A cluster of differentiation 14 (CD14) polymorphism (C-159T rs2569190) is associated with SARS-CoV-2 infection and mortality in the European population.
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ABSTRACT:
SUBMITTER: Pati A
PROVIDER: S-EPMC8083535 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The aim of this study was to investigate the relationship between the CD14 rs2569190 polymorphism and death related to septic shock in white European patients who underwent major cardiac or abdominal surgery. We carried out a retrospective study in 205 septic shock patients. The septic shock diagnosis was established by international consensus definitions. The outcome variable was the death within 28, 60 and 90 days after septic shock diagnosis. The CD14 rs2569190 polymorphism was analyzed by Agena Bioscience's MassARRAY platform. For the genetic association analysis with survival was selected a recessive inheritance model (GG vs. AA/AG). One hundred thirteen out of 205 patients (55.1%) died with a survival median of 39 days (95%CI = 30.6; 47.4). Patients with rs2569190 GG genotype had shorter survival probability than rs2569190 AA/AG genotype at 60 days (62.3% vs 50%; p = 0.035), and 90 days (62.3% vs 52.6%; p = 0.046). The rs2569190 GG genotype was associated with increased risk of septic shock-related death in the first 60 days (adjusted hazard ratio (aHR) = 1.67; p = 0.016) and 90 days (aHR = 1.64; p = 0.020) compared to rs2569190 AA/AG genotype. In conclusion, the presence of CD14 rs2569190 GG genotype was associated with death in shock septic patients who underwent major surgery. Further studies with bigger sample size are required to verify this relationship.
| S-EPMC5807421 | biostudies-literature
Project description:BACKGROUND:CD14 is a membrane glycoprotein that acts as a co-receptor for the detection of bacterial lipopolysaccharide (LPS). Mutual interaction between CD14 and LPS plays an important role in the innate immune system. Increased serum soluble CD14 levels have been described in hemodialysis (HD) patients, and linked to increased mortality risk, inflammation and protein-energy wasting. The expression of CD14 may be influenced by CD14 promoter gene C-159T polymorphism. This study aimed to clarify the possible association between CD14 promoter gene C-159T polymorphism and nutritional status in hemodialysis patients. MATERIAL/METHODS:The study population consisted of 185 (104 males; 81 females) long-term HD patients treated in 5 dialysis centers. The control group consisted of 112 apparently healthy volunteers (32 males and 80 females). Nutritional status was assessed using a modified SGA scale, and anthropometric methods (BMI, WHR, waist, hip and mid-arm circumferences, biceps, triceps, subocular and subscapular skinfolds). Biochemical parameters evaluated included: CRP, albumin, creatinine, urea, cholesterol, triglycerides and TIBC. CD14 promoter gene C-159T polymorphism was determined by restriction fragment length polymorphism, after digestion of the PCR product with Hae III restriction endonuclease. RESULTS:Genotype and allele frequencies were similar to controls and compliant with Hardy-Weinberg equilibrium. No between-group differences were detected in measured variables with the exception of lower triglyceride levels in carriers of C allele in comparison to TT genotype. CONCLUSIONS:CD14 promoter gene C-159T polymorphism does not seem to be associated with nutritional status parameters in HD patients. It does seem, however, to influence triglyceride blood levels.
| S-EPMC3524705 | biostudies-literature
Project description:Introduction:Previous epidemiological studies have suggested that CD14 rs2569190 C>T polymorphism plays an important role in ischemic stroke (IS) risk, but the results were inconsistent. Therefore, we conducted a meta-analysis to determine the association between CD14 rs2569190 C>T polymorphism and IS susceptibility. Methods:Online databases were searched from inception up to July 1, 2018, for studies concerning CD14 rs2569190 C>T polymorphism and its association with IS susceptibility. ORs and corresponding 95% CIs were calculated in the genetic models of each polymorphism locus with Stata Version 14.0. Furthermore, heterogeneity, meta-regression, accumulative analyses, sensitivity analyses, and publication bias were examined. Results:Overall, 10 observed studies involving 5,277 subjects were included in this meta-analysis on CD14 rs2569190 C>T polymorphism. Generally, no significant associations were found between CD14 rs2569190 C>T polymorphism and IS risk (allele contrast of T vs C: OR =1.03, 95% CI =0.96-1.12, P=0.41, I2=27.8%; co-dominant models of CT vs CC: OR =1.01, 95% CI =0.81-1.25, P=0.95, I2=51.9%; co-dominant models of TT vs CC: OR =1.04, 95% CI =0.89-1.22, P=0.62, I2=25.1%; dominant model of CT + TT vs CC: OR =1.02, 95% CI =0.84-1.25, P=0.82, I2=51.4%; recessive model of TT vs CC + CT: OR =1.07, 95% CI =0.95-1.22, P=0.28, I2=0%), similar to the results in the subgroup analysis. Conclusion:The current evidence indicated that CD14 rs2569190 C>T polymorphism was not a critical risk factor for IS development.
| S-EPMC6306072 | biostudies-literature
Project description: Not available
| S-EPMC7724738 | biostudies-literature
Project description:Microglia rapidly mount an inflammatory response to pathogens in the central nervous system (CNS). Heparan sulfate proteoglycans (HSPGs) have been attributed various roles in inflammation. To elucidate the relevance of microglial HSPGs in a pro-inflammatory response we isolated microglia from mice overexpressing heparanase (Hpa-tg), the HS-degrading endoglucuronidase, and challenged them with lipopolysaccharide (LPS), a bacterial endotoxin. Prior to LPS-stimulation, the LPS-receptor cluster-of-differentiation 14 (CD14) and Toll-like receptor 4 (TLR4; essential for the LPS response) were similarly expressed in Ctrl and Hpa-tg microglia. However, compared with Ctrl microglia, Hpa-tg cells released significantly less tumor necrosis factor-? (TNF?), essentially failed to up-regulate interleukin-1? (IL1?) and did not initiate synthesis of proCD14. Isolated primary astroyctes expressed TLR4, but notably lacked CD14 and in contrast to microglia, LPS challenge induced a similar TNF? response in Ctrl and Hpa-tg astrocytes, while neither released IL1?. The astrocyte TNF?-induction was thus attributed to CD14-independent TLR4 activation and was unaffected by the cells HS status. Equally, the suppressed LPS-response in Hpa-tg microglia indicated a loss of CD14-dependent TLR4 activation, suggesting that microglial HSPGs facilitate this process. Indeed, confocal microscopy confirmed interactions between microglial HS and CD14 in LPS-stimulated microglia and a potential HS-binding motif in CD14 was identified. We conclude that microglial HSPGs facilitate CD14-dependent TLR4 activation and that heparanase can modulate this mechanism.
| S-EPMC4463438 | biostudies-literature
Project description:BackgroundNeonatal sepsis is a health problem because it causes serious morbidity and mortality in neonate intensive care units. The susceptibility of neonates occurs due to the immaturity of immune system development as well as due to maternal and environmental risk factors that can cause infection. Identification of genetic variation in genes involved in the inflammatory process can help clarify the pathophysiology of sepsis in high-risk patients, useful for the development of new diagnostic tools, and specific management plans for more accurate predictions of patient's prognosis.AimThis study aims to determine the association between gene polymorphism of BPI rs4358188, CD14 rs2569190, IL1β rs1143643 or MMP16 rs2664349 and the incidence of neonatal sepsis.MethodsCross-sectional observational studies with genomic DNA samples from infants with sepsis and non-sepsis which were stored according to the standard storage of genetic materials in the Biomedical Laboratory of Faculty of Medicine Universitas Andalas Padang City, Indonesia. This study is part of a previous study by Rukmono P. Continued with PCR examination, sequencing and bioinformatics analysis.ResultsOnly IL1β rs1143643 G > A gene polymorphism was associated with the incidence of neonatal sepsis and was statistically significant (p = 0.017). No significant association was found between gene polymorphisms of BPI rs4358188 G > T, CD14 rs2569190 A>G or MMP16 rs2664349 G > A and neonatal sepsis (p > 0.05).ConclusionGene polymorphism of IL1β rs1143643 G > A is associated with the incidence of neonatal sepsis.
| S-EPMC6901854 | biostudies-literature
Project description:ContextCD14 functions as a multifunctional receptor for bacterial cell wall components including endotoxin and lipopolysaccharide and is likely to influence the cytokine profile and subsequent immunoglobulin E production in response to antigen/allergen contact in allergic phenotypes.AimsThe present study was to investigate genetic polymorphism in CD14 gene - 159C/T, which may be one of the risk factor for increased prevalence of Chronic Lung Diseases in the Central India.Settings and designSurvivors of Methyl isocyanates toxicity in Bhopal still suffering from various respiratory ailments were examined.Materials and methodsPolymerase chain reaction-restriction fragment length polymorphism was performed to determine the polymorphism of C-159T.ResultsThe genotype and allelic frequencies were in Hardy-Weinberg's equilibrium. Prevalence of CC, CT, and TT were 5.5%, 22.2% and 9.25% respectively in asthmatics; 16.6%, 20.3% and 5.5% respectively in chronic obstructive pulmonary disease (COPD) patients and 5.5%, 14.8% and 1.85 respectively among interstitial lung disorder (ILD) patients; whereas the control cohort with no methyl isocyanate exposure displayed (CC, CT, and TT) cytosine, thymine as 2%, 1.6% and 2% respectively. Increased risk of Asthma among those carrying TT genotype and T allele (odds ratio [OR] =2.61 and 2.02 respectively).ConclusionCOPD risk significantly found among those with CC genotype and C allele (OR = 2.81 and 1.50 respectively), whereas ILD risk found significantly among CT genotype and C allele (OR = 1.75 and 1.40 respectively). Therefore, single nucleotide polymorphism (SNP) C-159T polymorphism in CD14 gene might be a risk factor for development of CLD in this population.
| S-EPMC3758726 | biostudies-literature
Project description:Apical periodontitis (periapical lesions) is an infection-induced chronic inflammation in the jaw, ultimately resulting in the destruction of apical periodontal tissue. Toll-like receptors (TLRs) are prominent in the initial recognition of pathogens. Our previous study showed that TLR4 signaling is proinflammatory in periapical lesions induced by a polymicrobial endodontic infection. In contrast, the functional role of TLR2 in regulation of periapical tissue destruction is still not fully understood. Using TLR2 deficient (KO), TLR2/TLR4 double deficient (dKO), and wild-type (WT) mice, we demonstrate that TLR2 KO mice are highly responsive to polymicrobial infection-induced periapical lesion caused by over activation of TLR4 signal transduction pathway that resulted in elevation of NF-kB (nuclear factor kappa B) and proinflammatory cytokine production. The altered TLR4 signaling is caused by TLR2 deficiency-dependent elevation of CD14 (cluster of differentiation 14), which is a co-receptor of TLR4. Indeed, neutralization of CD14 strikingly suppresses TLR2 deficiency-dependent inflammation and tissue destruction in vitro and in vivo. Our findings suggest that a network of TLR2, TLR4, and CD14 is a key factor in regulation of polymicrobial dentoalveolar infection and subsequent tissue destruction. Anat Rec, 299:1281-1292, 2016. © 2016 Wiley Periodicals, Inc.
| S-EPMC4982827 | biostudies-literature
Project description:BackgroundThe C-159T polymorphism of the CD14 receptor gene can be associated with the development of atopic dermatitis. Probiotics can modulate chronic inflammation through activation of the CD14 receptor. So, the efficacy of probiotic therapy can be dependent on this genetic polymorphism.AimThe purpose of the study was to investigate the efficacy of adding probiotic (Lactobacillus acidophilus, LA-5 and Bifidobacterium animalis subsp. lactis, BB-12) to standard treatment (ointment of fluticasone propionate 0.005% and emollient) of atopic dermatitis in adults during 28 days, depending on the stratification of patients on CC or TT genotypes of the CD14 receptor gene.Material and methodsThe study included 37 adult patients with AD. There were identified 19 patients with exogenous (IgE-dependent) and 18 with endogenous (IgE-dependent) AD. To evaluate the efficacy of the probiotics all patients were divided into three groups for both exogenous and endogenous AD. The first group was selected from patients with CC genotype (C-159T) who received standard therapy (ointment of fluticasone propionate 0.005% - 2 times a day, emollients - 2 times a day) and probiotic (Lactobacillus acidophilus, LA-5 and Bifidobacterium animalis subsp. lactis, BB-12 - 1 capsule 2 times per day) The second group included patients with CC genotype, who received only standard therapy. The third group was presented by patients with TT genotype (C-159T) who received standard therapy and probiotic. The SCORAD and DLQI parameters were evaluated on Day 0, 14 and 28. The level of IL-4, IL-5, IL-10, TGF-β cytokines was determined on Day 0 and Day 28.ResultsThe results of our study found that the addition of probiotics (Lactobacillus acidophilus, LA-5 and Bifidobacterium animalis subsp. lactis, BB-12) to standard treatment (ointment of fluticasone propionate 0.005%, emollient) significantly increased the effectiveness of treatment of atopic dermatitis in adults with exogenous form and CC genotype (C-159T), confirmed by clinical (a significant decrease of SCORAD and DLQI indices) and immunological criteria (a significant decrease of IL-4 and an increase of TGF-β).ConclusionSimultaneous determination of the exogenous or endogenous form, identification of the C-159T genotypes, evaluation of the serum level of IL-4 and TGF-β can serve as an algorithm for the personalised treatment of patients with atopic dermatitis.
| S-EPMC6490491 | biostudies-literature
Project description:CD14 is a multifunctional receptor expressed on many cell types and has been shown to mediate immune response resulting in the activation of an inflammatory cascade, with polymorphism of its promoter (rs2569190) found to be associated with susceptibility to several diseases. In malaria infection, the CD14 gene demonstrated a pathogenic profile in regulating experimental cerebral malaria, with reports of elevated levels of soluble CD14 in serum of patients but no definitive conclusion. We present a detailed analysis of genetic diversity of CD14 promoter gene (snp -159 C/T; rs2519190) polymorphism between a malaria-infected group and uninfected controls and its association with clinical parameters of disease. Genomic DNA samples obtained from 106 Plasmodium falciparum malaria-infected patients and 277 uninfected controls were elucidated with a polymerase chain reaction-restriction fragment length polymorphism (RFLP) assay. Our results show a significant diversity (P = 3.32E-06) in the genotypic frequency (3.8% versus 22.4%) of the rs2569190 mutant variant between the malaria-infected group and controls, respectively. The mutant allele had the lowest frequency among the malaria-infected group demonstrating its necessity for infection. Mean parasitemia (parasites/μL of blood) was significantly regulated based on CD14 polymorphic profile (19 855 versus 37 041 versus 49 396 for homozygote mutants, heterozygotes, and homozygote wild type, respectively). Interestingly, we found no association between CD14 genetic variants with fever, age of patients, or anemia. How this affects disease severity between subregional and continental groups deserves further clarification, including extending these studies in a larger group and among severe and asymptomatic patients with malaria.
| S-EPMC5624288 | biostudies-literature