Background: Sepsis is now the leading cause of death in the non-cardiovascular intensive care unit (ICU). Recent research suggests that sepsis is likely to be due to an interaction between genetic and environmental factors. Genetic mutations of toll-like receptor 4 (TLR4) and cluster of differentiation 14 (CD14) genes are involved in the immune and (or) inflammatory response. These may contribute to the susceptibility to sepsis in patients. This study was designed to evaluate whether the TLR4 and cluster CD14 gene polymorphisms are associated with susceptibility to sepsis.
Methods: The single nucleotide polymorphisms (SNPs) of TLR4 (rs10759932, rs11536889, rs7873784, rs12377632, rs1927907, rs1153879) and CD14 (rs2569190 and rs2563298) in patients with sepsis and control subjects in the Guangxi Province were analyzed by using the polymerase chain reaction-single base extension (PCR-SBE) and DNA sequencing methods.
Results: The rs11536889 polymorphism in TLR4 and rs2563298 polymorphism in CD14 were significantly associated with the risk of sepsis when compared to the control group. The frequencies of rs11536889 and rs2563298 polymorphisms in the group with sepsis were higher than that in the control group (OR = 1.430, 95% CI, 1.032-1.981, P<0.05; OR = 2.454, 95% CI, 1.458-4.130, P<0.05, respectively). Followed up haplotype analysis suggested that there were two haplotypes in which increased risk factors for sepsis were indicated.
Conclusions: The rs11536889 polymorphism in TLR4 and rs2563298 polymorphism in CD14, and two haplotypes were associated with increased susceptibility to sepsis.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4411696 | PMC |
http://dx.doi.org/10.1186/s12881-014-0123-4 | DOI Listing |
J Immunother Cancer
January 2025
IRCCS Humanitas Research Hospital, Rozzano, Italy
Background: ACKR2 is an atypical chemokine receptor that plays a significant role in regulating inflammation by binding to inflammatory CC chemokines and facilitating their degradation. Previous findings suggest that the genetic absence of ACKR2 leads to heightened tumor growth in inflammation-driven models. Conversely, mice lacking ACKR2 exhibit protection against lung metastasis in melanoma and breast cancer models.
View Article and Find Full Text PDFJ Dermatol Sci
January 2025
Biosciences Department, Durham University, Durham, United Kingdom. Electronic address:
Background: Systemic Sclerosis (SSc) is an idiopathic rheumatic inflammatory disease that is characterised by inflammation and skin fibrosis. Type I interferon is significantly elevated in the disease.
Objective: The objective of this study is to determine the role of the TCA cycle metabolite fumarate in SSc.
J Hepatol
January 2025
Department of Biomedicine, University of Basel, Switzerland; University Centre for Gastrointestinal and Liver Disease Basel, Switzerland. Electronic address:
Background & Aims: Infectious complications determine the prognosis of cirrhosis patients. Their infection susceptibility relates to the development of immuneparesis, a complex interplay of different immunosuppressive cells and soluble factors. Mechanisms underlying the dynamics of immuneparesis of innate immunity remain inconclusive.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Biological Sciences, Virginia Tech, Blacksburg, VA, 24061-0910, USA.
Sepsis is a leading cause of death worldwide, with most patient mortality stemming from lingering immunosuppression in sepsis survivors. This is due in part to immune dysfunction resulting from monocyte exhaustion, a phenotype of reduced antigen presentation, altered CD14/CD16 inflammatory subtypes, and disrupted cytokine production. Whereas previous research demonstrated improved sepsis survival in Ticam2 mice, the contribution of TICAM2 to long-term exhaustion memory remained unknown.
View Article and Find Full Text PDFAdv Mater
January 2025
State Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, Tianjin, 300350, China.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!