To study the association of transforming growth factor β1 (TGF-β1) gene single nucleotide polymorphisms (SNPs) and plasma TGF-β1 levels with susceptibility to sepsis. The genotypes of the gene rs1800469, rs1800468, rs1800470, and rs1800471 loci in 285 sepsis patients (119 patients with severe sepsis and 166 patients with mild sepsis) and 285 healthy individuals (control group) were analyzed through Sanger sequencing. Enzyme-linked immunosorbent assay was used to detect the levels of plasma inflammatory factors. The gene SNP rs1800469 C allele was 0.56 times lower than the T allele in terms of risk of susceptibility to sepsis (95% confidence interval [CI]: 0.43-0.72, < 0.01). Carriers of the A allele at the rs1800468 locus of the were 2.82 times more susceptible to sepsis than those with the G allele (95% CI: 1.62-4.91, < 0.01). The T allele at the rs1800470 locus of produced a lower risk of sepsis than those with the C allele (odds ratio [OR] = 0.74, 95% CI: 0.57-0.94, = 0.02). The risk of susceptibility to sepsis in the rs1800471 locus G allele was 3.54 times higher than that of C allele (95% CI: 2.14-5.86, < 0.01). The gene rs1800469 T > C and rs1800470 C > T were associated with mild sepsis, whereas rs1800468 G > A and rs1800471 C > G were associated with severe sepsis ( < 0.01). The gene rs1800469 T > C and rs1800470 C > T were associated with lower plasma TGF-β1 levels, whereas rs1800468 G > A and rs1800471 C > G were associated with higher TGF-β1 levels ( < 0.05). The alleles T > C of rs1800469 and C > T of rs1800470 of the gene were associated with lower plasma TGF-β1 levels and a reduced risk of sepsis susceptibility, whereas the alleles rs1800468 G > A and rs1800471 C > G were associated with higher levels and risk of susceptibility to sepsis.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1089/gtmb.2020.0143 | DOI Listing |
Sci Adv
January 2025
Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Mitochondrial electron transport chain (ETC) function modulates macrophage biology; however, mechanisms underlying mitochondria ETC control of macrophage immune responses are not fully understood. Here, we report that mutant mice with mitochondria ETC complex III (CIII)-deficient macrophages exhibit increased susceptibility to influenza A virus (IAV) and LPS-induced endotoxic shock. Cultured bone marrow-derived macrophages (BMDMs) isolated from these mitochondria CIII-deficient mice released less IL-10 than controls following TLR3 or TLR4 stimulation.
View Article and Find Full Text PDFCureus
December 2024
Orthopaedic and Spine Surgery, National Institute of Traumatology and Orthopaedic Rehabilitation (NITOR), Dhaka, BGD.
Introduction: Ankylosing spondylitis (AS), a chronic inflammatory spondyloarthropathy affecting the spine, progressively leads to increased spinal stiffness. This condition increases the risk of spine fractures in patients, even from trivial injuries. The process of slow bone formation within the ligaments of the spine and the fusion of the spinal diarthrosis contribute to the most prominent symptom of progressive stiffness of joints, predominantly affecting the spine and sacroiliac joints.
View Article and Find Full Text PDFNeurotherapeutics
January 2025
Division of Neurosciences Critical Care, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Neurology, Johns Hopkins University School of Medicine, USA; Department of Anesthesiology & Critical Care Medicine, Johns Hopkins University School of Medicine, USA. Electronic address:
Cerebral autoregulation (CA) is the physiological process by which cerebral blood flow is maintained during fluctuations in arterial blood pressure (ABP). There are various validated methods to measure CA, either invasively, with intracranial pressure or brain tissue oxygenation monitors, or noninvasively, with transcranial Doppler ultrasound or near-infrared spectroscopy. Utilizing these monitors, researchers have been able to discern CA patterns in several pathological states, such as but not limited to acute ischemic stroke, spontaneous intracranial hemorrhage, aneurysmal subarachnoid hemorrhage, sepsis, and post-cardiac arrest, and they have found CA to be altered in these patients.
View Article and Find Full Text PDFInt J Mol Med
March 2025
Department of Clinical Laboratory, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Structural Birth Defect and Reconstruction, Chongqing 400014, P.R. China.
Sepsis is often a cause of mortality in patients admitted to the intensive care unit. Notably, the heart is the organ most susceptible to the impact of sepsis and this condition is referred to as sepsis‑induced cardiomyopathy (SIC). Low triiodothyronine (T3) syndrome frequently occurs in patients with sepsis, and the heart is one of the most important target organs for the action of T3.
View Article and Find Full Text PDFNarra J
December 2024
Department of Pediatric, Dr. Zainoel Abidin Hospital, Banda Aceh, Indonesia.
Sepsis is a systemic infection that significantly causes morbidity and mortality among neonates, which is associated with immature immune response. Variations in the tumor necrosis factor-alpha gene () -308G/A may be linked to neonatal sepsis mortality by modulating interleukins (ILs) involved in the immune response cascade, such as IL-6. The aim of this study was to investigate the association between -308G/A gene variation and IL-6 level with mortality of neonatal sepsis.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!