Overexpression of IL-38 protein in anticancer drug-induced lung injury and acute exacerbation of idiopathic pulmonary fibrosis

Respir Investig. 2017 Sep;55(5):293-299. doi: 10.1016/j.resinv.2017.06.001. Epub 2017 Aug 12.

Abstract

Background: Interleukin (IL)-38, a member of the IL-1 family, shows high homology to IL-1 receptor antagonist (IL-1Ra) and IL-36 receptor antagonist (IL-36Ra). Its function in interstitial lung disease (ILD) is still unknown.

Methods: To determine the expression pattern of IL-38 mRNA, a panel of cDNAs derived from various tissues was analyzed by quantitative real-time PCR. Immunohistochemical reactivity with anti-human IL-38 monoclonal antibody (clone H127C) was evaluated semi-quantitatively in lung tissue samples from 12 patients with idiopathic pulmonary fibrosis/usual interstitial pneumonia (IPF/UIP), 5 with acute exacerbation of IPF, and 10 with anticancer drug-induced ILD (bleomycin in 5 and epidermal growth factor receptor-tyrosine kinase inhibitor in 5). Control lung tissues were obtained from areas of normal lung in 22 lung cancer patients who underwent extirpation surgery.

Results: IL-38 transcripts were strongly expressed in the lung, spleen, synoviocytes, and peripheral blood mononuclear cells, and at a lower level in pancreas and muscle. IL-38 protein was not strongly expressed in normal pulmonary alveolar tissues in all 22 control lungs. In contrast, IL-38 was overexpressed in the lungs of 4 of 5 (80%) patients with acute IPF exacerbation and 100% (10/10) of the patients with drug-induced ILD. IL-38 overexpression was limited to hyperplastic type II pneumocytes, which are considered to reflect regenerative change following diffuse alveolar damage in ILD.

Conclusions: IL-38 may play an important role in acute and/or chronic inflammation in anticancer drug-induced lung injury and acute exacerbation of IPF.

Keywords: Anticancer drug; IL-38; Interstitial lung disease.

MeSH terms

  • Acute Lung Injury / chemically induced*
  • Acute Lung Injury / diagnosis*
  • Aged
  • Aged, 80 and over
  • Antineoplastic Agents / adverse effects*
  • Biomarkers / analysis
  • Disease Progression
  • Female
  • Gene Expression
  • Humans
  • Idiopathic Pulmonary Fibrosis / chemically induced*
  • Idiopathic Pulmonary Fibrosis / diagnosis*
  • Immunohistochemistry
  • Interleukins / analysis*
  • Interleukins / genetics
  • Interleukins / physiology*
  • Lung / metabolism
  • Male
  • Middle Aged

Substances

  • Antineoplastic Agents
  • Biomarkers
  • IL-38 protein, human
  • Interleukins