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Inflammation in Chronic Disease: Molecular Mechanisms and Signaling Pathways

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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: 31 December 2024 | Viewed by 3524

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Dr. Nadia Lampiasi

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Istituto per la Ricerca e l’Innovazione Biomedica (IRIB), Consiglio Nazionale delle Ricereche (CNR), 00185 Rome, Italy
Interests: inflammation; innate immunity; macrophages; mast cells; osteoimmunology
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Dear Colleagues,

Inflammation is a physiological response of the body to various insults, such as pathogens, injuries, toxic compounds, and irradiation. The goal of inflammation is to remove harmful stimuli and damaged cells, and to initiate the healing process to restore tissue homeostasis. It is, therefore, a defense mechanism involving cells of the innate and adaptive immune system, molecules, cytokines, and cellular signals. However, sometimes the stimuli or damaged cells are not removed efficiently and, thus, the inflammation degenerates and becomes chronic, which can contribute to the development of many diseases, including autoimmune diseases, cancer, and nerve disorders. Much progress has been made recently and many molecular mechanisms, cytokines, and pathways involved are now known. By way of example: histamine, prostaglandins, platelet activating factors, leukotrienes, cytokines, oxidative stress, and transcription factors, such as NF-kB, MAPKs signaling, and the JAK-STAT pathway. The role of these components continues to be studied to better define the underlying scenario and the cells involved in inflammation to identify new therapeutic targets that will change the face of medicine in the near future. This Special Issue aims to collect publications on the current understanding of the molecular basis of inflammation and possible therapeutic targets to prevent the development of diseases associated with inflammation.

Dr. Nadia Lampiasi
Guest Editor

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Keywords

inflammation
neuroinflammation
immune response
inflammation-associated disease
inflammation mediators (proteins, enzymes, ecc)
cytokines
macrophages
mast cells
monocytes
dendritic cells
oxidative stress
signaling pathways

Published Papers (3 papers)

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Research

16 pages, 1955 KiB

Open AccessArticle

Upregulation of Notch Signaling and Cell-Differentiation Inhibitory Transcription Factors in Stable Chronic Obstructive Pulmonary Disease Patients

by Antonino Di Stefano, Isabella Gnemmi, Umberto Rosani, Mauro Maniscalco, Silvestro Ennio D’Anna, Paola Brun, Vitina Carriero, Francesca Bertolini, Bruno Balbi and Fabio Luigi Massimo Ricciardolo

Int. J. Mol. Sci. 2024, 25(6), 3287; https://doi.org/10.3390/ijms25063287 - 14 Mar 2024

Viewed by 495

Abstract

Notch signaling is involved in the prevention of cell differentiation and cell fate in various organs, including the lungs. We aimed to determine the transcriptomic and protein expression of Notch receptors, their ligands, and related transcription factors in stable COPD. The expression and localization of Notch receptors, their ligands, and related transcription factors were measured in bronchial biopsies of individuals with stable mild/moderate (MCOPD) (n = 18) or severe/very severe (SCOPD) (n = 16) COPD, control smokers (CSs) (n = 13), and control nonsmokers (CNSs) (n = 11), and in the lung parenchyma of those with MCOPD (n = 13), CSs (n = 10), and CNSs (n = 10) using immunohistochemistry, ELISA tests, and transcriptome analyses. In the bronchial biopsies, Notch4 and HES7 significantly increased in the lamina propria of those with SCOPD compared to those with MCOPD, CSs, and CNSs. In the peripheral lung bronchiolar epithelium, Notch1 significantly increased in those with MCOPD and CSs compared to CNSs. ELISA tests of lung parenchyma homogenates showed significantly increased Notch2 in those with MCOPD compared to CSs and CNSs. Transcriptomic data in lung parenchyma showed increased DLL4 and HES1 mRNA levels in those with MCOPD and CSs compared to CNSs. These data show the increased expression of the Notch pathway in the lungs of those with stable COPD. These alterations may play a role in impairing the regenerative–reparative responses of diseased bronchioles and lung parenchyma. Full article

(This article belongs to the Special Issue Inflammation in Chronic Disease: Molecular Mechanisms and Signaling Pathways)

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22 pages, 6061 KiB

Open AccessArticle

Thrombin-Induced COX-2 Expression and PGE₂ Synthesis in Human Tracheal Smooth Muscle Cells: Role of PKCδ/Pyk2-Dependent AP-1 Pathway Modulation

by Chien-Chung Yang, I-Ta Lee, Yan-Jyun Lin, Wen-Bin Wu, Li-Der Hsiao and Chuen-Mao Yang

Int. J. Mol. Sci. 2023, 24(20), 15130; https://doi.org/10.3390/ijms242015130 - 13 Oct 2023

Cited by 2 | Viewed by 903

Abstract

In this study, we confirmed that thrombin significantly increases the production of COX-2 and PGE₂ in human tracheal smooth muscle cells (HTSMCs), leading to inflammation in the airways and lungs. These molecules are well-known contributors to various inflammatory diseases. Here, we investigated in detail the involved signaling pathways using specific inhibitors and small interfering RNAs (siRNAs). Our results demonstrated that inhibitors targeting proteins such as protein kinase C (PKC)δ, proline-rich tyrosine kinase 2 (Pyk2), c-Src, epidermal growth factor receptor (EGFR), phosphatidylinositol 3-kinase (PI3K), or activator protein-1 (AP-1) effectively reduced thrombin-induced COX-2 and PGE₂ production. Additionally, transfection with siRNAs against PKCδ, Pyk2, c-Src, EGFR, protein kinase B (Akt), or c-Jun mitigated these responses. Furthermore, our observations revealed that thrombin stimulated the phosphorylation of key components of the signaling cascade, including PKCδ, Pyk2, c-Src, EGFR, Akt, and c-Jun. Thrombin activated COX-2 promoter activity through AP-1 activation, a process that was disrupted by a point-mutated AP-1 site within the COX-2 promoter. Finally, resveratrol (one of the most researched natural polyphenols) was found to effectively inhibit thrombin-induced COX-2 expression and PGE₂ release in HTSMCs through blocking the activation of Pyk2, c-Src, EGFR, Akt, and c-Jun. In summary, our findings demonstrate that thrombin-induced COX-2 and PGE₂ generation involves a PKCδ/Pyk2/c-Src/EGFR/PI3K/Akt-dependent AP-1 activation pathway. This study also suggests the potential use of resveratrol as an intervention for managing airway inflammation. Full article

(This article belongs to the Special Issue Inflammation in Chronic Disease: Molecular Mechanisms and Signaling Pathways)

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14 pages, 1654 KiB

Open AccessArticle

High-Intensity Interval Training Ameliorates High-Fat Diet-Induced Metabolic Disorders via the Cyclic GMP-AMP Synthase-Stimulator of Interferon Gene Signaling Pathway

by Zhiwen Hu, Xi Li, Yangjun Yang, Zhe Zhang and Shuzhe Ding

Int. J. Mol. Sci. 2023, 24(18), 13840; https://doi.org/10.3390/ijms241813840 - 08 Sep 2023

Viewed by 1040

Abstract

Metabolic diseases are growing in prevalence worldwide. Although the pathogenesis of metabolic diseases remains ambiguous, the correlation between cyclic GMP-AMP synthase (cGAS)-stimulator of interferon gene (STING) and metabolic diseases has been identified recently. Exercise is an effective intervention protecting against metabolic diseases, however, the role of the cGAS-STING signaling pathway in this process is unclear, and the effect and mechanism of different exercise intensities on metabolic disorders are still unknown. Thus, we explored the association between exercise to ameliorate HFD-induced metabolic disorders and the cGAS-STING signaling pathway and compared the effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT). Male C57BL/6 mice (6–8 weeks old) were fed HFD for 8 weeks to establish a metabolic disease model and were subjected to 8-week MICT or HIIT training. Glucose tolerance tests (GTT) and insulin tolerance tests (ITT) were used to assess glucose metabolism. Serum triglyceride (TG) and total cholesterol (TC) were measured to evaluate lipid metabolism. Oil red staining was used to observe the lipid droplets in the gastrocnemius muscle. An enzyme-linked immunosorbent assay was used to detect the serum inflammatory factors IL-6 and IFN-β. The protein expression of the cGAS-STING signaling pathway was detected by the Wes^TM automatic protein expression analysis system. We reported that HFD induced metabolic disorders with obesity, abnormal glucolipid metabolism, and significant inflammatory responses. Both HIIT and MICT ameliorated the above adverse reactions, but MICT was superior to HIIT in improving glucolipid disorders. Additionally, HIIT significantly increased the expression of STING protein, as well as the phosphorylation of TBKI and the ratio of p-IRF3/IRF3. MICT only increased the expression of STING protein. Our findings suggest that HIIT may alleviate HFD-induced metabolic disorder phenotype through the cGAS-STING signaling pathway. However, the improvement of MICT on metabolic disorder phenotype is less associated with the cGAS-STING pathway, which needs to be further explored. Full article

(This article belongs to the Special Issue Inflammation in Chronic Disease: Molecular Mechanisms and Signaling Pathways)

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