The role of infection in sudden infant death syndrome

Studies on the potential role of infectious agents in sudden infant death syndrome (SIDS) have been published over the years in a variety of journals. The aim of this special issue of FEMS Immunology and Medical Microbiology is to bring together a group of the most recent studies from Europe, Australia and Canada which cover epidemiology and laboratory studies examining hypotheses relating to infection and inflammation in SIDS. The articles in this issue examine evidence for the involvement of specific micro-organisms in SIDS and the problems relating to experimental studies on infection in relation to the underlying pathology of these deaths. There is an update on the evidence for the common bacterial hypothesis proposed in 1987 examining risk factors identified in epidemiological studies, particularly how the prone sleeping position could affect bacterial colonisation or induction of toxins. Evidence for induction of inflammatory responses in SIDS infants is reviewed and the relation of these responses to mechanisms proposed as causes of death assessed. Factors found to be associated with reduction of the risk of SIDS (breast feeding and immunisation) are examined in relation to some of the toxigenic bacteria implicated in these deaths. Finally, the high incidence of SIDS in some ethnic groups is examined as a potential model to investigate the contributions of genetic, environmental and cultural differences to susceptibility of infants not only to SIDS but to serious respiratory tract infections.     

Toll-like Receptor 11 (TLR11) Prevents Salmonella Penetration into the Murine Peyer Patches

Toll-like receptors (TLRs) are key molecular sensors used by the mammalian innate immune system to detect microorganisms. Although TLR functions in colonic immune homeostasis and tolerance to commensal bacteria have been intensively researched, the precise roles of different TLRs in response to pathogen infection in the gut remain elusive. Peyer patches are the major entrance of Salmonella infection and antigen transportation in intestine. Here, we report that, in contrast to TLR5 as a “carrier of Salmonella,” TLR11 works as a “blocker of Salmonella” to prevent highly invasive Salmonella from penetrating into the murine Peyer patches and spreading systemically. TLR11 plays an important role in mediating TNF-α induction and systemic inflammation in response to Salmonella infection. Remarkably, in mice lacking TLR11, apparent hemorrhages at Peyer patches are induced by highly invasive Salmonella, a phenotype resembling human Salmonella infection. Therefore, our results indicate a potentially important role for TLR11 in preventing murine intestinal infection and modulating antigen transportation in the gut and imply an important role for various TLRs in cooperation with tight control of pathogens penetrating into Peyer patches. The TLR11 knock-out mouse can serve as a good animal model to study Salmonella infection.     

Involvement of cystic fibrosis transmembrane conductance regulator in infection-induced edema

Abnormal fluid accumulation in tissues, including the life-threatening cerebral and pulmonary edema, is a severe consequence of bacteria infection. Chlamydia (C.) trachomatis is an obligate intracellular gram-negative human pathogen responsible for a spectrum of diseases, causing tissue fluid accumulation and edema in various organs. However, the underlying mechanism for tissue fluid secretion induced by C. trachomatis and most of other infectious pathogens is not known. Here, we report that in mice C. trachomatis infection models, the expression of cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP activated chloride channel, is up regulated together with increased cytokine release and tissue fluid accumulation that can be reversed by treatment with antibiotic specific for C. trachomatis and CFTR channel blocker. However, C. trachomatis infection cannot induce tissue edema in CFTRtm1Unc mutant mice. Administration of exogenous IL-1beta to mice mimics the C. trachomatis infection-induced CFTR upregulation, enhanced CFTR channel activity and fluid accumulation, further confirming the involvement of CFTR in infection-induced tissue fluid secretion.     

博尔纳病病毒实时荧光定量PCR诊断试剂盒的评价与应用

目的 评价博尔纳病病毒(Borna disease virus,BDV)实时荧光定量PCR(FQ RT-PCR)试剂盒的各项指标,并了解其实际应用效果.方法 使用BDV OL持续感染细胞株、非BDV病毒序列转染的OL细胞、正常的OL细胞,对BDV RT-PCR试剂盒的敏感性、特异性、重复性和稳定性进行评估,同时检测部分临床病人和动物外周血液RNA.结果 试剂盒可以检测出的病毒RNA最低浓度为10~2,相当于1.5个病毒拷贝数.特异性好,无非特异检出.不同批次的试剂盒的检测结果变异系数接近1.加速破坏的试剂盒和正常试剂盒检测结果之间变异系数在2以内.对临床病人检测阳性率为3.6%,对动物检测阳性率为4.4%.结论 试剂盒敏感性、特异性、重复性和稳定性均佳,是BDV基础研究、流行病学调查、临床检测的良好工具.     

二氧化氯溶液消毒剂对呼吸道病毒的杀灭效果评估

目的:评估"菌bye-bye"消毒剂对甲型H1N1流感病毒PR8(PR8)、呼吸道合胞病毒(RSV)、3型腺病毒(ADV3)、人感染H7N9禽流感病毒(H7N9)的体外杀灭效果。方法:参考《消毒技术规范》和受试产品说明书进行细胞毒性试验、消毒剂中和试验和对PR8、RSV、ADV3、H7N9病毒的体外杀灭实验。结果:(1)候选中和剂选定0.02mol/L硫代硫酸钠(Na_2S_2O_4);(2)候选中和剂、"菌-bye-bye"消毒剂及两者混合物对细胞毒性低;(3)候选中和剂能完全中和消毒剂消毒效果;(4)随着"菌bye-bye"消毒剂的浓度增大,病毒杀灭效果亦越好。在其不稀释的条件下,除了PR8毒株外,其他3种病毒的平均灭活率均在99.99%以上,且平均病毒TCID50负对数值(log_(10)TCID_(50)/m L)均降低4 log_(10)或以上;对半稀释后对RSV的杀灭效果最好,而对ADV3的杀灭效果最差。结论:高浓度"菌bye-bye"消毒剂对呼吸道病毒的杀灭效果较好,且对细胞的毒性较小,是一种安全、高效的消毒剂,值得临床推广。     

重症急性胰腺炎患者并发感染的临床特征及相关危险因素分析

目的:分析重症急性胰腺炎(SAP)患者并发感染的临床特征及感染的相关危险因素。方法:选择我院2009年1月至2014年1月收治的SAP患者152例,所有患者入院后,根据有无发生并发感染分为感染组(n=48)和非感染组(n=105),详细记录两组临床资料,并对SAP患者并发感染的相关危险因素进行多因素回归分析。结果:152例SAP患者中有48例发生并发感染,并发感染率为31.58%,对感染组患者标本进行分析,检出病原菌58株,以肠杆菌属为主,其中阴沟肠杆菌最多,占比22.41%。经单因素及多因素回归分析显示年龄≥60岁、器官衰竭个数增加、禁食时间延长是SAP并发感染的独立危险因素(P0.05)。结论:内源性感染是SAP患者并发感染的主要原因,且临床诊治中应针对SAP并发感染的独立危险因素,及早给予必要的干预,降低SAP患者并发感染的风险。     

汾阳地区1 933例女性宫颈细胞样本HPV基因分型

目的了解汾阳地区女性人乳头瘤病毒(HPV)感染率及其各亚型的分布情况。方法选择2016年10月至2017年3月于山西省汾阳医院就诊的1 933例女性患者为研究对象。运用荧光定量PCR法对所采集的入选患者宫颈脱落细胞样本中21种HPV亚型进行检测。结果收集的1 933例样本中,有414例HPV阳性,感染率为21.42%;其中高危型HPV感染率为13.55%,感染率前3位的型别为HPV16,HPV52和HPV58。在HPV感染者中,单一感染最多,共296例,占总感染人数的71.50%。不同年龄患者HPV的感染率差异有统计学意义(χ~2=18.40,P0.01),其中≤25岁和≥56岁年龄段患者HPV感染率较高,与其他3组相比差异均有统计学意义(χ~2=8.33、16.34,P0.05)。结论汾阳地区女性患者主要以高危型HPV感染为主,其中单一感染最多。≤25岁和≥56岁年龄段患者HPV感染率相对较高。     

Plasmodium yoelii: combinatorial expression of variants of the 235 kDa rhoptry antigen during infection

The 235 kDa rhoptry protein Py235 of Plasmodium yoelii, has been implicated in erythrocyte invasion by the merozoite forms of the parasite. Py235 is encoded by a large, highly polymorphic gene family, members of which appear to be differentially transcribed. However, it is not clear how many variants are expressed at the protein level during an infection cycle and whether or not these variants are expressed selectively or combinatorially. Certain monoclonal antibodies to Py235 have been shown to attenuate parasite virulence upon passive transfer into mice, suggesting that this antigen or its derivatives may be useful vaccine candidates. To provide a basis for this, we sought to identify those variants that are recognised by the host immune system, and to establish the pattern of expression of the antigen in mice during infection. Using Py235 monoclonal antibodies as probes, we isolated distinct antigenic variants from an expression library, suggesting that the antigen repertoire is potentially large and that different Py235 variants may be produced during infection. The implications of these observations are discussed with respect to the ability of a cloned parasite line to express distinct antigenic variants in vivo.     

Propagation of HBV with spatial dependence

A mathematical model is proposed to simulate the hepatitis B virus (HBV) infection with spatial dependence. The existence of traveling waves is established via the geometric singular perturbation method. Numerical simulations show that the model admits non-monotone traveling profiles. Influences of various parameters on the minimum wave speed are also discussed.