Helicobacter pylori induces NOD1/NF-κB activation and IFN-βand IP-10 production in gastrics of mice
10.3969/j.issn.1000-484X.2015.07.007
- VernacularTitle:幽门螺杆菌激活小鼠胃组织中NOD1／NF-κB信号通路并诱导IFN-β和IP-10分泌
- Author:
Chuli XIAO
;
Sheng LIU
;
Xiao TAN
;
Jianye JIANG
;
Yan ZHANG
- Publication Type:Journal Article
- Keywords:
Helicobacter pylori;
NOD1;
IFN-β;
IP-10
- From:
Chinese Journal of Immunology
2015;(7):898-901,905
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To construct the Helicobacter pylori infected C57BL/6 mice model to observe the activation of NOD1/NF-κB signaling pathways in the gastric tissues,and study its roles in inflammatory response during Hp infection.Methods:6-8 week-old C57BL/6 mice were randomly divided into two groups,the Hp infection group and the control group,and mice were given by gavage every 48 h for five times with Hp or PBS,respectively.All the animals were sacrificed at different time point and the gastric tissue were stained with hematoxylin-eosin( HE);The mRNA expression of NOD1 and RIP2 in gastric tissues were examined by RT-PCR;Levels of IFN-βand IP-10 in mice serum were assessed by ELISA;Nuclear translocation of p65 in gastric tissue was detected by Western blot.Results:Hp infection elicits an inflammatory cell response,glands in gastric tissue were reduced or atrophic,as compared with that in the control group.The levels of IP-10 and IFN-βincreased in the model group, and peaked at 16 weeks after Hp infection.Hp infection increased the mRNA expression of NOD1 and the p65 content in nuclear between 24-120 h(P<0.05),and the highest level at 48 h,subsequently the expression levels were began to decrease.The mRNA expression level of RIP2 was up-regulated after Hp was administrated, peaked at 48 h and declined after 72 h.However, the expression levels would rise again at 120 h.Conclusion: Hp infection can activate the NOD1/NF-κB signaling pathways and induce the production of IFN-βand IP-10 in gastrics of mice.
