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New Insights into Oxidative Stress and Inflammation in the Pathophysiology and Treatment of Respiratory Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (31 May 2023) | Viewed by 2803

Special Issue Editor


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Guest Editor
1. Department of Physiology and Functional Explorations, Ambroise Paré and Bicêtre Hospitals, Assistance Publique Hôpitaux de Paris, 92104 Boulogne, France
2. Inserm U1179, University of Paris Saclay (UVSQ), 78000 Versailles, France
Interests: respiratory diseases; Nrf2/keap1-Bach1 signaling; macrophage; physiology; lung; immune regulation; monocyte–macrophage; inflammation; innate immunity; cell biology
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Special Issue Information

Dear Colleagues,

Recently, the importance of the respiratory system and the need for novel therapeutic strategies for respiratory diseases have been highlighted by SARS-CoV-2. The airways are constantly exposed to various inhaled pollutants and microbes, which induce oxidative stress and inflammation. Oxidative stress, known to increase the risk of developing many acute and chronic respiratory diseases, is defined by an imbalance between the production of reactive oxygen species and the capacity of antioxidants to counteract the deleterious effects of oxidants. Normal healthy lungs protect themselves against these oxidants with cellular and extracellular antioxidant defense mechanisms throughout the epithelial lining fluid and tissues. Recently, novel therapeutic targets have been implicated in the prevention, or treatment, of respiratory disease by modulating oxidative stress and inflammation. This Special Issue focuses on different aspects of oxidative stress and inflammation in the pathophysiology and treatment of respiratory diseases in animal models. IJMS is a journal of molecular science; thus, pure clinical studies will not be applicable. However, clinical submissions with biomolecular experiments are welcomed.

Prof. Dr. Marcel Bonay
Guest Editor

Manuscript Submission Information

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Keywords

  • oxidative stress
  • inflammation
  • lung
  • respiratory disease
  • molecular biology
  • infection
  • therapeutic strategies
  • antioxidants
  • innate immunity
  • animal models

Published Papers (1 paper)

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Research

18 pages, 7671 KiB  
Article
Ibrutinib Prevents Acute Lung Injury via Multi-Targeting BTK, FLT3 and EGFR in Mice
by Huanan Rao, Xiaominting Song, Jieting Lei, Peng Lu, Guiying Zhao, Xin Kang, Duanna Zhang, Tingrui Zhang, Yali Ren, Cheng Peng, Yuzhi Li, Jin Pei and Zhixing Cao
Int. J. Mol. Sci. 2022, 23(21), 13478; https://doi.org/10.3390/ijms232113478 - 03 Nov 2022
Cited by 2 | Viewed by 2181
Abstract
Ibrutinib has potential therapeutic or protective effects against viral- and bacterial-induced acute lung injury (ALI), likely by modulating the Bruton tyrosine kinase (BTK) signaling pathway. However, ibrutinib has multi-target effects. Moreover, immunity and inflammation targets in ALI treatment are poorly defined. We investigated [...] Read more.
Ibrutinib has potential therapeutic or protective effects against viral- and bacterial-induced acute lung injury (ALI), likely by modulating the Bruton tyrosine kinase (BTK) signaling pathway. However, ibrutinib has multi-target effects. Moreover, immunity and inflammation targets in ALI treatment are poorly defined. We investigated whether the BTK-, FLT3-, and EGFR-related signaling pathways mediated the protective effects of ibrutinib on ALI. The intratracheal administration of poly I:C or LPS after ibrutinib administration in mice was performed by gavage. The pathological conditions of the lungs were assessed by micro-CT and HE staining. The levels of neutrophils, lymphocytes, and related inflammatory factors in the lungs were evaluated by ELISA, flow cytometry, immunohistochemistry, and immunofluorescence. Finally, the expression of proteins associated with the BTK-, FLT3-, and EGFR-related signaling pathways were evaluated by Western blotting. Ibrutinib (10 mg/kg) protected against poly I:C-induced (5 mg/kg) and LPS-induced (5 mg/kg) lung inflammation. The wet/dry weight ratio (W/D) and total proteins in the bronchoalveolar lavage fluid (BALF) were markedly reduced after ibrutinib (10 mg/kg) treatment, relative to the poly I:C- and LPS-treated groups. The levels of ALI indicators (NFκB, IL-1β, IL-6, TNF-α, IFN-γ, neutrophils, and lymphocytes) were significantly reduced after treatment. Accordingly, ibrutinib inhibited the poly I:C- and LPS-induced BTK-, FLT3-, and EGFR-related pathway activations. Ibrutinib inhibited poly I:C- and LPS-induced acute lung injury, and this may be due to its ability to suppress the BTK-, FLT3-, and EGFR-related signaling pathways. Therefore, ibrutinib is a potential protective agent for regulating immunity and inflammation in poly I:C- and LPS-induced ALI. Full article
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