Vol 3-2 Commentary

Commentary: Novel Insight into the Genetic Basis of High Altitude Pulmonary Hypertension in Kyrgyz Highlanders

Tsering Stobdan1 and Gabriel G. Haddad1, 2, 3*

1Division of Respiratory Medicine, Department of Pediatrics, University of California, San Diego, La Jolla, CA 92093, USA

2Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093, USA

3Rady Children's Hospital, San Diego, CA 92123, USA

DOI: 10.29245/2689-999X/2019/2.1150 View / Download Pdf
Vol 3-2 Research Article

Complement Factor (C3) Level as Marker of Inflammation in Paediatric Asthma

AR Somashekar1*, KG Ramakrishnan1, Vanitha Gowda2

1Department of Pediatrics, M.S. Ramaiah Medical College and hospitals, Bangalore, India

2Department of Biochemistry, M.S. Ramaiah Medical College and hospitals, Bangalore, India

Aim: To assess the serum levels of a complement factors C3 in Indian asthmatic children and compare them with those of healthy controls in order to establish a relationship between the levels of these factors and asthma disease process.

Method: Serum c3 levels of 44 children with acute asthma and 44 controls of the age group of 6-16 years was determined and statistically compared. Lung function tests (FEV1%) was done and correlated with serum c3 levels using Pearson’s comparison coefficient.

Results: The mean serum c3 value of cases (138±32.99) is higher than the controls (112.82±14.6), with 32% cases showing higher than normal level of serum C3. Pearson’s correlation coefficient reveals negative correlation between FEV1% with serum C3 levels.

Conclusion: This study reveals that serum levels of complement c3 are statistically higher in subjects with asthma as compared to healthy subjects. Further, serum levels of c3 reflect the severity of the disease, with its levels being higher when disease is more severe.

DOI: 10.29245/2689-999X/2019/2.1151 View / Download Pdf
Vol 3-2 Mini Review

Epithelial-Mesenchymal Transition Contributes to Pulmonary Fibrosis via Aberrant Epithelial/Fibroblastic Cross-Talk

Charlotte Hill1, Mark G. Jones2,3, Donna E. Davies2,3,4 and Yihua Wang1,4*

1Biological Sciences, Faculty of Environmental and Life Sciences, University of Southampton, Southampton SO17 1BJ, UK.

2Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton SO16 6YD, UK.

3NIHR Respiratory Biomedical Research Centre, University Hospital Southampton, Southampton SO16 6YD, UK.

4Institute for Life Sciences, University of Southampton, Southampton SO17 1BJ, UK.

Idiopathic pulmonary fibrosis (IPF) is the prototypic progressive fibrotic interstitial lung disease. Median survival is only 3 years, and treatment options are limited. IPF is thought to be a result of a combination of genetic and environmental factors with repetitive micro-injuries to alveolar epithelial cells playing a central role. IPF is characterised by aberrant extra cellular matrix (ECM) deposition by activated myofibroblasts. Epithelial-mesenchymal transition (EMT) is a process where polarised epithelial cells undergo molecular changes allowing them to gain a mesenchymal phenotype, with a subsequent enhanced ability to produce ECM components and increased migration and/or invasion. The source of myofibroblasts in IPF has been debated for many years, and EMT has been proposed as a source of these cells. However, lineage tracing in transgenic mice suggests the contribution of epithelial cells, which have undergone EMT, to the fibroblast population may be negligible. Instead, recent findings suggest that alveolar epithelial type II (ATII) cells undergoing EMT promote a pro-fibrotic microenvironment through paracrine signalling activating local fibroblasts. This review paper explores the contribution of ATII cells, which have undergone EMT, in the context of pulmonary fibrosis.

DOI: 10.29245/2689-999X/2019/2.1149 View / Download Pdf
Vol 3-2 Review

Pulmonary Nano-Drug Delivery Systems for Lung Cancer: Current Knowledge and Prospects

Madumani Amararathna1, Kerry Goralski2, David W. Hoskin3,4, H. P. Vasantha Rupasinghe1,3*

1Department of Plant, Food, and Environmental Sciences, Faculty of Agriculture, Dalhousie University, Rm 219-C, Cox Institute Building, 50 Pictou Rd. PO Box 550, Truro, NS, B2N 5E3, Canada.

2College of Pharmacy and Department of Pharmacology, Dalhousie University, Halifax, NS B3H 4R2, Canada.

3Department of Pathology, Faculty of Medicine, Dalhousie University, Halifax, NS B3H 4R2, Canada.

4Department of Microbiology and Immunology, Faculty of Medicine, Dalhousie University, Halifax, NS B3H 4R2, Canada.

Treatment complexities and the cytotoxicity of anticancer drugs to normal cells often results in therapeutic failure. Biodegradable nanoparticles have gained attention as drug carriers due to their physicochemical characteristics. Nanoparticles are able to encapsulate anticancer drugs and deliver them to target malignant cells while sparing normal cells. Since lung cancer usually arises in lung epithelium, localized drug delivery could be an alternative strategy to effectively treat this disease. Encapsulation of lung cancer drugs in nanoparticles may facilitate intact drug delivery, avoid first-pass metabolism, and reduce cytotoxicity to normal cells, as well as being attractive to patients. However, nanoparticles should be formulated in such a way as to facilitate entrance, deposition, retention, and permeability on targeted lung tissues and escape mucociliary clearance and phagocytosis. Additionally, the patient’s diversity related to lung cancer type, stage of disease, and physical fitness should be considered when formulating a nanocarrier and a delivery device. The potential of localized drug delivery for lung cancer using nanoparticles is reviewed here.

Abbreviations: PLGA, poly(lactide-co-glycolide); MRP1, multidrug resistance associated protein 1; GST, glutathione-s-transferase; NAT, N-acetyltransferease; SULT, sulfotransferases; TRAIL, tumor necrosis factor-related apoptosis-inducing ligand.

DOI: 10.29245/2689-999X/2019/2.1148 View / Download Pdf