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The CRONIC-PPF Faculty

Leigh MARSH
Priv.-Doz. Dr. biol. hum.

Resolution of pulmonary fibrosis via immune cell reprogramming

Assistant Professor at the Otto Loewi Research Center, Lung Research Group, Head of Research Unit "Immune Cell Interaction"

Ludwig Boltzmann Institute for Lung Vascular Research, Medical University of Graz, Neue Stiftingtalstraße 6, 8010 Graz
Phone: +43-316-385 72911,  e-mail

WWW: Forschungsportal Med Uni Graz
ORCID: 0000-0002-1754-9249
PubMed: PubMed (nih.gov)

• Profile      • Curriculum vitae     • Publications    

Leigh Marsh is a molecular biologist specializing in uncovering the immune mechanisms underlying CLD. His research integrates computational flow cytometry, advanced data modelling, and transcriptomic analysis together with preclinical models. He has extensively characterized inflammatory cell profiles in both healthy and diseased human lungs, with a particular focus on the functional crosstalk between structural and recruited inflammatory cells. With broad expertise in animal models of CLD and relevant physiological assessments, his work contributes to a deeper understanding of disease progression and potential therapeutic targets.

Project

Resolution of pulmonary fibrosis via immune cell reprogramming
Co-PI: Katharina Jandl

Research interests

  1. Our group integrates computational flow cytometry, advanced data modeling, and transcriptomic analysis with preclinical models to dissect the interactions and interdependence of diverse immune cell populations in disease pathogenesis. Our extensive characterisation of human lungs has revealed the strong deviation in the immune profile in idiopathic pulmonary arterial hypertension. (Marsh et al., 2018 [↗]) and COPD (Bordag et al., 2025 [↗]), and inflammatory factors that drive remodelling (Jandl et al., 2022 [↗] Zabini et al., 2015 [↗])
  2. Our application of animal models of chronic lung disease has revealed the complex interaction in the immune system and aberrant expression of key downstream signalling molecules results in pathological inflammation and remodelling in vivo. (Reiter et al., 2025 [↗]; Hochgerner et al., 2022 [↗]; Schnoegl et al., 2022 [↗]; Bordag et al., 2020 [↗]; Theiler et al., 2019 [↗]; Gungl et al., 2018 [↗];
  3. Our third pillar applies data modelling and transcriptomic analysis to uncover mechanisms of disease pathogenesis. (Bordag et al., 2025 [↗]; Crnkovic et al., 2022 [↗]; Bordag et al., 2020 [↗]; Marsh et al., 2020 [↗]; Syarif, in preparation)