Immune Factor, CCL8, Identified as Possible IPF Diagnostic Marker

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by Magdalena Kegel |

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IPF research

The immune factor CCL8 could be a diagnostic marker of idiopathic pulmonary fibrosis (IPF), and it might be useful in predicting patients’ survival times, a recent study reports.

Researchers at the Soonchunhyang Graduate School and University Hospital in Korea published the study, Gene profile of fibroblasts identify relation of CCL8 with idiopathic pulmonary fibrosis,” in the journal Respiratory Research.

The team began by analyzing gene activity changes in lung fibroblasts from eight IPF patients and four controls. They focused on genes with an apparent change and ended up with a list of 15, 13 of which had not previously been explored in IPF. The gene with the greatest change in activity was CCL8. Further analysis showed that its protein levels — proteins can be produced by genes via messenger RNA — were nine-fold higher in IPF patients’ lung fibroblasts than levels seen in the controls.

Researchers then assessed levels of the factor in cells gathered from the bronchoalveolar washing liquid of 86 IPF patients (a procedure commonly used in clinical settings). CCL8 levels were significantly higher among IPF patients than in 41 controls. The levels were also higher than in patients with other interstitial lung diseases, including non-specific interstitial pneumonia, hypersensitivity pneumonitis, and sarcoidosis.

Those differences make CCL8 a potential marker that could be used to diagnose IPF, the team said.

Researchers also examined the patients’ survival data to determine whether CCL8 levels were linked to disease outcomes. (Participants had been followed for up to eight years.) The team found that patients with CCL8 levels above 28.61 pg/mL had shorter survival times.

CCL8 belongs to a group of immune factors called chemokines, which attract and activate other immune cells. Studies have shown that it signals T-cells that produce the cytokine IL-17 —a known mediator of autoimmune processes. Other cytokines, known to be involved in IPF disease processes, activate CCL8.

The researchers acknowledged that little is known about how CCL8 contributes to IPF’s development, and they said its role in mediating fibrosis needs to be explored.