A study recently published in Therapeutics and Clinical Risk Management showed for the first time that some interleukins (IL) were significantly upregulated in patients with both idiopathic pulmonary fibrosis (IPF) and lung cancer, providing novel evidence for their use as sensitive biomarkers for the early diagnosis of patients with both pathologies. This study offers new evidence for preventing and treating lung cancer-associated IPF.

Zhang et al enrolled 56 patients diagnosed with lung cancer-associated IPF, 59 lung cancer patients without IPF, and 60 healthy volunteers to serve as the control group to evaluate the expressions of IL-22, IL-23, and IL-17 using enzyme-linked immunosorbent assay (ELISA) kits.

The authors observed that IL-22, IL-23, and IL-17 were significantly upregulated in the serum of patients with lung cancer compared to that of healthy controls, which is consistent with previous findings.


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“Moreover, we first reported that the expression of both IL-22 and IL-23 were markedly increased in the serum of patients with combined lung cancer and IPF, compared with the lung cancer group, the area under the curve (AUC) of IL-17 was 0.8066 (95% confidence interval (CI), 0.7220 to 0.8912), the IL-22 was 0.7818 (95% CI, 0.6952 to 0.8684), and the IL-23 was 0.7324 (95% CI, 0.6419 to 0.8230),” the authors wrote, ”suggesting that IL-22 and IL-23 are effective biomarkers to distinguish patients with combined lung cancer and IPF with the lung cancer patients.”

The findings are relevant since IPF and lung cancer have similar risk factors (for example, age, family history, and smoking history), which might confound the results of these studies. Furthermore, the authors described some somatic alterations in both IPF-associated lung cancer and fibrosing lung tissue. For example, KRAS or tumor protein 53 (TP53) mutations were found to be higher in lung tissue samples from patients with IPF and lung cancer than in those from patients with IPF but no lung cancer.

Long-term inflammation and infiltration of immune cells frequently characterize IPF, as does aberrant collagen deposition, which leads to the remodeling of the lungs. Although the specific pathogenesis remains unclear, the results of previous studies suggest this disease may originate from a lesion in the alveolus, and the long-term inflammatory condition could further damage its structure, including apoptosis of type I epithelial cells, overproliferation of the type II cells, and thickening of small airways and arterial walls.

Reference

Zhang Q, Tong L, Wang B, Wang T, Ma H. Diagnostic value of serum levels of IL-22, IL-23, and IL-17 for idiopathic pulmonary fibrosis associated with lung cancer. Ther Clin Risk Manag. 2022;18:429-437. doi:10.2147/tcrm.s349185