Biomedical subjects

Colin F Robertson

Publications and source records attributed to Colin F Robertson.

22 records · Page 2Linked to original sources

PubMed2002

Long-term outcome of childhood asthma.

What we know: The outcome of childhood asthma is dependent on the pattern of asthma through childhood. Episodic asthma in childhood tends to resolve in adolescence and through mid-adult years, with no impairment of lung function. Persistent asthma in childhood is more likely to persist into adult years, with modest impairment of lung function. The impairment of lung function occurs early in the disease process and is not progressive, despite continuing symptoms. What we need to know: Are there clearly identifiable phenotypes of childhood asthma that have different aetiologies, response to treatment, genotypes and natural history? Does early treatment with anti-inflammatory agents prevent impairment of lung function? Can an algorithm be developed to predict the likelihood of persistent asthma on first presentation?

Adolescent↗

PubMed2002

Angiogenesis in paediatric airway disease.

A number of characteristic changes occur in the bronchial wall in paediatric airway diseases. The process of remodelling is usually associated with specific changes to the vasculature, resulting in an increase in vessel numbers, vasodilatation, vessel leakage and cellular margination with transmigration to target tissues. This combined action in conditions such as asthma, cystic fibrosis and bronchiolitis lead to airway wall thickening and reduced airflow. Each component of the vascular response has been shown to be controlled by a range of inflammatory mediators and growth factors. These factors are regulated by a complex process involving gene expression, transcription and translation at the molecular level, protein release, binding to matrix elements and receptors on endothelial cells, then the endothelial response itself. A number of commonly used airway medications are potentially capable of modulating the vascular response to inflammatory stimuli. New therapies may be able to improve airflow through better regulation of vessel growth, dilatation and leakage in the airway wall.

Animals↗

PubMed2002

The Melbourne Asthma Study: 1964-1999.

A group of children with a past history of wheezing was randomly selected from the Melbourne community at the age of 7 years in 1964, and a further group of children with severe wheezing was selected from the same birth cohort at the age of 10 years. These subjects have been followed prospectively at 7-year intervals, with the last review in 1999, when their average age was 42 years. Eighty-seven percent of the original cohort who were still alive participated in the 1999 review. This study showed that the majority of children who had only a few episodes of wheezing associated with symptoms of a respiratory infection had a benign course, with many ceasing to wheeze by adult life. Most who continued with symptoms into adult life were little troubled by them. Conversely, those children with asthma mostly continued with significant wheezing into adult life, and the more troubled they were in childhood, the more likely symptoms continued. There was a loss in lung function by the age of 14 years in those with severe asthma, but the loss did not progress in adult life. The childhood asthma had been treated before the availability of inhaled steroids. There was no significant loss of lung function in those with milder symptoms.

Adolescent↗

PubMed2002

Polyclonal and allergen-induced cytokine responses in adults with asthma: resolution of asthma is associated with normalization of IFN-gamma responses.

BACKGROUND: Atopic disease is associated with skewing of immune responses away from a T(H)1 toward a T(H)2 profile. Previous studies have implicated this cytokine imbalance in the development of disease. However, it is not known whether normalization of this imbalance is conversely associated with disease resolution. OBJECTIVE: To further delineate the role of reduced T(H)1 and increased T(H)2 cytokine production in the pathogenesis of atopic disease and to determine whether disease resolution is associated with alteration of cytokine profiles, we investigated cytokine responses in a cohort of adult patients with asthma followed from childhood. METHODS: A cohort of wheezy children and control subjects aged 7 to 10 years were recruited from 1964 to 1967. Subjects were reevaluated every 7 years to monitor the outcome of childhood asthma. At the 42-year follow-up, 89 subjects from this cohort were evaluated for mitogen and house dust mite (HDM)-induced T(H)1 (IFN-gamma) and T(H)2 (IL-4, IL-5, and IL-13) cytokine responses. Cytokine responses were compared in patients with ongoing asthma, patients with resolved asthma, and control subjects. RESULTS: Patients with severe ongoing asthma had significantly reduced HDM-induced IFN-gamma production compared with that of control subjects and patients with resolved asthma. In contrast, HDM-induced IFN-gamma production in patients with resolved asthma was equivalent to that seen in control subjects. Patients with ongoing and resolved asthma produced significantly higher levels of IL-5 in response to HDM compared with that seen in control subjects, with levels being equivalent in patients with active and resolved asthma. HDM-induced IL-13 production was significantly increased in the patients with resolved asthma when compared with that seen in the control subjects. PHA-induced cytokine responses did not parallel HDM-induced responses. CONCLUSION: Patients with persistent and severe atopic asthma have a reduced HDM-induced T(H)1 response, whereas those with resolved asthma do not. This suggests that reduced HDM-induced IFN-gamma production might be an important factor contributing to ongoing severe asthma and that normalization of allergen-induced T(H)1 responses might be important for disease resolution. The finding that all subjects with a history of asthma displayed increased HDM-induced T(H)2 (IL-5 and IL-13) cytokine responses, irrespective of the presence or absence of asthma, suggests that increased T(H)2 responses reflect the presence of the atopic state per se rather than being specifically linked to asthma.

Adult↗