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Genetic Variation in CCL18 Gene Influences CCL18 Expression and Correlates with Survival in Idiopathic Pulmonary Fibrosis: Part A
Open AccessArticle

Genetic Variation in CCL18 Gene Influences CCL18 Expression and Correlates with Survival in Idiopathic Pulmonary Fibrosis—Part B

1
Department of Respiratory Medicine, Hannover Medical School and Biomedical Research in End-stage and Obstructive Lung Disease Hannover, German Lung Research Center (DZL), 30265 Hannover, Germany
2
Fraunhofer Institute for Toxicology and Experimental Medicine, 30625 Hannover, Germany
3
Dept of Pulmonology, Interstitial Lung Diseases Center of Excellence, St Antonius Hospital, 3435 CM Nieuwegein, The Netherlands
4
Department of Medicine and Human Genetics, University of Pittsburgh, Pittsburgh, PA 15261, USA
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
J. Clin. Med. 2020, 9(6), 1993; https://doi.org/10.3390/jcm9061993
Received: 25 May 2020 / Revised: 16 June 2020 / Accepted: 23 June 2020 / Published: 25 June 2020
(This article belongs to the Special Issue The New Perspective in Pulmonary Fibrosis)
Idiopathic pulmonary fibrosis (IPF) is a progressive disease with high mortality. CC-chemokine ligand 18 (CCL18) is predictive of survival in IPF. We described correlation of CCL18 serum levels with the genotype of rs2015086 C > T polymorphism the CCL18-gene, which was associated with survival in a pre-antifibrotic cohort (Part-A). Herein (Part-B), we aimed to validate these findings and to study the effects of antifibrotics. Two cohorts were prospectively recruited, cohort-A (n = 61, pre-antifibrotic) and cohort B (n = 101, received antifibrotics). Baseline CCL18 serum level measurement by enzyme-linked immunosorbent assay (ELISA, serially in cohort B) and genotyping of rs2015086 was performed and correlated with clinical outcomes. The CT genotype was present in 15% and 31% of patients. These patients had higher CCL18 levels compared to the TT-genotype (cohort-A: 234 vs. 115.8 ng/mL, p < 0.001; cohort B: 159.5 vs. 120 ng/mL, p = 0.0001). During antifibrotic therapy, CCL18 increased (p = 0.0036) regardless of rs2015086-genotype and antifibrotic-agent. In cohort-A, baseline CCL18-cutoff (>120 ng/mL) and CT-genotype were associated with mortality (p = 0.041 and p = 0.0051). In cohort-B, the CCL18-cutoff (>140 ng/mL) was associated with mortality (p = 0.003) and progression (p = 0.004), but not the CT/CC-genotype. In conclusion, we validated the correlation between rs2015086-genotype and CCL18 serum levels, which was predictive of (progression-free)-survival in two prospective validation cohorts. View Full-Text
Keywords: idiopathic pulmonary fibrosis; antifibrotics; CCL18; interstitial lung disease idiopathic pulmonary fibrosis; antifibrotics; CCL18; interstitial lung disease
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Caliskan, C.; Seeliger, B.; Jäger, B.; Fuge, J.; Welte, T.; Terwolbeck, O.; Freise, J.; van Moorsel, C.H.M.; Zhang, Y.; Prasse, A. Genetic Variation in CCL18 Gene Influences CCL18 Expression and Correlates with Survival in Idiopathic Pulmonary Fibrosis—Part B. J. Clin. Med. 2020, 9, 1993.

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