Chronic pulmonary diseases are a major cause of morbidity and mortality and their impact is expected to increase in the future. Respiratory viruses are the commonest cause of acute respiratory infections and it is increasingly recognized that respiratory viruses are a major cause of acute exacerbations of chronic pulmonary diseases such as asthma, chronic obstructive pulmonary disease and cystic fibrosis.

There is now increasing evidence that the host response to virus infection is dysregulated in these diseases, and a better understanding of the mechanisms of abnormal immune responses has the potential to lead to the development of new therapies for respiratory virus infections.

The aim of this article is to review the current knowledge regarding the role of viruses and immune modulation in chronic pulmonary diseases and discuss avenues for future research and therapeutic implications.

BACKGROUND: Based on surface brushings and BAL fluid Hilty, et al. demonstrated microbiomes in the human lung characteristic of asthma and chronic obstructive pulmonary disease (COPD), which have now been confirmed by others. The present study extends these findings to human lung tissue samples.

METHODS: DNA from lung tissue samples were obtained from non-smokers (n=8), smokers without COPD (n=8), very severe COPD (GOLD 4) patients (n=8), and patients with cystic fibrosis (n=8). The latter served as a positive control, with sterile water as a negative control. All bacterial community analyses were based on PCR amplified 16S rRNA gene fragments. Total bacterial populations were measured by quantitative PCR (QPCR) and bacterial community composition was assessed by terminal restriction fragment length polymorphism (TRFLP) analysis and pyrotag sequencing.

RESULTS: Total bacterial populations within lung tissue were small (20-1252 bacterial cells/1000 human cells) but greater in all four sample groups versus the negative control (P<0.001). TRFLP analysis and sequencing distinguished three distinct bacterial community compositions: one common to the non-smoker and smoker groups, a second to the GOLD 4 group, and the third to the cystic fibrosis positive control group. Pyrotag sequencing identified greater than 1400 unique bacterial sequences and showed an increase in the firmicute phylum in GOLD 4 patients versus all other groups (P<0.003) attributable to an increase in the Lactobacillus genus (P<0.0007).

CONCLUSION: There is a detectable bacterial community within human lung tissue that changes in patients with very severe COPD.

PURPOSE: Although honeycombing is one of the key features for the diagnosis of idiopathic pulmonary fibrosis (IPF), its origin and evolution are still poorly understood. The aim of our study was to analyse the natural history of honeycombing in patients treated with single-lung transplantation.

MATERIALS AND METHODS: We considered seven patients who underwent single-lung transplantation; two of them (28.6%) were excluded from our analysis because they died in the posttransplantation period, whereas the remaining five (71.4%) were evaluated with computed tomography (CT) over 67.6±38.56 months. Each CT scan was assessed for disease extension and cyst size (visual score and size of target cysts); CT scans acquired after 2006 were also assessed for native lung volume.

RESULTS: All patients showed disease progression (with a concurrent reduction in lung volume in two, 40%) and a progression of honeycombing, with increased number and size of cysts in four (80%). We observed dimensional changes in all target cysts (enlargement or reduction); three patients (60%) also had radiological evidence of complications, such as spontaneous rupture with pneumothorax and development of mycetomas within the cysts.

CONCLUSIONS: Honeycombing is a dynamic process in which the overall trend is represented by a dimensional increase in cystic pattern; however, single cysts may have a different evolution (enlargement, reduction or complications). This behaviour could be explained by the variety of the pathogenetic processes underlying honeycombing, with cysts that may present abnormal communication with the airway, including the development of a check-valve mechanism.

INTRODUCTION: Patients with CF experience pulmonary exacerbations. These are often initially empirically treated with intravenous antibiotics, with antibiotic choice refined after susceptibility testing.

METHODS: We completed a 5-year retrospective review of children attending the Paediatric CF Unit, Nottingham. The respiratory sampling, antibiotic prescribing and susceptibility testing guidance were audited. Episodes were classified according to the concordance between the antibiotics prescribed and antibiotic susceptibility testing.

RESULTS: Of 52 patients who had previously isolated Pseudomonas aeruginosa, 103 antibiotic courses were commenced that coincided with an isolation of P. aeruginosa. P. aeruginosa was fully susceptible, partially susceptible or fully resistant on 33%, 44.7% or 16.5% of occasions respectively. The antibiotic prescriptions were never changed following antibiotic susceptibility testing. We found no association between change in FEV(1) (p=0.54), change in BMI (p=0.12) or time to next exacerbation (p=0.66) and concordance between antibiotic susceptibility and the antibiotics administered.

CONCLUSION: This study contributes to mounting evidence questioning the utility of routine antibiotic susceptibility testing.