Westernized diets and lifestyle are linked to the development of metabolic syndrome, characterized by obesity, type 2 diabetes, and increased cardiovascular disease risk. Systemic low-grade inflammation is a common feature of chronic metabolic disorders and is believed to promote disease progression. Therefore, modulating inflammation is a commonly explored strategy to prevent obesity-associated co-morbidities. In this review, how current knowledge on the recently described concept of innate immune memory could underline metaflammation in the context of metabolic syndrome is explored. It is hoped that these insights provide a new perspective to address the question of innate immune activation during disease progression.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/mnfr.201900480 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
5-FU Weakens Defensive Functions of the Junctional Epithelium.
J Periodontal Res
January 2025
Department of Surgery, Stanford University School of Medicine, Stanford, California, USA.
Aim: To investigate additional factors contributing to the pathophysiology of chemotherapy-induced oral mucositis and periodontitis beyond the systemic immune suppression caused by the chemotherapeutic agent 5-Fluorouracil (5-FU).
Methods: 5-Fluorouracil was topically delivered to the non-keratinized, rapidly proliferating junctional epithelium (JE) surrounding the dentition, and acts as an immunologic and functional barrier to bacterial ingression. Various techniques, including EdU incorporation, quantitative immunohistochemistry (qIHC), histology, enzymatic activity assays, and micro-computed tomographic (μCT) imaging, were employed to analyze the JE at multiple time points following topical 5-FU treatment.
[Advances in the study of viruses inhibiting the production of advanced autophagy or interferon through Rubicon to achieve innate immune escape].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
January 2025
Department of Pathogen Biology and Immunology, Kunming Medical University, Kunming 650500, China. *Corresponding authors, E-mail:
The innate immune response is the first line of defense for the host against viral infections. Targeted degradation of pathogenic microorganisms through autophagy, in conjunction with pattern recognition receptors synergistically inducing the production of interferon (IFN), constitutes an important pathway for the body to resist viral infections. Rubicon, a Run domain Beclin 1-interacting and cysteine-rich domain protein, has an inhibitory effect on autophagy and IFN production.
View Article and Find Full Text PDFEvolution of Omicron lineage towards increased fitness in the upper respiratory tract in the absence of severe lung pathology.
Nat Commun
January 2025
Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.
The emergence of the Omicron lineage represented a major genetic drift in SARS-CoV-2 evolution. This was associated with phenotypic changes including evasion of pre-existing immunity and decreased disease severity. Continuous evolution within the Omicron lineage raised concerns of potential increased transmissibility and/or disease severity.
View Article and Find Full Text PDFExploring the Impact of Interferon-Gamma Single Nucleotide Polymorphisms on HTLV-1 Infection: Unraveling Genetic Influences in Viral Pathogenesis.
Crit Rev Oncol Hematol
January 2025
Department of Haematology, Bayero University Kano and Aminu Kano Teaching Hospital, Kano, Nigeria.
Human T-lymphotropic virus-1 (HTLV-1) induces neoplastic adult T-cell leukemia/lymphoma (ATLL) and neurological HTLV-1 associated myelopathy (HAM) in approximately 3%-5% of infected individuals. The precise factors that facilitate disease manifestation are still unknown; interaction between the virus and the host's immune response is key. Cytokines regulates physiological activities and their dysregulation may initiate the pathogenesis of various malignant and infectious diseases.
View Article and Find Full Text PDFBaicalin ameliorates neuroinflammation by targeting TLR4/MD2 complex on microglia via PI3K/AKT/NF-κB signaling pathway.
Neuropharmacology
January 2025
National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China, The Key Laboratory of Medicinal Resources and Natural Pharmaceutical Chemistry, The Ministry of Education, College of Life Sciences, Shaanxi Normal University, Xi'an, Shaanxi 710119, China. Electronic address:
This study aims to elucidate the target and mechanism of baicalin, a clinically utilized drug, in the treatment of neuroinflammatory diseases. Neuroinflammation, characterized by the activation of glial cells and the release of various pro-inflammatory cytokines, plays a critical role in the pathogenesis of various diseases, including spinal cord injury (SCI). The remission of such diseases is significantly dependent on the improvement of inflammatory microenvironment.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!