INTERFERON LAMBDA-3 AS A NEW CANDIDATE GENE INVOLVED IN THE PROGRESSION OF IDIOPATHIC PULMONARY FIBROSIS

Hamdi, Eman; Abdelrehim, Amany B.; Higazi, Aliaa; Ahmed, Abo Bakr F.; Thabet, Khaled

doi:10.21608/bfsa.2022.271824

INTERFERON LAMBDA-3 AS A NEW CANDIDATE GENE INVOLVED IN THE PROGRESSION OF IDIOPATHIC PULMONARY FIBROSIS

Document Type : Original Article

Authors

¹ Department of Biochemistry, Faculty of Pharmacy, Minia University, Minia, 61519, Egypt

² Department of Clinical pathology, Faculty of Medicine, Minia University, Minia, 61519, Egypt

³ Department of Microbiology and Immunology, Faculty of Pharmacy, Minia University, Minia, 61519, Egypt

10.21608/bfsa.2022.271824

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive fibrosing interstitial respiratory illness with an unknown origin, which leads to inevitably fatal outcomes in the majority of cases. The pro-inflammatory cytokine interferon lambda-3 (IFN-λ3) has been recently identified as a risk factor for the development of lung fibrosis in scleroderma patients. In this study, we examined the involvement of IFN-λ3 in IPF by utilizing the mouse model of BLM-induced pulmonary fibrosis. Our study identifies a remarkable overexpression in the mRNA of IFNL3, and a positive significant correlation between the IFNL3 mRNA levels and the various pro-inflammatory cytokines for instance NF-kB, TNF-α, IL-1β and TGF-β throughout the three-weeks study. These findings have proven the impact of IFNL3 on BLM-induced pulmonary fibrosis occurrence and progression. Moreover, the data suggest that the pro-inflammatory and pro-fibrotic capacities of IFNL3 may be provoked by additional pro-inflammatory cytokines NF-kB, TNF-α, IL-1β, and TGF-β. In conclusion, IFN-λ3 looks like a promising target in the therapeutic development of new drug candidates for pulmonary fibrosis.

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