly impairs salbutamol-mediated airway relaxation. The findings of the present study suggest that cigarette smoke and respiratory virus infection may intefere with the ability of commonly prescribed therapies to effectively bronchodilate the airways.
? 2016 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.


[h=4]KEYWORDS:[/h] chronic obstructive pulmonary disease; influenza; pharmacology

PMID: 27128804 [PubMed - in process]

 

[tetano]

Clin Sci (Lond). 2016 May 1;130(10):829-37. doi: 10.1042/CS20160093. Epub 2016 Apr 10.
[h=1]Influenza A virus infection and cigarette smoke impair bronchodilator responsiveness to β-adrenoceptor agonists in mouse lung.[/h] Donovan C[SUP]1[/SUP], Seow HJ[SUP]2[/SUP], Bourke JE[SUP]1[/SUP], Vlahos R[SUP]3[/SUP].
[h=3]Author information[/h]

[h=3]Abstract[/h] β2-adrenoceptor agonists are the mainstay therapy for patients with asthma but their effectiveness in cigarette smoke (CS)-induced lung disease such as chronic obstructive pulmonary disease (COPD) is limited. In addition, bronchodilator efficacy of β2-adrenoceptor agonists is decreased during acute exacerbations of COPD (AECOPD), caused by respiratory viruses including influenza A. Therefore, the aim of the present study was to assess the effects of the β2-adrenoceptor agonist salbutamol (SALB) on small airway reactivity using mouse precision cut lung slices (PCLS) prepared from CS-exposed mice and from CS-exposed mice treated with influenza A virus (Mem71, H3N1). CS exposure alone reduced SALB potency and efficacy associated with decreased β2-adrenoceptor mRNA expression, and increased tumour necrosis factor α (TNFα) and interleukin-1β (IL-1β) expression. This impaired relaxation was restored by day 12 in the absence of further CS exposure. In PCLS prepared after Mem71 infection alone, responses to SALB were transient and were not well maintained. CS exposure prior to Mem71 infection almost completely abolished relaxation, although β2-adrenoceptor and TNFα and IL-1β expression were unaltered. The present study has shown decreased sensitivity to SALB after CS or a combination of CS and Mem71 occurs by different mechanisms. In addition, the PCLS technique and our models of CS and influenza infection provide a novel setting for assessment of alternative bronchodilators.
? 2016 The Author(s).


[h=4]KEYWORDS:[/h] acute exacerbations of COPD (AECOPD); chronic obstructive pulmonary disease (COPD); influenza; respiratory virus; small airways; β-adrenoceptor

PMID: 27128803 [PubMed - in process]