Alteration of histone H3 lysine 9 dimethylation in peripheral white blood cells of septic patients with trauma and cancer

Abstract

The present study aimed to investigate the clinical significance of histone methylation in sepsis. A total of 43 blood samples from trauma and esophageal cancer patients with or without sepsis were collected. Immunofluorescence staining of isolated peripheral white blood cells (WBCs) was conducted. Co-stained 293T cells served as a reference, to allow the levels of histone methylation in different types of WBCs from patients to be determined. Immunostaining analyses revealed different levels of histone 3 lysine 9 dimethylation (H3K9me2) in neutrophils (Neu), lymphocytes (Lym), and monocytes (Mon) from trauma patients. Compared with trauma patients, the levels of H3K9me2 were elevated in the three types of WBCs from cancer patients. When combined with sepsis, trauma patients demonstrated increased H3K9me2 levels in Neu (P=0.0005) and Mon (P=0.0002), whereas cancer patients had a significant decrease of H3K9me2 levels in the three types of WBCs (Neu, P=0.0003; Lym, P=0.007; Mon, P=0.007). The H3K9me2 alterations in patients with trauma and cancer were different with the occurrence of sepsis. A larger cohort study is warranted to explore the diagnostic significance and prognostic implications of altered histone methylation in septic patients.

LTR-retrotransposon transcriptome modulation in response to endotoxin-induced stress in PBMCs

“…From an in vivo point of view, this approach paves the way for systematic deciphering of modulated retroviral elements associated with autoimmune diseases such as systemic lupus erythematosus, inflammatory diseases such as type 1 diabetes [ 79 ] inherited autoimmune and auto-inflammatory disorders such as type 1 interferonopathies (reviewed in [ 80 , 81 ]), and virus- or drug-induced immunocompromised states [ 82 ], as well as resulting from a compensatory response to hyperinflammation such as in sepsis [ 83 ]. Notably, it would be of interest to investigate whether the altered histone methylation recently observed for genes in LPS-induced tolerance and in septic patients [ 75 , 84 ] may affect HERV expression and contribute to sepsis.…”

Abnormal liver phosphatidylcholine synthesis revealed in patients with acute respiratory distress syndrome

“…The methy l-D 3 -SAMe enrichment in patients was higher at the initial time point and showed a rapid decline until 24 h followed by a steady state decay, which was lower than that of controls, indicating that SAMe may be prioritized to maintain methyl balance or used for other methyl-dependent pathways instead of PEMT-mediated hepatic PC synthesis. While no direct evidence is available that increased hepatic SAMe turnover contributes to the pathogenesis of ARDS, increased SAMe-dependent histone methylation is an important component of the inflammatory response in sepsis and cancer ( 30 ). Alternatively, enhanced SAMe turnover could have been partly due to decreased synthesis, and inhibition of liver SAMe synthetase has been reported in an endotoxic rat model of septic shock ( 31 ).…”

Post-Translational Modifications in NETosis and NETs-Mediated Diseases

“…As mentioned earlier, curcumin inhibits TREM-1 by suppressing the methylation and acetylation of H3K4, and studies have suggested that curcumin is also able to inhibit tumor growth [181,200]. In addition, Jiang et al (2016) examined the clinical significance of histone methylation in esophageal cancer patients, and results show that increased levels of H3K9me2 are to be found in neutrophils when compared with samples acquired from trauma patients [201]. Another study examined the epigenetic alterations of the ALX/FPR 2 gene, which activation exerts anti-inflammatory effects, and its potential in breast cancer treatment [202].…”