Viruses exacerbating chronic pulmonary disease: the role of immune modulation

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 most common 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 virus-induced exacerbations. 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

Protocol of the baseline assessment for the Environments for Healthy Living (EHL) Wales cohort study

Background Health is a result of influences operating at multiple levels. For example, inadequate housing, poor educational attainment, and reduced access to health care are clustered together, and are all associated with reduced health. Policies which try to change individual people's behaviour have limited effect when people have little control over their environment. However, structural environmental change and an understanding of the way that influences interact with each other, has the potential to facilitate healthy choices irrespective of personal resources. The aim of Environments for Healthy Living (EHL) is to investigate the impact of gestational and postnatal environments on health, and to examine where structural change can be brought about to optimise health outcomes. The baseline assessment will focus on birth outcomes and maternal and infant health. Methods/Design EHL is a longitudinal birth cohort study. We aim to recruit 1000 pregnant women in the period April 2010 to March 2013. We will examine the impact of the gestational environment (maternal health) and the postnatal environment (housing and neighbourhood conditions) on subsequent health outcomes for the infants born to these women. Data collection will commence during the participants' pregnancy, from approximately 20 weeks gestation. Participants will complete a questionnaire, undergo anthropometric measurements, wear an accelerometer, compile a food diary, and have environmental measures taken within their home. They will also be asked to consent to having a sample of umbilical cord blood taken following delivery of their baby. These data will be complemented by routinely collected electronic data such as health records from GP surgeries, hospital admissions, and child health and development records. Thereafter, participants will be visited annually for follow-up of subsequent exposures and child health outcomes. Discussion The baseline assessment of EHL will provide information concerning the impact of gestational and postnatal environments on birth outcomes and maternal and infant health. The findings can be used to inform the development of complex interventions targeted at structural, environmental factors, intended to reduce ill-health. Long-term follow-up of the cohort will focus on relationships between environmental exposures and the later development of adverse health outcomes, including obesity and diabetes

Prevalence of sleep disordered breathing symptoms among Malay school children in a primary school in Malaysia

Sleep disordered breathing (SDB) is increasingly being diagnosed in children. However, there is no prevalence study done in Malaysia. The study objective was to evaluate the prevalence of SDB symptoms based on parental reports and associated risk factors among Malay school children aged 6 to 10 years old in a primary school using a translated University Michigan Paediatric Sleep Questionnaire (Malay UM-PSQ). The children whose parents responded to the questionnaire and consented were examined, documenting height, weight, skin fold thickness, neck and abdominal circumference, tonsillar size, nostril examination and presence of micrognathia or retrognathia. There were 550 respondents. The prevalence of parental report of SDB symptoms was 14.9 % (95 % CI 11.9, 17.9). Two hundred and eighty-five (51.8%) school children were males with mean age of 8.5 years (SD 1.1). The associated risk factors for SDB symptoms are male, obesity, large neck and waist circumference, positive history of asthma, history of recurrent tonsillitis, enlarged tonsil (> 4+) and enlarged nasal turbinate. Multivariate analysis showed that male gender is the only significant independent risk factor of SDB symptom

Rhinovirus exacerbates house-dust-mite induced lung disease in adult mice

Human rhinovirus is a key viral trigger for asthma exacerbations. To date, murine studies investigating rhinovirus-induced exacerbation of allergic airways disease have employed systemic sensitisation/intranasal challenge with ovalbumin. In this study, we combined human-rhinovirus infection with a clinically relevant mouse model of aero-allergen exposure using house-dust-mite in an attempt to more accurately understand the links between human-rhinovirus infection and exacerbations of asthma. Adult BALB/c mice were intranasally exposed to low-dose house-dust-mite (or vehicle) daily for 10 days. On day 9, mice were inoculated with human-rhinovirus-1B (or UV-inactivated human-rhinovirus-1B). Forty-eight hours after inoculation, we assessed bronchoalveolar cellular inflammation, levels of relevant cytokines/serum antibodies, lung function and responsiveness/sensitivity to methacholine. House-dust-mite exposure did not result in a classical TH 2 -driven response, but was more representative of noneosinophilic asthma. However, there were significant effects of house-dustmite exposure on most of the parameters measured including increased cellular inflammation (primarily macrophages and neutrophils), increased total IgE and house-dust-mite-specific IgG 1 and increased responsiveness/sensitivity to methacholine. There were limited effects of human-rhinovirus-1B infection alone, and the combination of the two insults resulted in additive increases in neutrophil levels and lung parenchymal responses to methacholine (tissue elastance). We conclude that acute rhinovirus infection exacerbates house-dust-mite-induced lung disease in adult mice. The similarity of our results using the naturally occurring allergen house-dust-mite, to previous studies using ovalbumin, suggests that the exacerbation of allergic airways disease by rhinovirus infection could act via multiple or conserved mechanisms. © 2014 Phan et al