LPS-Induced Acute Lung Injury: Analysis of the Development and Suppression by the TNF-α-Targeting Aptamer

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Abstract

Acute lung injury (ALI) is a specific form of lung inflammation characterized by diffuse alveolar damage, noncardiogenic pulmonary edema, as well as a pulmonary and systemic inflammation. The pathogenesis of ALI involves a cascade inflammatory response accompanied by an increase in the local and systemic levels of proinflammatory cytokines and chemokines. The development of molecular tools targeting key components of cytokine signaling appears to be a promising approach in ALI treatment. The development of lipopolysaccharide (LPS)-induced ALI, as well as the feasibility of suppressing it by an aptamer targeting the proinflammatory cytokine TNF-α, was studied in a mouse model. The TNF-α level was shown to increase significantly and remain steadily high during the development of ALI. LPS-induced morphological signs of inflammation in the respiratory system become most pronounced 24 h after induction. Intranasal administration of TNF-α-targeting aptamers conjugated with polyethylene glycol (PEG-aptTNF-α) to mice with ALI reduced the intensity of inflammatory changes in lung tissue. Assessment of the levels of potential TNF-α target genes (Usp18, Traf1, and Tnfaip3) showed that their expression levels in the lungs increase during ALI development, while declining after the application of PEG-aptTNF-α. Therefore, topical use of TNF-α-targeting aptamers may be an efficient tool for treating ALI and other inflammatory lung diseases.

About the authors

A. V. Sen’kova

Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of the Russian Academy of Sciences

Author for correspondence.
Email: alsenko@mail.ru
Russian Federation, Novosibirsk, 630090

I. A. Savin

Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of the Russian Academy of Sciences

Email: alsenko@mail.ru
Russian Federation, Novosibirsk, 630090

E. L. Chernolovskaya

Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of the Russian Academy of Sciences

Email: alsenko@mail.ru
Russian Federation, Novosibirsk, 630090

A. S. Davydova

Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of the Russian Academy of Sciences

Email: alsenko@mail.ru
Russian Federation, Novosibirsk, 630090

M. I. Meschaninova

Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of the Russian Academy of Sciences

Email: alsenko@mail.ru
Russian Federation, Novosibirsk, 630090

A. Bishani

Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of the Russian Academy of Sciences

Email: alsenko@mail.ru
Russian Federation, Novosibirsk, 630090

M. A. Vorobyeva

Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of the Russian Academy of Sciences

Email: alsenko@mail.ru
Russian Federation, Novosibirsk, 630090

M. A. Zenkova

Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of the Russian Academy of Sciences

Email: alsenko@mail.ru
Russian Federation, Novosibirsk, 630090

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Copyright (c) 2024 Sen’kova A.V., Savin I.A., Chernolovskaya E.L., Davydova A.S., Meschaninova M.I., Bishani A., Vorobyeva M.A., Zenkova M.A.

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