Analyzing the relationship between programmed cell death of Helicobacter pylori(apoptosis), persistence and host immunity

螺杆pylori cdrA对细胞分裂有抑制作用。在动物模型和患者持续感染过程中发现cdrA的丢失。因此，我们研究了cdrA是否影响体外和体内的宿主免疫应答。在与野生型或cdrA破坏菌株共培养的AGS细胞中以及在来自感染cdrA阳性或cdrA阴性菌株的患者的活检标本中比较IL-8水平。CDRA干扰株诱导的AGS中IL-8水平显著低于对照组（P<0. 05）。01)与野生型相比：对应于野生型的50%-60%，这与使用来自cdrA阳性和cdrA阴性组的活检标本的体内数据一致。因此，由cdrA阴性或cdrA功能失调的菌株定殖导致IL-8产生减少和NF-κB抑制，并因此减弱宿主免疫力，导致持续感染。

The H. pylori cdrA has a repressive role on cell division. Loss of cdrA was found during persistent infection in animal model and patients. Thus we investigated whether the cdrA affects on the host immune response in vitro and vivo. The IL-8 level was compared in AGS cells co-cultured with wild-type or cdrA-disruptant strains and in biopsy specimens from patients infected by cdrA-positive or cdrA-negative strains. IL-8 level induced in AGS by a cdrA-disruptant strain was significantly lower(P<0. 01) compared to wild-type : corresponding to 50%-60% of those of wild-type, which coincided with in vivo data using biopsy specimens from cdrA-positive and cdrA-negative groups. Therefore, colonization by a cdrA-negative or cdrA-dysfunctional strain resulted in decreased IL-8 production and repression of NF-κB, and hence, attenuate the host immunity leading to persistent infection.