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Electronic cigarettes (e-cigarettes) are often perceived to be a less harmful alternative to tobacco cigarettes. Potentially due to this perception, they are used by people with pre-existing respiratory conditions, such as asthma, who otherwise would not smoke. Despite this, there are few studies exploring the health effects of e-cigarette use on pre-existing asthma.
Early-life immune development is a critical factor in predicting the risk of childhood respiratory infections, asthma, and poor vaccine responses. Identifying immune endotypes that predispose children to these conditions could lead to the development of predictive biomarkers and early interventions, potentially improving long-term health outcomes.
Risk factors for non-communicable diseases (NCDs, cardiovascular diseases, cancers, chronic respiratory diseases, diabetes, and mental disorders) arise in adolescence but are mostly framed as relevant to health in adulthood; little is known about the relationship between co-occurring NCD risks and mental wellbeing in young people.
Poor maternal diet during pregnancy is a risk factor for severe lower respiratory infections in the offspring, but the underlying mechanisms remain elusive. Here, we demonstrate that in mice a maternal low-fiber diet led to enhanced LRI severity in infants because of delayed plasmacytoid dendritic cell recruitment and perturbation of regulatory T cell expansion in the lungs.
Citation: Donovan GM, Wang KCW, Elliot JG, James AL, Noble PB. Quantifying airway remodelling for research or clinical purposes: How should we
Asthma is among the commonest noncommunicable diseases of childhood and often occurs with other atopic comorbidities. A previous case-control study found evidence that compared to children who received acellular pertussis (aP) vaccines in early infancy, children who received one or more doses of whole-cell pertussis (wP) vaccine had lower risk of developing IgE-mediated food allergy. We hypothesized that wP vaccination in early infancy might protect against atopic asthma in childhood.
Airway-associated adipose tissue increases with body mass index and is a local source of pro-inflammatory adipokines that may contribute to airway pathology in asthma co-existing with obesity. Genetic susceptibility to airway adiposity was considered in the present study through kisspeptin/kisspeptin receptor signalling, known to modulate systemic adiposity and potentially drive airway remodelling.
Environmental exposure to phthalates and bisphenol A (BPA), chemicals used in the production of plastics, may increase risk for asthma and allergies. However, little is known about the long-term effects of early life exposure to these compounds.
Abnormalities of the airway smooth muscle (ASM) layer in asthma may develop before birth. We hypothesize that antenatal inflammation causes physiological abnormalities of the ASM that predisposes asthma. This study determined the short-term effects of antenatal inflammation on the developing ASM.
In obstructive airway diseases such as asthma and chronic obstructive pulmonary disease (COPD), the extracellular matrix (ECM) protein amount and composition of the airway smooth muscle (ASM) is often remodelled, likely altering tissue stiffness. The underlying mechanism of how human ASM cell (hASMC) mechanosenses the aberrant microenvironment is not well understood.