The promoter polymorphisms of receptor for advanced glycation end products were associated with the susceptibility and progression of sepsis

Shao, Yiming; Shao, Xin; He, Junbing; Cai, Yujie; Zhao, Jianghao; Chen, Feng; Tao, Hua; Yin, Zihan; Tan, Xinzhang; He, Yiping; Lin, Yao; Li, Keshen; Cui, Lili

doi:10.1111/cge.12800

Cited by 8 publications

(5 citation statements)

References 59 publications

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“…Although the pathological mechanism of sepsis remains unclear, numerous lines of evidence have demonstrated that variations in genes associated with the inflammatory immune response play vital roles in the pathomechanism and progression of sepsis [4–7]. Progress in genetic sequencing and association studies between different immunological profiles and disease outcomes may someday allow for genetic diagnosis and interventional treatment of sepsis, ultimately improving outcomes for critically ill patients [8–10].…”

Section: Introductionmentioning

confidence: 99%

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Association study of MCP-1 promoter polymorphisms with the susceptibility and progression of sepsis

Chen

Lin

et al. 2017

PLoS ONE

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Previous studies have indicated that the monocyte chemo-attractant protein 1 (MCP-1), also referred to as C-C motif chemokine ligand 2 (CCL2), plays a significant role in the pathogenesis of sepsis, and this study investigated the clinical relevance of two MCP-1 gene polymorphisms on sepsis onset and progression. The Multiplex SNaPshot genotyping method was used to detect MCP-1 gene polymorphisms in the Chinese Han population (403 sepsis patients and 400 controls). MCP-1 mRNA expression levels were measured using real-time quantitative PCR, and enzyme-linked immunosorbent assays were used to analyze MCP-1, tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6) and interleukin-1 beta (IL-1β) plasma concentrations. The rs1024611 polymorphism analysis showed lower frequencies of minor homozygous genotype (AA) and allele (A) in sepsis patients compared to the healthy controls (19.4% vs. 31.5%, P = 0.0001 and 45.9% vs. 54.8%, P = 0.0004, respectively). And the frequencies of GG genotype and G allele were lower in sepsis patients compared to the controls (19.6% vs. 31.3%, P = 0.0002 and 46.0% vs. 54.5%, P = 0.0007, respectively). The rs1024611 AG/GG and rs2857656 GC/CC genotypes were both overrepresented in patients with severe sepsis (both P = 0.0005) and septic shock (P = 0.010 and P = 0.015, respectively) compared to the patients with mild sepsis. Moreover, among sepsis patients, the rs1024611 AG/GG and rs2857656 GC/CC carriers exhibited significant increases in expression levels of MCP-1 (P = 0.025), TNF-α (P = 0.034) and IL-6 (P = 0.043) compared with the rs1024611 AA or rs2857656 GG carriers. This study provides valuable clinical evidence that the MCP-1/CCL2 polymorphisms rs1024611 and rs2857656 are associated with sepsis susceptibility and development. We conclude that MCP-1/CCL2 plays a significant role in the pathogenesis of sepsis, which has potentially important therapeutic implications.

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Section: Introductionmentioning

confidence: 99%

“…A growing body of work has demonstrated that many variations in genes associated with the inflammatory and immune responses contribute to the occurrence and progression of sepsis [4–7]. However, to the best of our knowledge, the clinical relevance of MCP-1 genetic polymorphisms to sepsis has not been determined, adequately.…”

Section: Introductionmentioning

confidence: 99%

Association study of MCP-1 promoter polymorphisms with the susceptibility and progression of sepsis

Chen

Lin

et al. 2017

PLoS ONE

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“…Two variants located in the promoter region of RAGE were significantly associated with the risk of sepsis. In total, four studies on RAGE rs1800625-429 T/C were conducted by Zeng et al [19] and Shao et al [20]. The primary meta-analysis of the four studies showed significant associations between the risk of sepsis and RAGE rs1800625-429 T/C in all three genetic models (OR = 0.59, 95% CI = 0.45–0.73, P < 0.001 for the dominant model, OR = 0.47, 95%CI = 0.24–0.96, P = 0.04 for the recessive model, and OR = 0.61, 95%CI = 0.51–0.74, P < 0.0001 for the allelic model) with a high level of evidence.…”

Section: Resultsmentioning

confidence: 99%

Host genetic variants in sepsis risk: a field synopsis and meta-analysis

Wen

Wang

et al. 2019

Crit Care

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BackgroundPublished data revealed that host genetic variants have a substantial influence on sepsis susceptibility. However, the results have been inconsistent. We aimed to systematically review the published studies and quantitatively evaluate the effects of these variants on the risk of sepsis.MethodsWe searched the PubMed, EMBASE, Medline, Web of Knowledge, and HuGE databases to identify studies that investigated the associations between genetic variants and sepsis risk. Then, we conducted meta-analyses of the associations for genetic variants with at least three study populations and applied the Venice criteria to assess the association result credibility.ResultsA literature search identified 349 eligible articles that investigated 405 variants of 172 distinct genes. We performed 204 primary and 185 subgroup meta-analyses for 76 variants of 44 genes. The results showed that 29 variants of 23 genes were significantly associated with the risk of sepsis, including 8 variants of pattern recognition receptors (PRRs), 14 variants of cytokines, one variant of an immune-related gene and 6 variants of other genes. Furthermore, the cumulative epidemiological evidence of a significant association between each variant and the risk of sepsis was classified as strong or moderate for 18 variants. For the 329 variants with fewer than three study populations, 63 variants of 48 genes have been reported to be significantly associated with the risk of sepsis in a systematic review.ConclusionWe identified several genetic variants that could influence the susceptibility to sepsis by systematic review and meta-analysis. This study provides a comprehensive overview of the genetic architecture of variants involved in sepsis susceptibility and novel insight that may affect personalized targeted treatment in the future clinical management of sepsis.Electronic supplementary materialThe online version of this article (10.1186/s13054-019-2313-0) contains supplementary material, which is available to authorized users.

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“…In addition, the SLE patients with neurologic disorder carrying CC or CG genotypes seem to exhibit relatively higher levels of expression S100B compared with those carrying the GG genotype. It is known that polymorphisms in the promoter region of certain genes might regulate their expression by altering the binding sites of transcription factors (Sun, et al , 2007; Shao, et al , 2017). We hypothesized that the synonymous SNP rs1051169 located in the exon of S100B may exert an influence on splicing, thereby affecting the levels of serum S100B, which ultimately potentiate S100B-mediated pro-inflammatory processes, increase SLE risk, and promote neurologic disorder development.…”

Section: Discussionmentioning

confidence: 99%

Association of S100B polymorphisms and serum S100B with risk of systemic lupus erythematous in a Chinese population

Huang

Liu

et al. 2019

Genet. Mol. Biol.

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The aim of this study was to investigate whether the S100B polymorphisms are associated with systemic lupus erythematous (SLE) in a Chinese population. A total of 313 SLE patients and 396 control subjects were enrolled in the present study. The genotypes of three SNPs (rs9722, rs881827 and rs1051169) in S100B gene were detected by single base extension polymerase chain reaction (SBE-PCR). Serum S100B levels were determined by enzyme-linked immunosorbent assay (ELISA). Rs1051169 was associated with an increased risk of SLE (C vs. G: adjusted OR=1.46, 95% CI, 1.18-1.80, p =0.001; CC vs. GG: adjusted OR=1.99, 95% CI, 1.32-3.02, p =0.001; CC+GC vs. GG: adjusted OR=1.54, 95% CI, 1.13-2.11, p =0.007; CC vs. GC+GG: adjusted OR=1.67, 95% CI, 1.16-2.42, p =0.006). Haplotype analysis showed that the G-G-C haplotype was associated with an increased risk of SLE (OR=1.50, 95% CI, 1.14-1.98, p =0.004). Stratified analyses showed that the rs1051169 polymorphism was associated with an increased risk of neurologic disorder in SLE patients (C vs. G: OR=1.78, 95% CI, 1.22-2.59, p =0.003; GC vs. GG: OR=2.33, 95% CI, 1.14-4.77, P=0.019; CC vs. GG: OR=3.02, 95% CI, 1.39-6.53, p =0.004; CC+GC vs. GG: OR=2.57, 95% CI=1.31-5.04, p =0.005). In addition, SLE patients with neurologic disorder carrying the rs1051169 GC/CC genotypes present a higher serum S100B levels compared with that carrying the GG genotype ( p < 0.05). Our results indicate that the rs1051169 polymorphism may be involved in the pathogenesis of SLE.

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The promoter polymorphisms of receptor for advanced glycation end products were associated with the susceptibility and progression of sepsis

Cited by 8 publications

References 59 publications

Association study of MCP-1 promoter polymorphisms with the susceptibility and progression of sepsis

Association study of MCP-1 promoter polymorphisms with the susceptibility and progression of sepsis

Host genetic variants in sepsis risk: a field synopsis and meta-analysis

Association of S100B polymorphisms and serum S100B with risk of systemic lupus erythematous in a Chinese population

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