Moscovis Sophia M, Gordon Ann E, Al Madani Osama M, Gleeson Maree, Scott Rodney J, Hall Sharron T, Burns Christine, Blackwell Caroline
School of Biomedical Sciences, Faculty of Health and Medicine, University of Newcastle and Hunter Medical Research Institute , Newcastle, NSW , Australia ; Hunter Medical Research Institute , New Lambton, NSW , Australia.
Medical Microbiology, University of Edinburgh , Edinburgh , UK.
Front Immunol. 2015 Jul 27;6:374. doi: 10.3389/fimmu.2015.00374. eCollection 2015.
Dysregulation of the inflammatory responses has been suggested to contribute to the events leading to sudden infant deaths. Our objectives were (1) to analyze a single nucleotide polymorphism (SNP) associated with high levels of tumor necrosis factor-α (TNF-α) responses, TNF G-308A, in sudden infant death syndrome (SIDS) infants, SIDS and control parents, and ethnic groups with different incidences of SIDS; (2) the effects of two risk factors for SIDS, cigarette smoke and virus infection, on TNF-α responses; and (3) to assess effects of genotype, cigarette smoke, and gender on TNF-α responses to bacterial toxins identified in SIDS infants. TNF G-308A genotypes were determined by real-time polymerase chain reaction for SIDS infants from Australia, Germany, and Hungary; parents of SIDS infants and their controls; and populations with high (Aboriginal Australian), medium (Caucasian), and low (Bangladeshi) SIDS incidences. Leukocytes from Caucasian donors were stimulated in vitro with endotoxin or toxic shock syndrome toxin-1 (TSST-1). TNF-α responses were measured by L929 bioassay (IU/ml) and assessed in relation to genotype, smoking status, and gender. There was a significantly higher proportion of the minor allele AA genotype among Australian SIDS infants (6/24, 24%) compared to 3/62 (4.8%) controls (p = 0.03). There were no significant differences in TNF-α responses by TNF G-308A genotypes when assessed in relation to smoking status or gender. Given the rarity of the TNF G-308A A allele in Caucasian populations, the finding that 24% of the Australian SIDS infants tested had this genotype requires further investigation and cautious interpretation. Although non-smokers with the AA genotype had higher TNFα responses to both TSST-1 and endotoxin, there were too few subjects with this rare allele to obtain statistically valid results. No effects of genotype, smoking, or gender were observed for TNF-α responses to these toxins.
炎症反应失调被认为与导致婴儿猝死的事件有关。我们的目标是:(1)分析与高水平肿瘤坏死因子-α(TNF-α)反应相关的单核苷酸多态性(SNP),即TNF G-308A,在婴儿猝死综合征(SIDS)婴儿、SIDS婴儿及对照父母,以及SIDS发病率不同的种族群体中的情况;(2)两种SIDS风险因素,即香烟烟雾和病毒感染,对TNF-α反应的影响;(3)评估基因型、香烟烟雾和性别对SIDS婴儿中鉴定出的细菌毒素的TNF-α反应的影响。通过实时聚合酶链反应确定来自澳大利亚、德国和匈牙利的SIDS婴儿、SIDS婴儿的父母及其对照,以及SIDS发病率高(澳大利亚原住民)、中(白种人)和低(孟加拉人)的人群的TNF G-308A基因型。用内毒素或中毒性休克综合征毒素-1(TSST-1)体外刺激白种人供体的白细胞。通过L929生物测定法(IU/ml)测量TNF-α反应,并根据基因型、吸烟状况和性别进行评估。与3/62(4.8%)的对照相比,澳大利亚SIDS婴儿中次要等位基因AA基因型的比例显著更高(6/24,24%)(p = 0.03)。当根据吸烟状况或性别评估时,TNF G-308A基因型的TNF-α反应没有显著差异。鉴于TNF G-308A A等位基因在白种人群体中很罕见,24%接受检测的澳大利亚SIDS婴儿具有这种基因型这一发现需要进一步研究并谨慎解读。尽管具有AA基因型的非吸烟者对TSST-1和内毒素的TNFα反应较高,但具有这种罕见等位基因的受试者太少,无法获得统计学上有效的结果。未观察到基因型、吸烟或性别对这些毒素的TNF-α反应有影响。