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Research

Autophagy modulates growth and development in the moss Physcomitrium patens

Physcomitrium patens apical growing protonemal cells have the singularity that they continue to undergo cell divisions as the plant develops. This feature provides a valuable tool to study autophagy in the context of a multicellular apical growing tissue coupled to development. Herein, we showed that the core autophagy machinery is present in the moss P. patens, and characterized the 2D and 3D growth and development of atg5 and atg7 loss-of-function mutants under optimal and nutrient-deprived conditions.

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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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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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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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Vitamin D supplementation of initially vitamin D-deficient mice diminishes lung inflammation with limited effects on pulmonary epithelial integrity

In disease settings, vitamin D may be important for maintaining optimal lung epithelial integrity and suppressing inflammation, but less is known of its effects prior to disease onset.

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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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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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Bile signalling promotes chronic respiratory infections and antibiotic tolerance

Bile acid signalling is a leading trigger for the development of chronic phenotypes underlying the pathophysiology of chronic respiratory disease

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Effect of human rhinovirus infection on airway epithelium tight junction protein disassembly and transepithelial permeability

HRV-1B infection directly alters human airway epithelial TJ expression leading to increased epithelial permeability potentially via antiviral response of IL-15

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The genetic and epigenetic landscapes of the epithelium in asthma

Genetic factors in airway epithelial cells that are functionally associated with asthma pathogenesis