From the perspective of epidemiology, viral immunology and current clinical research, pulmonary fibrosis may become one of the complications of patients with Coronavirus Disease 2019 (COVID-19). Cytokine storm is a major cause of new coronavirus death. The purpose of this study was to explore the effects of antiviral drug arbidol on cytokine storm and pulmonary fibrosis. Here, we use a mouse model of bleomycin-induced pulmonary fibrosis and a mouse model of fecal dilution-induced sepsis to evaluate the effects of arbidol on pulmonary fibrosis and cytokine storm. The results showed that arbidol significantly reduced the area of pulmonary fibrosis and improved lung function (reduced inspiratory resistance, lung dynamic compliance and forced vital capacity increased). Treatment with arbidol promoted reduced sepsis severity 48 h after sepsis induction, based on weight, murine sepsis score and survival rate. Arbidol observably alleviates inflammatory infiltrates and injury in the lungs and liver. Finally, we also found that arbidol reduced serum levels of pro-inflammatory factors such as TNF-α and IL-6 induced by fecal dilution. In conclusion, our results indicate that arbidol can alleviate the severity of pulmonary fibrosis and sepsis, and provide some reference for the treatment of cytokine storm and sequelae of pulmonary fibrosis in patients with COVID-19.
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http://dx.doi.org/10.3389/fphar.2020.607075 | DOI Listing |
Pharmaceutics
January 2025
School of Pharmacy, Queen's University Belfast, Belfast BT9 7BL, UK.
This paper presents a comprehensive review of the current literature, clinical trials, and products approved for the delivery of antibiotics to the lungs. While there are many literature reports describing potential delivery systems, few of these have translated into marketed products. Key challenges remaining are the high doses required and, for powder formulations, the ability of the inhaler and powder combination to deliver the dose to the correct portion of the respiratory tract for maximum effect.
View Article and Find Full Text PDFPathogens
January 2025
Division of Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.
The lung is a vital organ for the body as the main source of oxygen input. Importantly, it is also an internal organ that has direct contact with the outside world. Innate immunity is a vital protective system in various organs, whereas, in the case of the lung, it helps maintain a healthy, functioning cellular and molecular environment and prevents any overt damage caused by pathogens or other inflammatory processes.
View Article and Find Full Text PDFJ Clin Med
January 2025
2nd Pulmonary Department, General University Hospital "Attikon", Medical School, National and Kapodistrian University of Athens, 12462 Athens, Greece.
: Long-term lung sequelae in severe COVID-19 survivors, as well as their treatment, are poorly described in the current literature. : To investigate lung fibrotic sequelae in survivors of severe/critical COVID-19 pneumonia and their fate according to a "non-interventional" approach. : Prospective study of the above COVID-19 survivors after hospital discharge from March 2020 to October 2022.
View Article and Find Full Text PDFLife (Basel)
January 2025
Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, Italy.
Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease with a median survival of 3-5 years. Antifibrotic therapies like pirfenidone and nintedanib slow progression, but the outcomes vary. Gender may influence disease presentation, progression, and response to treatment.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Institute of Biomedicine & Department of Cell Biology, College of Life Science and Technology, Jinan University, Guangzhou 510632, China.
Following the COVID-19 pandemic, the prevalence of pulmonary fibrosis has increased significantly, placing patients at higher risk and presenting new therapeutic challenges. Current anti-fibrotic drugs, such as Nintedanib, can slow the decline in lung function, but their severe side effects highlight the urgent need for safer and more targeted alternatives. This study explores the anti-fibrotic potential and underlying mechanisms of an endogenous peptide (P5) derived from fibroblast growth factor 2 (FGF2), developed by our research team.
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