Carolyn J. Baglole

Lung-targeted overexpression of the NF-κB member RelB inhibits cigarette smoke-induced inflammation.

Genetic ablation of the aryl hydrocarbon receptor causes cigarette smoke-induced mitochondrial dysfunction and apoptosis.

Genetic and histologic evidence for autophagy in asthma pathogenesis.

Cigarette smoke increases TLR4 and TLR9 expression and induces cytokine production from CD8(+) T cells in chronic obstructive pulmonary disease.

Autocrine-regulated airway smooth muscle cell migration is dependent on IL-17-induced growth-related oncogenes.

Th17-associated cytokines promote human airway smooth muscle cell proliferation.

IL-8 production in response to cigarette smoke is decreased in epithelial cells from COPD patients.

Differential roles of CXCL2 and CXCL3 and their receptors in regulating normal and asthmatic airway smooth muscle cell migration.

Genetic deletion of IL-17A reduces cigarette smoke-induced inflammation and alveolar type II cell apoptosis.

The NF-κB family member RelB regulates microRNA miR-146a to suppress cigarette smoke-induced COX-2 protein expression in lung fibroblasts.

Aryl hydrocarbon receptor (AhR) attenuation of subchronic cigarette smoke-induced pulmonary neutrophilia is associated with retention of nuclear RelB and suppression of intercellular adhesion molecule-1 (ICAM-1).

Aryl hydrocarbon receptor-dependent regulation of miR-196a expression controls lung fibroblast apoptosis but not proliferation.

Alterations in the expression of the NF-κB family member RelB as a novel marker of cardiovascular outcomes during acute exacerbations of chronic obstructive pulmonary disease.

Upregulation of IL-17A/F from human lung tissue explants with cigarette smoke exposure: implications for COPD.

Decreased expression of the NF-κB family member RelB in lung fibroblasts from Smokers with and without COPD potentiates cigarette smoke-induced COX-2 expression.

Fibroblast-epithelial cell interactions drive epithelial-mesenchymal transition differently in cells from normal and COPD patients.

The aryl hydrocarbon receptor suppresses cigarette-smoke-induced oxidative stress in association with dioxin response element (DRE)-independent regulation of sulfiredoxin 1.

Club Cell-16 and RelB as Novel Determinants of Arterial Stiffness in Exacerbating COPD Patients.

Dihydromethysticin (DHM) Blocks Tobacco Carcinogen 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-Induced O(6)-Methylguanine in a Manner Independent of the Aryl Hydrocarbon Receptor (AhR) Pathway in C57BL/6 Female Mice.

Bioinformatic analysis of microRNA and mRNA Regulation in peripheral blood mononuclear cells of patients with chronic obstructive pulmonary disease.

Differential Contribution of the Aryl-Hydrocarbon Receptor and Toll-Like Receptor Pathways to IL-8 Expression in Normal and Cystic Fibrosis Airway Epithelial Cells Exposed to .

Aryl hydrocarbon receptor (AhR)-dependent regulation of pulmonary miRNA by chronic cigarette smoke exposure.

Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter.

RelB attenuates cigarette smoke extract-induced apoptosis in association with transcriptional regulation of the aryl hydrocarbon receptor.

Pulmonary and diaphragmatic pathology in collagen type I α1 mutant mice with osteogenesis imperfecta.

Smoke-induced neuromuscular junction degeneration precedes the fibre type shift and atrophy in chronic obstructive pulmonary disease.

The Aryl Hydrocarbon Receptor and the Maintenance of Lung Health.

Endocrine aryl hydrocarbon receptor signaling is induced by moderate cutaneous exposure to ultraviolet light.

Pulmonary neutrophilia caused by absence of the NF-κB member RelB is dampened by exposure to cigarette smoke.

Neutrophils from severe asthmatic patients induce epithelial to mesenchymal transition in healthy bronchial epithelial cells.

Differential Regulation of the Asthmatic Phenotype by the Aryl Hydrocarbon Receptor.

Endogenous regulation of the Akt pathway by the aryl hydrocarbon receptor (AhR) in lung fibroblasts.

Involvement of the ACE2/Ang-(1-7)/MasR Axis in Pulmonary Fibrosis: Implications for COVID-19.

HuR drives lung fibroblast differentiation but not metabolic reprogramming in response to TGF-β and hypoxia.

Role of Human Antigen R (HuR) in the Regulation of Pulmonary ACE2 Expression.

Differential impact of JUUL flavors on pulmonary immune modulation and oxidative stress responses in male and female mice.

Standardized Cannabis Smoke Extract Induces Inflammation in Human Lung Fibroblasts.

Receptor-mediated effects of Δ -tetrahydrocannabinol and cannabidiol on the inflammatory response of alveolar macrophages.

Modulation of pulmonary immune function by inhaled cannabis products and consequences for lung disease.

Differential inflammatory profile in the lungs of mice exposed to cannabis smoke with varying THC:CBD ratio.

Dynamic relationship between the aryl hydrocarbon receptor and long noncoding RNA balances cellular and toxicological responses.

Regulation of long non-coding RNA expression by aryl hydrocarbon receptor activation.

Sex-specific alterations in pulmonary metabolic, xenobiotic and lipid signalling pathways after e-cigarette aerosol exposure during adolescence in mice.

Alveolar macrophage function is impaired following inhalation of berry e-cigarette vapor.

Cannabis vaping elicits transcriptomic and metabolomic changes involved in inflammatory, oxidative stress, and cancer pathways in human bronchial epithelial cells.

The effect of cannabis-derived terpenes on alveolar macrophage function.

Transcriptomic changes in oxidative stress, immunity, and cancer pathways caused by cannabis vapor on alveolar epithelial cells.