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Studies of human airway virome are relatively recent and still very limited. Culture-independent microbial techniques showed growing evidence of numerous viral communities in the respiratory microbial ecosystem. The significance of different acute respiratory viruses is already known in the pathogenesis of chronic conditions, such as asthma, cystic fibrosis (CF), or chronic obstructive lung disease (COPD), and their exacerbations. Viral pathogens, such as influenza, metapneumovirus, parainfluenza, respiratory syncytial virus, or rhinovirus, have been associated with impaired immune response, acute exacerbations, and decrease in lung function in chronic lung diseases. However, more data have attributed a role to Herpes family viruses or the newly identified Anelloviridae family of viruses in chronic diseases, such as asthma, idiopathic pulmonary fibrosis (IPF), or CF. Impaired antiviral immunity, bacterial colonization, or used medication, such as glucocorticoids or antibiotics, contribute to the imbalance of airway microbiome and may shape the local viral ecosystem. A specific part of virome, bacteriophages, frames lung microbial communities through direct contact with its host, the specific bacteria known as Pseudomonas aeruginosa or their biofilm formation. Moreover, antibiotic resistance is induced through phages via horizontal transfer and leads to more severe exacerbations of chronic airway conditions. Morbidity and mortality of asthma, COPD, CF, and IPF remains high, despite an increased understanding and knowledge about the impact of respiratory virome in the pathogenesis of these conditions. Thus, more studies focus on new prophylactic methods or therapeutic agents directed toward viral⁻host interaction, microbial metabolic function, or lung microbial composition rearrangement.

Background and Aims: Inhaled corticosteroids (ICSs) are crucial anti-inflammatory medications for chronic airway diseases. Studies investigating the relationship between ICSs and fractures in Asian populations are scant. We investigated whether ICSs increased the risk of low-energy fractures in patients with chronic airway diseases., Methods: We used the Longitudinal Health Insurance Database to select patients aged 20 years and older with chronic airway diseases (asthma and COPD) between 2000 and 2011 as the base cohort. We identified ICS users and ICS non-users matched by propensity score method at 1:1 ratio. Cox proportional hazard regression models were used to calculate the adjusted hazard ratio (aHR) and 95% confidence interval (CI) for factors associated with the risk of fracture., Results: A total of 1,182 ICS users and 1,182 controls were enrolled. After adjustment for age, gender, annual exacerbation number of acute respiratory events, comorbidity and medications, the risk of fracture was 1.10 for ICS users (aHR = 1.20; 95% CI = 1.10-1.31) compared with ICS non-users. The ICS users exhibited significantly 1.63-fold risk of hip fracture and 1.24-fold risk of ulna and radius fracture than did the ICS non-users. Patients with medium and high doses of ICS use were associated with significantly increased risks of fracture (aHR = 1.48, 95% CI = 1.25-1.76 for medium dose and aHR = 1.55, 95% CI = 1.39-1.72 for high dose) compared with those in ICS non-users., Conclusions: Patients with medium and high doses of ICS use are associated with an increased risk of fracture., (© 2017 John Wiley & Sons Ltd.)

Overexpression of PC5/6A and BMP-2 in the human nasal epithelial cell line RPMI-2650 demonstrated that PC5/6A can activate BMP-2. Dec-RVKR-CMK also decreased expression of PC5/6A, but not furin, another PC member, suggesting the involvement of PC5/6A in squamous differentiation of HNECs. Keywords: Nasal Polyp; Squamous Metaplasia; Squamous Differentiation; Chronic Airway Disease; Human Nasal Epithelial Cell EN Nasal Polyp Squamous Metaplasia Squamous Differentiation Chronic Airway Disease Human Nasal Epithelial Cell 1 1 1 03/02/21 20150627 NES 150627 Background Squamous metaplasia in airway epithelium is a pathological process arising from abnormal remodeling/repair responses to injury. [Extracted from the article]