Lung Research Program
Lung Research Program
The RAH Lung Research Program conducts a broad range of projects in pulmonary disease from basic cell biology through to investigator – initiated clinical trials. A particular strength is the close links between the lab and clinical arms, facilitating the acquisition of samples from well-phenotype clinical groups.
The program is divided into four labs namely:
Current research projects:
Chronic Inflammatory Airways Diseases Laboratory
- Macrophage modulation as a therapy for Chronic Obstructive Pulmonary Disease (COPD)
- The impact of e-Cigarettes on airway health
- The role of Autophagy and its potential modulation in COPD
- Overcoming Steroid resistance as a therapeutic strategy in COPD
- Macrolides as an anti-inflammatory therapies in Asthma and COPD
- Macrophage dysfunction in brinchiectasis
Gene & Cell Therapy / Pulmonary vascular disease laboratory
- Cell and Gene Therapy Strategies for Pulmonary Arterial Hypertension
- Extracellular vesicles as candidate therapies for PAH
Lung Transplantation Laboratory
- The role of pro-inflammatory Cytokines in Chronic Lung Allograft Dysfunction
- The role of anxiety and depression in lung transplant outcomes The role of BMPR2 in Lung Cancer
- Development of biomarkers for prediction of disease progression in Interstitial Lung Disease
Interventional Pulmonology / Lung Cancer Laboratory
- New strategies for improving diagnostic yield from bronchoscopic procedures for pulmonary diseases
- The role of cytokine modulation in therapeutic responses to Bronchial Thermoplasty
Sandra Hodge, Greg Hodge, Mark Holmes, Hubertus Jersmann, Paul N. Reynolds. Increased CD8 T-cell granzyme B in COPD is suppressed by treatment with low-dose azithromycin. Respirology 2015 Jan;20(1):95-100.
Harper, RL, Reynolds AM, Bonder C, Reynolds PN. BMPR2 gene therapy for PAH alters Smad signaling. Respirology. Jan 2016 ePub
Feng F, Harper RL, Reynolds PN. BMPR2 gene therapy for PAH upregulates eNOS and counteracts TGF-B induced effects in endothelial and smooth muscle cells. Respirology. 2016 Apr;21(3):526-32
Gao P, Gibson PG, Baines KJ, Yang IA, Upham JW, Reynolds PN, Hodge S, James AL, Jenkins C, Peters MJ, Zhang J, Simpson JL. Anti-inflammatory deficiencies in neutrophilic asthma: reduced galectin-3 and IL-1RA/IL-1β.Respir Res. 2015 Jan 24;16:5.
Hodge G, Jersmann H, Tran HB, Holmes M, Reynolds PN, Hodge S. Lymphocyte senescence in COPD is associated with loss of glucocorticoid receptor expression by pro-inflammatory/cytotoxic lymphocytes. Respir Res. 2015 Jan 9;16:2.
Hodge G, Jersmann H, Tran HB, Roscioli E, Holmes M, Reynolds PN, Hodge S. Lymphocyte senescence in COPD is associated with decreased histone deacetylase 2 expression by pro-inflammatory lymphocytes. Respir Res. 2015 Oct 24;16:130.
Simpson JL, Daly J, Baines KJ, Yang IA, Upham JW, Reynolds PN, Hodge S, James AL, Hugenholtz P, Willner D, Gibson PG. Airway dysbiosis: Haemophilus influenzae and Tropheryma in poorly controlled asthma. Eur Respir J. 2015 Dec 2.
Hodge S, Hodge G, Simpson JL, Yang IA, Upham J, James A, Gibson PG, Reynolds PN. Blood cytotoxic/inflammatory mediators in non-eosinophilic asthma. Clin Exp Allergy. 2016 Jan;46(1):60-70.
Tran HB, Barnawi J, Ween M, Hamon R, Roscioli E, Hodge G, Reynolds PN, Pitson SM, Davies LT, Haberberger R, Hodge S. Cigarette smoke inhibits efferocytosis via deregulation of sphingosine kinase signaling: reversal with exogenous S1P and the S1P analogue FTY720. J Leukoc Biol. 2016 Jan 20.
Simpson JL, Carroll M, Yang IA, Reynolds PN, Hodge S, James AL, Gibson PG, Upham JW. Reduced Antiviral Interferon Production in Poorly Controlled Asthma Is Associated With Neutrophilic Inflammation and High-Dose Inhaled Corticosteroids. Chest. 2016 Mar;149(3):704-13
Ween M, Ahern J, Carroll A, Hodge G, Pizzutto S, Jersmann H, Reynolds P, Hodge S. A small volume technique to examine and compare alveolar macrophage phagocytosis of apoptotic cells and non typeable Haemophilus influenzae (NTHi). J Immunol Methods. 2016 Feb;429:7-14