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The role of Tumor necrosis factor alpha -308 G>A promoter polymorphism in pediatric community acquired pneumonia

机译:肿瘤坏死因子α-308g在儿科群落中促进剂多态性的作用患有肺炎

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Background:Tumor necrosis factor alpha (TNF-α) ?308 G>A promoter polymorphism might be associated with excessive production of the proinflammatory cytokine TNF-α, modulating host response to pulmonary infections. Our objective was to evaluate the association of TNF-α gene ?308?G>A polymorphism with susceptibility to, and severity of, community-acquired pneumonia (CAP).ResultsThis was a cross-sectional study including 45 Egyptian children hospitalized for CAP in addition to 45 healthy children who served as a control group. Pneumonia severity was assessed on admission by the World Health Organization (WHO) guidelines; Pediatric Respiratory Severity Score (PRESS) score; Predisposition, Infection, Response and Organ failure (PIROm) score; and Respiratory Index of Severity in Children (RISC) score. Genotyping of TNF-α polymorphism was performed to all individuals by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). Patients were monitored till hospital discharge. Frequency of AG genotype was lower among patients compared with control [odds ratio (OR) and 95% confidence interval (CI) = 0.13 (0.03–0.63); p = 0.012]. Prevalence of genotypes AA+AG was lower among patients compared with controls [OR and 95% CI = 0.34 (0.12–0.99); p = 0,048]. The “A” allele prevalence was higher among controls, but no significant association was found with CAP [OR and 95% CI = 0.58 (0.25–1.35); p = 0.21]. When PRESS score was used to classify patients into “severe pneumonia” and “non-severe pneumonia,” no significant association of any of the alleles or genotypes with CAP severity was found.ConclusionTNF-α ?308 G>A polymorphism confers protection from pediatric CAP but is not associated with indicators of CAP severity. Larger studies are needed to confirm these findings in pediatric patients from different ethnicities.
机译:背景:肿瘤坏死因子α(TNF-α)?308g>启动子多态性可能与过量产生的促炎细胞因子TNF-α相关,调节脑响应肺部感染。我们的目的是评估TNF-α基因的关联吗?308?G>具有易感性和严重程度的多态性,社区获得的肺炎(CAP).Resultsthis是一个横断面研究,包括45名埃及儿童住院的帽子除了45名担任对照组的健康儿童。世界卫生组织(世卫组织)准则的入学评估了肺炎严重程度;儿科呼吸严重程度评分(新闻)得分;倾向,感染,反应和器官衰竭(Pirom)得分;和儿童严重程度的呼吸指数(RISC)得分。通过聚合酶链反应和限制性片段长度多态性(PCR-RFLP)对所有个体进行TNF-α多态性的基因分型。患者监测到医院排放。患者的Ag基因型的频率降低,与对照[差距(或)和95%置信区间(CI)= 0.13(0.03-0.63); p = 0.012]。与对照相比,患者的基因型AA + AG的患病率降低[或95%CI = 0.34(0.12-0.99); p = 0.048]。对照组的“a”等位基因患病率较高,但帽子[或95%Ci = 0.58(0.25-1.35)没有明显关联。 p = 0.21]。当压分用于将患者分类为“严重肺炎”和“非严重肺炎”时,没有发现任何等位基因或基因型的显着关联.ConclusionTNF-α?308g>多态性赋予儿科保护帽子但与CAP严重程度的指标无关。需要更大的研究来确认来自不同种族的儿科患者的这些发现。

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