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Thomas Iosifidis

Research Officer

Thomas Iosifidis

Research Officer

BSc BMedSci(Hons) PhD

thomas.iosifidis@thekids.org.au

+61 8 6319 1807

Tom Iosifidis received his PhD in Paediatrics (UWA 2018) and is currently a Postdoctoral Research Officer in the Airway Epithelial Research at The Kids Research Institute Australia.

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.

Projects

Kids Easy Breathing Study

As both bronchiolitis and bronchiectasis are diseases of the airway surface, we will comprehensively study the airway surface and factors affecting the airway surface in infants hospitalised with bronchiolitis.

Compound Repurposing Into Novel Therapeutics In COVID-19 At risk Lungs (CRITICAL Study)

Mechanisms of Acute Viral Respiratory Illness in Children (MAVRIC)

Published research

Transcriptomic analysis of primary nasal epithelial cells reveals altered interferon signalling in preterm birth survivors at one year of age

Many survivors of preterm birth (<37 weeks gestation) have lifelong respiratory deficits, the drivers of which remain unknown. Influencers of pathophysiological outcomes are often detectable at the gene level and pinpointing these differences can help guide targeted research and interventions. This study provides the first transcriptomic analysis of primary nasal airway epithelial cells in survivors of preterm birth at approximately 1 year of age.

AI-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.

Nasal 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.

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.

Dysregulated 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.

Development 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.

Reduced 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.

ACE2 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.

Education and Qualifications
  • PhD (Paediatrics) - UWA 2018
  • BMedSci(Hons) - UWA 2011
  • Bsc - Curtin University 2010
Active Collaborations

Local: active collaborations with local cohort studies (ORIGINS, WAERP, AREST CF, MAVRIC and MAP); The University of Western Australia; King Edward Memorial Hospital; Ear Science Institute Australia; Burns Unit, Fiona Stanley Hospital;

National: Australian Translational Medicinal Chemistry Facility, Monash University;

International: Wake Forest University, USA; Imperial College London, UK; University of Wisconsin, USA; SickKids Hospital, Canada; University of Toronto, Canada; Galaru Pharmaceutical Co., Ltd, China;