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Repressing cytokine storm-like response in macrophages by targeting the eIF2α-integrated stress response pathway.
Int 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 PDFAssociation of Hyperinflammatory Subphenotype With Code Status De-Escalation in Patients With Acute Respiratory Failure.
CHEST Crit Care
December 2024
Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine (A. C. M., S. M. N., C. S., I. J. B., B. J. M., and G. D. K.), University of Pittsburgh School of Medicine; the Department of Critical Care Medicine (I. J. B., D. B. W., and B. J. M.), University of Pittsburgh School of Medicine; and the Department of Medicine (H. Z.), University of Kentucky.
Diagnostic Challenges and Therapeutic Considerations in Adult-Onset Still's Disease: A Clinical Case Report.
Cureus
November 2024
Diabetes and Endocrinology, United Lincolnshire Hospitals NHS Trust, Boston, GBR.
Adult-onset Still's disease (AOSD) is an uncommon systemic inflammatory disorder that presents with diverse, overlapping symptoms, complicating the diagnostic process due to its nonspecific clinical features and the absence of a definitive diagnostic test. Diagnosis is often challenging and relies on excluding other conditions while maintaining a high index of suspicion, supported by specific diagnostic criteria such as Yamaguchi or Fautrel. Prompt recognition and a multidisciplinary approach are essential, as AOSD can progress to life-threatening multiorgan dysfunction due to a hyperinflammatory response.
View Article and Find Full Text PDFHDAC10 switches NLRP3 modification from acetylation to ubiquitination and attenuates acute inflammatory diseases.
Cell Commun Signal
December 2024
Department of Immunology, School of Basic Medical Sciences, Cheeloo college of Medicine, Shandong University, Jinan, 250012, China.
Background: The NOD-like receptor protein (NLRP)3 inflammasome is at the signaling hub center to instigate inflammation in response to pathogen infection or oxidative stress, and its tight control is pivotal for immune defense against infection while avoiding parallel intensive inflammatory tissue injury. Acetylation of NLRP3 is critical for the full activation of NLRP3 inflammasome, while the precise regulation of the acetylation and deacetylation circuit of NLRP3 protein remained to be fully understood.
Methods: The interaction between histone deacetylase 10 (HDAC10) and NLRP3 was detected by immunoprecipitation and western blot in the HDAC10 and NLRP3 overexpressing cells.
A predictive model for Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis.
Front Immunol
December 2024
Clinical Laboratory, Children's Hospital Affiliated to Shandong University, Jinan, Shandong, China.
Background: Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis (EBV-HLH) is a severe hyperinflammatory disorder induced by overactivation of macrophages and T cells. This study aims to identify the risk factors for the progression from infectious mononucleosis (EBV-IM) to EBV-HLH, by analyzing the laboratory parameters of patients with EBV-IM and EBV-HLH and constructing a clinical prediction model. The outcome of this study carries important clinical value for early diagnosis and treatment of EBV-HLH.
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