ICAM-1 and other potential biomarkers for IPF flagged


By Mardi Chapman

8 Apr 2019

 A number of proteins found in lung biopsy samples of patients with idiopathic pulmonary disease (IPF) have the potential to be useful in predicting the trajectory of disease.

An immunohistochemical study of 29 samples from the Australian IPF Registry found the potential biomarkers could identify which patients had rapidly progressing disease (a fall in FVC ≥10% or DLco ≥15% or death within 1 year from baseline) or stable disease.

Dr Sukhwinder Sohal, head of the University of Tasmania’s Respiratory Translational Research Group, told the TSANZSRS 2019 meeting that intracellular adhesion molecule-1 (ICAM-1), matrix metalloproteinase (MMP)-7, osteopontin and the chemokine CXCL13 and were all increased in the tissue of patients identified as rapid decliners.

He identified ICAM-1 as a protein of particular interest.

“ICAM-1 is expressed in endothelial cells, macrophages and fibroblasts. It’s a pro-inflammatory marker.”

“It’s also a very important molecule in infections. These patients get a lot of exacerbations as well, and the [ICAM-1] protein is used by the rhinovirus to hang on to the epithelium.”

“In this scenario what we looked at was ICAM-1 increased in rapidly progressive disease and less in stable disease. If you had low levels of ICAM-1 then it leads to better transplant-free survival, which makes sense. If you have more of this protein you have more infections – a mechanism we want to look at down the track.”

Dr Sohal said he was hopeful ICAM-1 might prove useful to predict disease early and measure progression over time.

“It should be helpful from a diagnosis point of view, and also in understanding the disease mechanism. If we can do that, then we can look at therapeutic targets specific to those mechanisms.”

He added that ICAM-1 was also increased in smokers and in patients with COPD.

Given the pathology of COPD and IPF were quite different, he said ICAM-1 might be contributing to each disease via completely different mechanisms.

Associate Professor Tamera Corte, Chair of the Australian IPF Registry, said patients often struggled with delayed diagnosis, and the fact that no one can tell them why they have the disease or how quickly their condition will progress.

“This research removes some of those uncertainties and hopefully will lead to a more personalised approach to tailoring treatment to the individual with IPF,” she said.

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