Research Officer
BSc BMedSci(Hons) PhD
Tom Iosifidis received his PhD in Paediatrics (UWA 2018) and is currently a Postdoctoral Research Officer in the Airway Epithelial Research at the Telethon Kids Institute.
Tom utilises a broad skill base including unique paediatric samples such as cells lining the airways, known as airway epithelial cells. In addition, he also uses cutting-edge omics data analyses and organotypic airway models to develop better treatments for childhood lung diseases, such as pre-school wheeze and asthma.
His research interests lie in understanding the molecular mechanisms underlying airway repair and lung disease development. He is currently leading drug screening efforts to target epithelial injuries. In addition, he has a strong interest in biomarkers for the identification of at-risk individuals that would benefit from targeted treatments.
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Publications
January 2022
Exacerbation of chronic cigarette-smoke induced lung disease by rhinovirus in mice
A significant proportion of chronic obstructive pulmonary disease exacerbations are strongly associated with rhinovirus infection (HRV). In this study, we combined long-term cigarette smoke exposure with HRV infection in a mouse model.
Published research Pregnancy and Early Life Immunology Airway Epithelial Research Children's Lung Health P4 Respiratory Health for Kids Respiratory Environmental Health Respiratory viral infectionsMay 2022AI-Driven Cell Tracking to Enable High-Throughput Drug Screening Targeting Airway Epithelial Repair for Children with Asthma
The airway epithelium of children with asthma is characterized by aberrant repair that may be therapeutically modifiable. The development of epithelial-targeting therapeutics that enhance airway repair could provide a novel treatment avenue for childhood asthma.
Published research Airway Epithelial Research P4 Respiratory Health for Kids Subsite: WalyanDecember 2021Dysregulated Notch Signaling in the Airway Epithelium of Children with Wheeze
The airway epithelium of children with wheeze is characterized by defective repair that contributes to disease pathobiology. Dysregulation of developmental processes controlled by Notch has been identified in chronic asthma. However, its role in airway epithelial cells of young children with wheeze, particularly during repair, is yet to be determined.
Asthma Published research Airway Epithelial Research P4 Respiratory Health for Kids Bacterial Respiratory Infectious Disease Group Subsite: WalyanJanuary 2021ACE2 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.
Asthma Published research Airway Epithelial ResearchNovember 2021Development and validation of a miniaturized bacteriophage host range screening assay against antibiotic resistant Pseudomonas aeruginosa
Antimicrobial resistance is a current global health crisis, and the increasing emergence of multidrug resistant infections has led to the resurgent interest in bacteriophages as an alternative treatment.
Published research Airway Epithelial Research Subsite: WalyanJune 2021Nasal airway epithelial repair after very preterm birth
Nasal epithelial cells from very preterm infants have a functional defect in their ability to repair beyond the first year of life, and failed repair may be associated with antenatal steroid exposure.
Published research Airway Epithelial Research Children's Lung Health Pre-term birthApril 2021Reduced socs1 expression in lung fibroblasts from patients with ipf is not mediated by promoter methylation or mir155
The interleukin (IL)-6 family of cytokines and exaggerated signal transducer and activator of transcription (STAT)3 signaling is implicated in idiopathic pulmonary fibrosis (IPF) pathogenesis, but the mechanisms regulating STAT3 expression and function are unknown. Suppressor of cytokine signaling (SOCS)1 and SOCS3 block STAT3, and low SOCS1 levels have been reported in IPF fibroblasts and shown to facilitate collagen production. Fibroblasts and lung tissue from IPF patients and controls were used to examine the mechanisms underlying SOCS1 down-regulation in IPF.
Published research Genetics and Health Airway Epithelial Research -
Education and Qualifications
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Active Collaborations