Article
Biotechnology & Applied Microbiology
Meizhu Chen, Xueping Huang, Minzhao Gao, Zhipeng Yang, Zhaoxiong Fang, Jinqi Wei, Baihe Wu
Summary: This study found that H. pylori infection and VacA treatment promote the secretion of inflammatory factors through the NF-kappa B signaling pathway and induce lung injury. In both in vivo and in vitro models, VacA treatment inhibits cell proliferation, promotes cell apoptosis, and increases phosphorylation of NF-kappa B protein.
Article
Pharmacology & Pharmacy
Yan Wang, Mengling Liao, Yu Zhang, Fei Deng, Jing Luo, Nuoyan Wang, Min Liu, Lin Ao, Qimei Fang, Qingchun Wang, Hong Zhou
Summary: The study demonstrated that artesunate has immunomodulatory effects on hydrocortisone-induced immunosuppression, enhancing bacterial clearance ability and increasing inflammatory response. Artesunate's effect is related to the improvement of the TLR4/NF-kappa B signal transduction pathway by inhibiting the upregulation of GILZ mRNA. Further investigation into the immunomodulatory effects of artesunate is warranted.
EUROPEAN JOURNAL OF PHARMACOLOGY
(2021)
Article
Cell Biology
Gina M. Gallucci, Bader Alsuwayt, Adam M. Auclair, James L. Boyer, David N. Assis, Nisanne S. Ghonem
Summary: Fenofibrate has anti-inflammatory effects in chronic liver diseases by inhibiting NF-kappa B signaling and reducing the secretion of pro-inflammatory cytokines.
Article
Biochemistry & Molecular Biology
Britta Marko, Paulina Heurich, Patrick Thon, Frieda Zimmer, Lars Bergmann, Hartmuth Nowak, Katharina Rump, Bjorn Koos, Michael Adamzik, Matthias Unterberg, Tim Rahmel
Summary: The NF-kappa B1 promoter polymorphism (-94ins/delATTG) is functionally important and plays a significant role in inflammation and sepsis. This study found that individuals with the deletion allele of this polymorphism exhibited lower nuclear activity of subunit p50, leading to aggravated inflammation and mitochondrial dysfunction.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Biochemistry & Molecular Biology
Panagiotis Theofilis, Marios Sagris, Evangelos Oikonomou, Alexios S. Antonopoulos, Gerasimos Siasos, Costas Tsioufis, Dimitris Tousoulis
Summary: Maintenance of endothelial cell integrity is crucial for human health, as dysfunction can lead to various diseases. Activated and injured endothelial cells release inflammatory mediators and enter a pro-thrombotic state, ultimately promoting atherosclerosis progression. Various pathways and mechanisms contribute to endothelial dysfunction, highlighting the complexity of this process.
Article
Biochemistry & Molecular Biology
Paola Galozzi, Ola Negm, Sara Bindoli, Patrick Tighe, Paolo Sfriso, Leonardo Punzi
Summary: This study aimed to increase understanding of the inflammatory pathways in the development of monogenic autoinflammatory diseases (mAIDs). The researchers evaluated signaling pathways and inflammatory mediators in mAIDs patients and observed upregulation of multiple intermediates in the signaling pathways, as well as differences in cytokine and chemokine levels between patients with different diseases. These findings suggest ongoing subclinical inflammation and define an elevated inflammatory cytokine signature. The activation of Th17-related cytokines also highlights the important role of Th17 and/or Th17-like cells in mAIDs.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Immunology
Daniel Arthur Corpuz Fisher, Jared Scott Fowles, Amy Zhou, Stephen Tracy Oh
Summary: Myeloid neoplasms such as AML, MPNs, and MDS involve clonal dominance and remodeling of bone marrow niche leading to malignant hematopoiesis. Inflammatory signaling hyperactivation and cytokine overproduction play critical roles, with cytokines like TNF potentially contributing to malignant clonal dominance. Targeting cytokine-mediated signaling may be a promising therapeutic strategy.
FRONTIERS IN IMMUNOLOGY
(2021)
Article
Multidisciplinary Sciences
Huibin Yu, Chen Peng, Chi Zhang, Ana M. M. Stoian, Loubna Tazi, Greg Brennan, Stefan Rothenburg
Summary: This study investigates the interaction between the Myxoma virus and the host protein kinase R (PKR). The results show that the MYXV M156 protein inhibits PKR in brush rabbits more strongly than in European rabbits. The moderate inhibition of PKR in European rabbits leads to the activation of the proinflammatory nuclear factor kappa B (NF-kappa B) pathway, which may contribute to the increased virulence of MYXV in European rabbits.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2022)
Article
Endocrinology & Metabolism
Zahirrah BM. Rasheed, Yun S. S. Lee, Sung H. H. Kim, Tg Teoh, David A. A. MacIntyre, Phillip R. R. Bennett, Lynne Sykes
Summary: The study found that 15dPGJ2 has differential effects on inflammatory modulation depending on cell type, and is therefore unlikely to be a useful therapeutic agent for the prevention of preterm birth.
FRONTIERS IN ENDOCRINOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Bulbul Ahmed, Hongwei Si
Summary: The study revealed that aging adipocytes chronologically accumulated lipids and increased pro-inflammatory markers such as interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-alpha (TNF-alpha); at the same time, NF-kappa B p50 markers were also increased while I kappa B alpha protein was decreased significantly in conditioned medium.
Article
Pharmacology & Pharmacy
Priscilla Natalia, Julia Zwirchmayr, Ieva Rudzionyte, Alexandra Pulsinger, Johannes M. Breuss, Pavel Uhrin, Judith M. Rollinger, Rainer de Martin
Summary: Based on scientific research and traditional use, this study investigated the anti-inflammatory potential of red sandalwood in IL-1 stimulated endothelial cells. The results showed that red sandalwood extract can suppress the induction of molecules that mediate leukocyte adhesion to the endothelium, while stimulating the activation of the JNK signaling pathway. Gene expression profiling revealed that red sandalwood extract selectively inhibits certain IL-1 induced genes and stimulates the expression of negative regulatory genes.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Pharmacology & Pharmacy
Wei Liu, Yanghui Ou, Yumeng Yang, Xuemei Zhang, Liqi Huang, Xiaohua Wang, Buling Wu, Mingcheng Huang
Summary: The study demonstrated that punicalagin has a protective effect on HUVECs activation through an endothelial-mediated mechanism, which may be used in the treatment of various disorders such as cancer, rheumatoid arthritis, and cardiovascular disease. This effect is achieved by reducing adhesion of monocyte cells to HUVECs, decreasing expression of ICAM-1 and VCAM-1, and inhibiting permeability, proliferation, migration, and tube formation in VEGF-induced HUVECs. Additionally, punicalagin suppresses IKK-mediated activation of NF-kappa B signaling and inhibits VEGFR2 activation and downstream p-PAK1.
FRONTIERS IN PHARMACOLOGY
(2021)
Article
Neurosciences
Philippa Malko, Xiaoling Jia, Ian Wood, Lin-Hua Jiang
Summary: Microglial cell function and inflammation are regulated by the activation of Piezo1 channel. This study found that the activation of Piezo1 channel can inhibit the pro-inflammatory activation and production of pro-inflammatory cytokines in microglial cells by initiating intracellular Ca2+ signaling to inhibit the NF-kappa B inflammatory signaling pathway.
Article
Biochemistry & Molecular Biology
Rakhee K. Ramakrishnan, Khuloud Bajbouj, Maha Guimei, Surendra Singh Rawat, Zaina Kalaji, Mahmood Y. Hachim, Bassam Mahboub, Saleh M. Ibrahim, Rifat Hamoudi, Rabih Halwani, Qutayba Hamid
Summary: Subepithelial fibrosis is a characteristic feature of airway remodeling in asthma, and current medications have limited effectiveness in treating fibrosis. The study shows that Bcl10-mediated NF-κB activation is elevated in severe asthmatic bronchial fibroblasts, and is associated with an increased expression of pro-fibrotic cytokines induced by lipopolysaccharide (LPS). Inhibition of the Bcl10-mediated NF-κB pathway shows potential in ameliorating inflammation and fibrosis in severe asthma.
Article
Medicine, Research & Experimental
Ling Lin, Shuyi Chen, Hua Wang, Bin Gao, Bhaskar Kallakury, Krithika Bhuvaneshwar, Katherine Cahn, Yuriy Gusev, Xue Wang, Yunan Wu, John L. Marshall, Xiuling Zhi, Aiwu Ruth He
Summary: This study found that the loss of SPTBN1 in HCC cells leads to an increase in pro-inflammatory cytokines, further affecting the activation of the NF-kappa B pathway, promoting the formation and development of liver cancer. The loss of SPTBN1 can affect the inflammatory response and tumor development of HCC cells by regulating the SOCS1/p65 pathway.