Marco Contoli

TL;DR: In this paper, the authors show deficient induction of interferon-λs by rhinovirus in primary bronchial epithelial cells and alveolar macrophages, which was highly correlated with severity of rhinovirus induced asthma exacerbation and virus load in experimentally infected human volunteers.

TL;DR: Increased RV-induced clinical illness severity in asthmatic compared with normal subjects is demonstrated, evidence of strong relationships between virus load, lower airway virus-induced inflammation and asthma exacerbation severity is provided, and indicates augmented Th2 or impaired Th1 or IL-10 immunity are likely important mechanisms.

TL;DR: A new model of COPD exacerbation is developed that strongly supports a causal relationship between rhinovirus infection and COPD alleviation and impaired IFN production and neutrophilic inflammation may be important mechanisms in virus-induced COPd exacerbations.

TL;DR: Increased expression of the Th17‐related cytokines IL‐17A, IL‐22 and IL‐23 in COPD patients may reflect their involvement, and that of specific IL‐ 17‐producing cells, in driving the chronic inflammation seen in COPd.

TL;DR: Rinovirus infections are frequently followed by secondary bacterial infections in COPD and cleavage of the antimicrobial peptides SLPI and elafin by virus-induced neutrophil elastase may precipitate these secondaryacterial infections.