The intracellular pathway of Janus kinase/signal transducer and activator of transcription (JAK/STAT) and modification of nucleosome histone marks regulate the expression of proinflammatory mediators, playing an essential role in carcinogenesis, antiviral immunity and the interaction of host proteins with Herpesviral particles. The pathway has also been suggested to play a vital role in the clinical course of the acute infection caused by severe acute respiratory syndrome coronavirus type 2 (SARS‑CoV‑2; known as coronavirus infection‑2019), a novel human coronavirus initially identified in the central Chinese city Wuhan towards the end of 2019, which evolved into a pandemic affecting nearly two million people worldwide. The infection mainly manifests as fever, cough, myalgia and pulmonary involvement, while it also attacks multiple viscera, such as the liver. The pathogenesis is characterized by a cytokine storm, with an overproduction of proinflammatory mediators. Innate and adaptive host immunity against the viral pathogen is exerted by various effectors and is regulated by different signaling pathways notably the JAK/STAT. The elucidation of the underlying mechanism of the regulation of mediating factors expressed in the viral infection would assist diagnosis and antiviral targeting therapy, which will help overcome the infection caused by SARS‑CoV‑2.
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http://dx.doi.org/10.3892/mmr.2024.13163 | DOI Listing |
Ecotoxicol Environ Saf
January 2025
NHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, Jilin 130021, PR China. Electronic address:
Exposure of PM2.5 can cause different degrees of lung injury, which is referred with inflammatory response. Some evidences showed that low-dose radiation (LDR) induces hormesis in immune, however, it is unknown if LDR ameliorates the PM2.
View Article and Find Full Text PDFEcotoxicol Environ Saf
January 2025
Department of Occupational Health and Environment Health, School of Public Health, Anhui Medical University, Hefei 230032, China. Electronic address:
A mounting number of studies have been documenting strong pro-inflammatory and pro-fibrotic effects of carbon nanotube (CNT). However, the molecular mechanisms of single-walled CNT (SWCNT)-provoked lung injury remain to be elucidated. Here, we established a mice model of SWCNT-induced lung injury by intratracheal instillation and found that C5a-C5a receptor-1 (C5aR1) signaling was significantly activated along with abundant neutrophils recruitment in lungs at early phase post SWCNT administration, which were positively correlated with early lung inflammation and late pulmonary fibrosis.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Department of Geriatric Medicine, Qilu Hospital of Shandong University, Shandong University, Jinan, Shandong Province, China. Electronic address:
Cytokine storm is a life-threatening systemic hyper-inflammatory state caused by different etiologies, in which the bulk production of pro-inflammatory cytokines from activated macrophages has a central role. Integrated stress response (ISR) comprises several protective signaling pathways, leading to phosphorylation of eukaryotic initiation factor 2α (eIF2α) and repression of protein translation. Emerging evidence suggests that ISR induction may elicit anti-inflammatory effects.
View Article and Find Full Text PDFTransl Stroke Res
January 2025
Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, 6431 Fannin Street, Houston, TX, 77030, USA.
The role of chromatin biology and epigenetics in disease progression is gaining increasing recognition. Genes that escape X chromosome inactivation (XCI) can impact neuroinflammation through epigenetic mechanisms. Our previous study has suggested that the X escapee genes Kdm6a and Kdm5c are involved in microglial activation after stroke in aged mice.
View Article and Find Full Text PDFInflammation
January 2025
Department of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
Microglia-mediated neuroinflammation plays a crucial role in multiple neurological diseases. We have previously found that Atglistatin, the mouse Adipose Triglyceride Lipase (ATGL) inhibitor, could promote lipid droplets (LDs) accumulation and suppress LPS-induced neuroinflammation in mouse microglia. However, Atglistatin was species-selective, which limited its use in clinical settings.
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