Hamdi, E., Abdelrehim, A., Higazi, A., Ahmed, A., Thabet, K. (2022). INTERFERON LAMBDA-3 AS A NEW CANDIDATE GENE INVOLVED IN THE PROGRESSION OF IDIOPATHIC PULMONARY FIBROSIS. test, 45(2), 1109-1119. doi: 10.21608/bfsa.2022.271824
Eman Hamdi; Amany B. Abdelrehim; Aliaa Higazi; Abo Bakr F. Ahmed; Khaled Thabet. "INTERFERON LAMBDA-3 AS A NEW CANDIDATE GENE INVOLVED IN THE PROGRESSION OF IDIOPATHIC PULMONARY FIBROSIS". test, 45, 2, 2022, 1109-1119. doi: 10.21608/bfsa.2022.271824
Hamdi, E., Abdelrehim, A., Higazi, A., Ahmed, A., Thabet, K. (2022). 'INTERFERON LAMBDA-3 AS A NEW CANDIDATE GENE INVOLVED IN THE PROGRESSION OF IDIOPATHIC PULMONARY FIBROSIS', test, 45(2), pp. 1109-1119. doi: 10.21608/bfsa.2022.271824
Hamdi, E., Abdelrehim, A., Higazi, A., Ahmed, A., Thabet, K. INTERFERON LAMBDA-3 AS A NEW CANDIDATE GENE INVOLVED IN THE PROGRESSION OF IDIOPATHIC PULMONARY FIBROSIS. test, 2022; 45(2): 1109-1119. doi: 10.21608/bfsa.2022.271824

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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