Association of the genes for tumor necrosis factor-α and myelin basic protein with delayed encephalopathy after acute carbon monoxide poisoning

Abstract

ABSTRACT. There is structural damage to myelin and secondary immune injury in the development of delayed encephalopathy after acute carbon monoxide (CO) poisoning (DEACMP). In order to assess the role of genetic factors in this mechanism, we studied the association between tumor necrosis factor-α308 (TNF-α308) and myelin basic protein (MBP) 5ꞌ-side tetranucleotide repetitive sequence (TGGA) n gene polymorphism and DEACMP. We selected 109 DEACMP patients from the Han population in the Northern Henan Province as the case group, and 115 patients without delayed encephalopathy (called the acute CO poisoning group or the control group). There were no significant differences in TNF-α308 and MBP 5ꞌ-side TGGA n genotype distribution and allele frequency between the DEACMP group and the acute CO poisoning group (all P > 0.05). When the population was stratified by gender, only the MBP 5ꞌ-side TGGA n allele frequency was significantly different, and the frequency of allele L in the DEACMP group was significantly higher than that of the acute CO poisoning group in males (χ 2 = 4.089, P = 0.043, odds ratio = 2.103, 95% confidence interval = 1.014-4.363). The results showed that there was association between MBP 5ꞌ-side TGGA n gene polymorphism and DEACMP, and that allele L could increase the risk of occurrence in male patients with DEACMP. DEACMP may be the result of interaction of environmental and genetic factors.

DNA Pooling Base Genome-Wide Association Study Identifies Variants at NRXN3 Associated with Delayed Encephalopathy after Acute Carbon Monoxide Poisoning

“…However, the occurrence varied greatly, even in patients with similar age, sex and intoxication level, which suggested that individual differences exist, and that genetic factors might play an important role. In our previous report, the case-control study showed that there was an association between the MBP TGGAn gene polymorphism and DEACMP [13] .…”

The Relationship between Cadherin Polymorphisms and the Risk of Delayed Encephalopathy after Acute Carbon Monoxide Poisoning in the Chinese Han Population

“…For example, MAPK activation can regulate the expression of proinflammatory cytokines, including IL-1, IL-6, and TNF- α , as well as cyclooxygenase-2 (COX2) and inducible nitric oxide synthase (iNOS) [ 24 ]. The onset of DEACMP is closely related to many immune cells and inflammatory factors, such that the infiltration of T cells, B cells, macrophages, and neutrophils and the cascade-like release of inflammatory factors such as interferon- γ , interferon- α , IL-6, IL-8, and others participate in the occurrence of DEACMP [ 8 ]. Thus, it is plausible that alterations in cadherin function through genetic variation results in changes in ROCK and MAPK signaling that impact the repair of demyelination damage and inflammatory responses during DEACMP pathogenesis.…”

“…We conducted genome-wide association studies (GWAS) of single-nucleotide polymorphisms (SNP) on peripheral blood samples of 175 DEACMP and 244 ACMP Chinese patients. Our results identified genes such as neurexin 3, Parkinson disease 2, myelin basic protein (MBP), neuron-specific enolase (NSE), and leucine-rich repeats and calponin homology domain containing 1 (LRCH1) which were associated with DEACMP [ 8 – 12 ]. In this study, we now extend this analysis to consider the contribution of genetic variation in cadherin family genes to the development of DEACMP.…”