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Research

Macrophage PD-1 associates with neutrophilia and reduced bacterial killing in early cystic fibrosis airway disease

Macrophages are the major resident immune cells in human airways coordinating responses to infection and injury. In cystic fibrosis, neutrophils are recruited to the airways shortly after birth, and actively exocytose damaging enzymes prior to chronic infection, suggesting a potential defect in macrophage immunomodulatory function.

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ACE2 expression is elevated in airway epithelial cells from older and male healthy individuals but reduced in asthma

COVID-19 is complicated by acute lung injury, and death in some individuals. It is caused by SARS-CoV-2 that requires the ACE2 receptor and serine proteases to enter AEC. We determined what factors are associated with ACE2 expression particularly in patients with asthma and COPD. We obtained lower AEC from 145 people from two independent cohorts, aged 2-89 years, Newcastle (n = 115) and Perth (n = 30), Australia. The Newcastle cohort was enriched with people with asthma (n = 37) and COPD (n = 38). Gene expression for ACE2 and other genes potentially associated with SARS-CoV-2 cell entry was assessed by qPCR, and protein expression was confirmed with immunohistochemistry on endobronchial biopsies and cultured AEC.

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Persistent induction of goblet cell differentiation in the airways: Therapeutic approaches

Here we review the current knowledge of key molecular pathways that are dysregulated during persistent goblet cell differentiation

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Accumulation mode particles and LPS exposure induce TLR-4 dependent and independent inflammatory responses in the lung

We aimed to delineate the effects of LPS and AMP on airway inflammation, and potential contribution to airway disease by measuring airway inflammatory responses

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Impaired airway epithelial cell responses from children with asthma to rhinoviral infection

Human rhinovirus infection delays repair and inhibits apoptotic processes in epithelial cells from non-asthmatic and asthmatic children

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Identification of epithelial phospholipase A2 receptor 1 as a potential target in asthma

PLA2R1 is increased in the airway epithelium in asthma, and serves as a regulator of airway hyperresponsiveness, airway permeability, antigen sensitization, and airway inflammation

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Conditionally reprogrammed primary airway epithelial cells maintain morphology, lineage and disease specific functional characteristics

Here, we show that conditionally reprogrammed airway epithelial cells (CRAECs) can be established from both healthy and diseased phenotypes.

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Defective cell migration as a mechanism of dysregulated asthmatic airway repair

The findings from this study show that in children with asthma this protective barrier is different from children without asthma.

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The airway epithelium is a direct source of matrix degrading enzymes in bronchiolitis obliterans syndrome

Long-term survival after lung transplantation is hindered by the development of bronchiolitis obliterans syndrome (BOS).

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Suppression of adrenomedullin contributes to vascular leakage and altered epithelial repair during asthma

The anti-inflammatory peptide, adrenomedullin (AM), and its cognate receptor are expressed in lung tissue, but its pathophysiological significance in airway...