INTERFERON LAMBDA-3 AS A NEW CANDIDATE GENE INVOLVED IN THE PROGRESSION OF IDIOPATHIC PULMONARY FIBROSIS | ||
Bulletin of Pharmaceutical Sciences Assiut University | ||
Volume 45, Issue 2, December 2022, Pages 1109-1119 PDF (1.16 M) | ||
Document Type: Original Article | ||
DOI: 10.21608/bfsa.2022.271824 | ||
Authors | ||
Eman Hamdi1; Amany B. Abdelrehim1; Aliaa Higazi2; Abo Bakr F. Ahmed3; Khaled Thabet* 1 | ||
1Department of Biochemistry, Faculty of Pharmacy, Minia University, Minia, 61519, Egypt | ||
2Department of Clinical pathology, Faculty of Medicine, Minia University, Minia, 61519, Egypt | ||
3Department of Microbiology and Immunology, Faculty of Pharmacy, Minia University, Minia, 61519, Egypt | ||
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. | ||
Keywords | ||
idiopathic pulmonary fibrosis; interferon lambda-3 | ||
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