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TNF and ROS Crosstalk in Inflammation
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TNF and ROS Crosstalk in Inflammation

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

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 9468

Special Issue Editor

Dr. Takuya Noguchi

E-Mail Website
Guest Editor
Department of Biopharmaceutical Science, Tohoku University, Sendai 980-8578, Japan
Interests: apoptosis; signaling pathways; phosphorylation; signal transduction; cell signaling; reactive oxygen species; molecular cell biology; cell biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Tumor necrosis factor-α (TNF-α) is a representative pro-inflammatory cytokine that contributes to host defense by inducing a wide variety of cellular responses, including cell growth, differentiation, inflammatory responses, and cell death. TNF-α also promotes production of reactive oxygen species (ROS) as second messengers to stimulate ROS-responsive signaling pathways. Conversely, previous studies demonstrated that signalling mechanisms activated by ROS upregulates the expression of TNF-α. Accumulating evidence indicates the involvement of intricate crosstalk between TNF-α and ROS in the pathological process of inflammatory diseases and cancer. Therefore, uncovering the molecular mechanisms of the crosstalk between TNF-α and ROS would lead to a better understanding of the pathogenetic mechanisms of TNF-α- and ROS-related diseases, which may be one of the strategies to overcome these diseases. In this Special Issue, studies of novel signalling mechanisms and pathological process mediated by TNF-α and ROS are welcome.

Dr. Takuya Noguchi
Guest Editor

Manuscript Submission Information

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Published Papers (3 papers)

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Research

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24 pages, 5558 KiB  
Article
ROS/TNF-α Crosstalk Triggers the Expression of IL-8 and MCP-1 in Human Monocytic THP-1 Cells via the NF-κB and ERK1/2 Mediated Signaling
by Nadeem Akhter, Ajit Wilson, Reeby Thomas, Fatema Al-Rashed, Shihab Kochumon, Areej Al-Roub, Hossein Arefanian, Ashraf Al-Madhoun, Fahd Al-Mulla, Rasheed Ahmad and Sardar Sindhu
Int. J. Mol. Sci. 2021, 22(19), 10519; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910519 - 29 Sep 2021
Cited by 33 | Viewed by 3826
Abstract
IL-8/MCP-1 act as neutrophil/monocyte chemoattractants, respectively. Oxidative stress emerges as a key player in the pathophysiology of obesity. However, it remains unclear whether the TNF-α/oxidative stress interplay can trigger IL-8/MCP-1 expression and, if so, by which mechanism(s). IL-8/MCP-1 adipose expression was detected in [...] Read more.
IL-8/MCP-1 act as neutrophil/monocyte chemoattractants, respectively. Oxidative stress emerges as a key player in the pathophysiology of obesity. However, it remains unclear whether the TNF-α/oxidative stress interplay can trigger IL-8/MCP-1 expression and, if so, by which mechanism(s). IL-8/MCP-1 adipose expression was detected in lean, overweight, and obese individuals, 15 each, using immunohistochemistry. To detect the role of reactive oxygen species (ROS)/TNF-α synergy as a chemokine driver, THP-1 cells were stimulated with TNF-α, with/without H2O2 or hypoxia. Target gene expression was measured by qRT-PCR, proteins by flow cytometry/confocal microscopy, ROS by DCFH-DA assay, and signaling pathways by immunoblotting. IL-8/MCP-1 adipose expression was significantly higher in obese/overweight. Furthermore, IL-8/MCP-1 mRNA/protein was amplified in monocytic cells following stimulation with TNF-α in the presence of H2O2 or hypoxia (p ˂ 0.0001). Synergistic chemokine upregulation was related to the ROS levels, while pre-treatments with NAC suppressed this chemokine elevation (p ≤ 0.01). The ROS/TNF-α crosstalk involved upregulation of CHOP, ERN1, HIF1A, and NF-κB/ERK-1,2 mediated signaling. In conclusion, IL-8/MCP-1 adipose expression is elevated in obesity. Mechanistically, ROS/TNF-α crosstalk may drive expression of these chemokines in monocytic cells by inducing ER stress, HIF1A stabilization, and signaling via NF-κB/ERK-1,2. NAC had inhibitory effect on oxidative stress-driven IL-8/MCP-1 expression, which may have therapeutic significance regarding meta-inflammation. Full article
(This article belongs to the Special Issue TNF and ROS Crosstalk in Inflammation)
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19 pages, 4278 KiB  
Article
Intestinal SIRT1 Deficiency-Related Intestinal Inflammation and Dysbiosis Aggravate TNFα-Mediated Renal Dysfunction in Cirrhotic Ascitic Mice
by Yu-Te Chou, Tze-Tze Liu, Ueng-Cheng Yang, Chia-Chang Huang, Chih-Wei Liu, Shiang-Fen Huang, Tzu-Hao Li, Hsuan-Miao Liu, Ming-Wei Lin, Ying-Ying Yang, Tzung-Yan Lee, Yi-Hsiang Huang, Ming-Chih Hou and Han-Chieh Lin
Int. J. Mol. Sci. 2021, 22(3), 1233; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031233 - 27 Jan 2021
Cited by 10 | Viewed by 2248
Abstract
In advanced cirrhosis, the TNFα-mediated intestinal inflammation and bacteria dysbiosis are involved in the development of inflammation and vasoconstriction-related renal dysfunction. In colitis and acute kidney injury models, activation of SIRT1 attenuates the TNFα-mediated intestinal and renal abnormalities. This study explores the impacts [...] Read more.
In advanced cirrhosis, the TNFα-mediated intestinal inflammation and bacteria dysbiosis are involved in the development of inflammation and vasoconstriction-related renal dysfunction. In colitis and acute kidney injury models, activation of SIRT1 attenuates the TNFα-mediated intestinal and renal abnormalities. This study explores the impacts of intestinal SIRT1 deficiency and TNFα-mediated intestinal abnormalities on the development of cirrhosis-related renal dysfunction. Systemic and renal hemodynamics, intestinal dysbiosis [cirrhosis dysbiosis ratio (CDR) as marker of dysbiosis], and direct renal vasoconstrictive response (renal vascular resistance (RVR) and glomerular filtration rate (GFR)) to cumulative doses of TNFα were measured in bile duct ligated (BDL)-cirrhotic ascitic mice. In SIRT1IEC-KO-BDL-ascitic mice, the worsening of intestinal dysbiosis exacerbates intestinal inflammation/barrier dysfunction, the upregulation of the expressions of intestinal/renal TNFα-related pathogenic signals, higher TNFα-induced increase in RVR, and decrease in GFR in perfused kidney. In intestinal SIRT1 knockout groups, the positive correlations were identified between intestinal SIRT1 activity and CDR. Particularly, the negative correlations were identified between CDR and RVR, with the positive correlation between CDR and GFR. In mice with advanced cirrhosis, the expression of intestinal SIRT1 is involved in the linkage between intestinal dysbiosis and vasoconstriction/hypoperfusion-related renal dysfunction through the crosstalk between intestinal/renal TNFα-related pathogenic inflammatory signals. Full article
(This article belongs to the Special Issue TNF and ROS Crosstalk in Inflammation)
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Review

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13 pages, 2728 KiB  
Review
Redox Responsive Copolyoxalate Smart Polymers for Inflammation and Other Aging-Associated Diseases
by Berwin Singh Swami Vetha, Angela Guma Adam and Azeez Aileru
Int. J. Mol. Sci. 2021, 22(11), 5607; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22115607 - 25 May 2021
Cited by 3 | Viewed by 2391
Abstract
Polyoxalate (POx) and copolyoxalate (CPOx) smart polymers are topics of interest the field of inflammation. This is due to their drug delivery ability and their potential to target reactive oxygen species (ROS) and to accommodate small molecules such as curcumin, vanilline, and p-Hydroxybenzyl [...] Read more.
Polyoxalate (POx) and copolyoxalate (CPOx) smart polymers are topics of interest the field of inflammation. This is due to their drug delivery ability and their potential to target reactive oxygen species (ROS) and to accommodate small molecules such as curcumin, vanilline, and p-Hydroxybenzyl alcohol. Their biocompatibility, ultra-size tunable characteristics and bioimaging features are remarkable. In this review we discuss the genesis and concept of oxylate smart polymer-based particles and a few innovative systemic delivery methods that is designed to counteract the inflammation and other aging-associated diseases (AADs). First, we introduce the ROS and its role in human physiology. Second, we discuss the polymers and methods of incorporating small molecule in oxalate backbone and its drug delivery application. Finally, we revealed some novel proof of concepts which were proven effective in disease models and discussed the challenges of oxylate polymers. Full article
(This article belongs to the Special Issue TNF and ROS Crosstalk in Inflammation)
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