Oxidative Stress and Inflammation, 2nd Volume

Topic Information

Dear Colleagues,

Oxidative stress is viewed as an imbalance between the production of reactive oxygen species (ROS) and their elimination by protective mechanisms, which can lead to chronic inflammation. The incorrect lifestyle and the intake of external unhealthy chemicals are the major causes of age-related chronic diseases and cancer. Their study includes diseases pathology pathway, lifestyle, treatment, protection, and prevention of oxidative stress and inflammation. ROS are normally produced within the body in limited amount and are essential compounds involved in the regulation of processes capable of maintaining cell homeostasis and functions (signal transduction, gene expression, and activation of receptors). This imbalance may cause oxidative stress, which can lead to lipid peroxidation, gene mutation, inflammation and other complications. The harmful oxidative activity of ROS can be counteracted only by antioxidant/anti-inflammatory compounds, which may be both synthetic and natural, but are often characterized by several stability issues, such as poor water solubility and low bioavailability, that compromise their in vivo activities. The research papers of this Topic are looked forward to providing an overview of the status of research on both natural and synthetic products with antioxidant properties and capable of counteracting inflammatory diseases, including, but not necessarily restricted to, chemical compounds synthetic or of natural origin, vitamins, peptides, micronutrients, non-starch polysaccharides, probiotics, postbiotics, prebiotics formulations containing functional foods or nutraceutical or cosmeceutical products and their innovative oral, systemic or topical delivery capable to overcome their stability issues.

Dr. Maria Letizia Manca
Dr. Amparo Nacher
Dr. Mohamad Allaw
Dr. Matteo Perra
Dr. Ines Castangia
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biomedicines biomedicines	4.7	3.7	2013	15.4 Days	CHF 2600	Submit
Cells cells	6.0	9.0	2012	16.6 Days	CHF 2700	Submit
International Journal of Molecular Sciences ijms	5.6	7.8	2000	16.3 Days	CHF 2900	Submit
Life life	3.2	2.7	2011	17.5 Days	CHF 2600	Submit
Oxygen oxygen	-	-	2021	22.7 Days	CHF 1000	Submit

MDPI Topics is cooperating with Preprints.org and has built a direct connection between MDPI journals and Preprints.org. Authors are encouraged to enjoy the benefits by posting a preprint at Preprints.org prior to publication:

1. Immediately share your ideas ahead of publication and establish your research priority;
2. Protect your idea from being stolen with this time-stamped preprint article;
3. Enhance the exposure and impact of your research;
4. Receive feedback from your peers in advance;
5. Have it indexed in Web of Science (Preprint Citation Index), Google Scholar, Crossref, SHARE, PrePubMed, Scilit and Europe PMC.

Published Papers (4 papers)

Order results

Content type Publication Date

Result details

Normal Extended Compact

Journals

All Biomedicines Cells IJMS Life Oxygen

Show export options expand_more Show export options expand_less

Select all

Export citation of selected articles as:

Plain Text BibTeX BibTeX (without abstracts) Endnote Endnote (without abstracts) Tab-delimited RIS

Error

Oops... you haven't selected anything for export.

Ok

clear

attachment

Supplementary material:
Supplementary File 1 (ZIP, 39 KiB)

24 pages, 5974 KiB  

Open AccessArticle

Human Macrophages Activate Bystander Neutrophils’ Metabolism and Effector Functions When Challenged with Mycobacterium tuberculosis

by Dearbhla M. Murphy, Anastasija Walsh, Laura Stein, Andreea Petrasca, Donal J. Cox, Kevin Brown, Emily Duffin, Gráinne Jameson, Sarah A. Connolly, Fiona O’Connell, Jacintha O’Sullivan, Sharee A. Basdeo, Joseph Keane and James J. Phelan

Int. J. Mol. Sci. 2024, 25(5), 2898; https://doi.org/10.3390/ijms25052898 - 01 Mar 2024

Viewed by 1312

Abstract

Neutrophils are dynamic cells, playing a critical role in pathogen clearance; however, neutrophil infiltration into the tissue can act as a double-edged sword. They are one of the primary sources of excessive inflammation during infection, which has been observed in many infectious diseases [...] Read more.

Neutrophils are dynamic cells, playing a critical role in pathogen clearance; however, neutrophil infiltration into the tissue can act as a double-edged sword. They are one of the primary sources of excessive inflammation during infection, which has been observed in many infectious diseases including pneumonia and active tuberculosis (TB). Neutrophil function is influenced by interactions with other immune cells within the inflammatory lung milieu; however, how these interactions affect neutrophil function is unclear. Our study examined the macrophage–neutrophil axis by assessing the effects of conditioned medium (MΦ-CM) from primary human monocyte-derived macrophages (hMDMs) stimulated with LPS or a whole bacterium (Mycobacterium tuberculosis) on neutrophil function. Stimulated hMDM-derived MΦ-CM boosts neutrophil activation, heightening oxidative and glycolytic metabolism, but diminishes migratory potential. These neutrophils exhibit increased ROS production, elevated NET formation, and heightened CXCL8, IL-13, and IL-6 compared to untreated or unstimulated hMDM-treated neutrophils. Collectively, these data show that MΦ-CM from stimulated hMDMs activates neutrophils, bolsters their energetic profile, increase effector and inflammatory functions, and sequester them at sites of infection by decreasing their migratory capacity. These data may aid in the design of novel immunotherapies for severe pneumonia, active tuberculosis and other diseases driven by pathological inflammation mediated by the macrophage–neutrophil axis. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)

►▼ Show Figures

Figure 1

attachment

Supplementary material:
Supplementary File 1 (ZIP, 483 KiB)

22 pages, 18029 KiB  

Open AccessArticle

Reactive Oxygen Species-Dependent Activation of EGFR/Akt/p38 Mitogen-Activated Protein Kinase and JNK1/2/FoxO1 and AP-1 Pathways in Human Pulmonary Alveolar Epithelial Cells Leads to Up-Regulation of COX-2/PGE₂ Induced by Silica Nanoparticles

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

Biomedicines 2023, 11(10), 2628; https://doi.org/10.3390/biomedicines11102628 - 25 Sep 2023

Viewed by 1096

Abstract

The risk of lung exposure to silica nanoparticles (SiNPs) and related lung inflammatory injury is increasing with the wide application of SiNPs in a variety of industries. A growing body of research has revealed that cyclooxygenase (COX)-2/prostaglandin E₂ (PGE₂) up-regulated [...] Read more.

The risk of lung exposure to silica nanoparticles (SiNPs) and related lung inflammatory injury is increasing with the wide application of SiNPs in a variety of industries. A growing body of research has revealed that cyclooxygenase (COX)-2/prostaglandin E₂ (PGE₂) up-regulated by SiNP toxicity has a role during pulmonary inflammation. The detailed mechanisms underlying SiNP-induced COX-2 expression and PGE₂ synthesis remain unknown. The present study aims to dissect the molecular components involved in COX-2/PGE₂ up-regulated by SiNPs in human pulmonary alveolar epithelial cells (HPAEpiCs) which are one of the major targets while SiNPs are inhaled. In the present study, we demonstrated that SiNPs induced COX-2 expression and PGE₂ release, which were inhibited by pretreatment with a reactive oxygen species (ROS) scavenger (edaravone) or the inhibitors of proline-rich tyrosine kinase 2 (Pyk2, PF-431396), epidermal growth factor receptor (EGFR, AG1478), phosphatidylinositol 3-kinase (PI3K, LY294002), protein kinase B (Akt, Akt inhibitor VIII), p38 mitogen-activated protein kinase (MAPK) (p38 MAPK inhibitor VIII), c-Jun N-terminal kinases (JNK)1/2 (SP600125), Forkhead Box O1 (FoxO1, AS1842856), and activator protein 1 (AP-1, Tanshinone IIA). In addition, we also found that SiNPs induced ROS-dependent Pyk2, EGFR, Akt, p38 MAPK, and JNK1/2 activation in these cells. These signaling pathways induced by SiNPs could further cause c-Jun and FoxO1 activation and translocation from the cytosol to the nucleus. AP-1 and FoxO1 activation could increase COX-2 and PGE₂ levels induced by SiNPs. Finally, the COX-2/PGE₂ axis might promote the inflammatory responses in HPAEpiCs. In conclusion, we suggested that SiNPs induced COX-2 expression accompanied by PGE₂ synthesis mediated via ROS/Pyk2/EGFR/PI3K/Akt/p38 MAPK- and JNK1/2-dependent FoxO1 and AP-1 activation in HPAEpiCs. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)

►▼ Show Figures

Figure 1

attachment

Supplementary material:
Supplementary File 1 (ZIP, 133 KiB)

13 pages, 7445 KiB  

Open AccessArticle

Chlorogenic Acid Alleviates LPS-Induced Inflammation and Oxidative Stress by Modulating CD36/AMPK/PGC-1α in RAW264.7 Macrophages

by Tiantian Gu, Zhiguo Zhang, Jinyu Liu, Li Chen, Yong Tian, Wenwu Xu, Tao Zeng, Weicheng Wu and Lizhi Lu

Int. J. Mol. Sci. 2023, 24(17), 13516; https://doi.org/10.3390/ijms241713516 - 31 Aug 2023

Cited by 3 | Viewed by 1239

Abstract

Chlorogenic acid (CGA) is a bioactive substance with anti-inflammatory activities. Clusters of CD36 have been suggested to be widely involved in inflammatory damage. However, the mechanism of CGA protecting against LPS-induced inflammation involving the CD36 regulation is unclear. Here, we demonstrated that CGA [...] Read more.

Chlorogenic acid (CGA) is a bioactive substance with anti-inflammatory activities. Clusters of CD36 have been suggested to be widely involved in inflammatory damage. However, the mechanism of CGA protecting against LPS-induced inflammation involving the CD36 regulation is unclear. Here, we demonstrated that CGA protected against LPS-induced cell death and decreased the production of ROS. Moreover, the SOD, CAT, and GSH-Px activities were also upregulated in CGA-treated cells during LPS stimulation. CGA reduced COX-2 and iNOS expression and IL-1β, IL-6, and TNF-α secretion in LPS-stimulated RAW264.7 macrophages. In addition, CGA treatment widely involved in immune-related signaling pathways, including NF-κB signaling, NOD-like receptor signaling, and IL-17 signaling using transcriptomic analysis and CD36 also markedly reduced during CGA pretreatment in LPS-induced RAW264.7 cells. Furthermore, the CD36 inhibitor SSO attenuated inflammation and oxidative stress by enabling activation of the AMPK/PGC-1α cascade. These results indicate that CGA might provide benefits for the regulation of inflammatory diseases by modulating CD36/AMPK/PGC-1α to alleviate oxidative stress. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)

►▼ Show Figures

Figure 1

16 pages, 1024 KiB  

Open AccessReview

Antioxidant Therapy as an Effective Strategy against Noise-Induced Hearing Loss: From Experimental Models to Clinic

by Anna Pisani, Fabiola Paciello, Raffaele Montuoro, Rolando Rolesi, Jacopo Galli and Anna Rita Fetoni

Life 2023, 13(4), 1035; https://doi.org/10.3390/life13041035 - 17 Apr 2023

Cited by 2 | Viewed by 3449

Abstract

Cochlear redox unbalance is the main mechanism of damage involved in the pathogenesis of noise-induced-hearing loss. Indeed, the increased free radical production, in conjunction with a reduced efficacy of the endogenous antioxidant system, plays a key role in cochlear damage induced by noise [...] Read more.

Cochlear redox unbalance is the main mechanism of damage involved in the pathogenesis of noise-induced-hearing loss. Indeed, the increased free radical production, in conjunction with a reduced efficacy of the endogenous antioxidant system, plays a key role in cochlear damage induced by noise exposure. For this reason, several studies focused on the possibility to use exogenous antioxidant to prevent or attenuate noise-induce injury. Thus, several antioxidant molecules, alone or in combination with other compounds, have been tested in both experimental and clinical settings. In our findings, we tested the protective effects of several antioxidant enzymes, spanning from organic compounds to natural compounds, such as nutraceuticals of polyphenols. In this review, we summarize and discuss the strengths and weaknesses of antioxidant supplementation focusing on polyphenols, Q-Ter, the soluble form of CoQ10, Vitamin E and N-acetil-cysteine, which showed great otoprotective effects in different animal models of noise induced hearing loss and which has been proposed in clinical trials. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)

►▼ Show Figures

Graphical abstract

Show export options expand_more Show export options expand_less

Select all

Export citation of selected articles as:

Plain Text BibTeX BibTeX (without abstracts) Endnote Endnote (without abstracts) Tab-delimited RIS

 

Error

Oops... you haven't selected anything for export.

Ok

clear

Displaying articles 1-4