Coinfection with Enterohepatic Helicobacter Species Can Ameliorate or Promote Helicobacter pylori-Induced Gastric Pathology in C57BL/6 Mice
Coinfection with Enterohepatic Helicobacter Species Can Ameliorate or Promote Helicobacter pylori-Induced Gastric Pathology in C57BL/6 Mice
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DOI：
10.1128/iai.05357-11
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发表时间：
2011-10-01
影响因子：
3.1
通讯作者：
Fox, James G.
中科院分区：
文献类型：
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作者：
Ge, Zhongming;Feng, Yan;Fox, James G.
为探讨不同种肠肝螺杆菌（EHS）对幽门螺杆菌（Hp）胃粘膜病理的影响，用C57 BL/6小鼠分别感染肝螺杆菌（Hp）和鼠螺杆菌（Hp），然后再感染H.幽门螺杆菌感染2周后。与H. pylori感染小鼠、H. muridarum和H.在接种后6个月和11个月，HmHp小鼠的组织病理学活动指数（HAI）评分显著降低（P < 0.0001）。然而，感染H. hepaticus和H. pylori（HhHp小鼠）在6 MPI时胃病理学表现更严重（P = 0.01），在11 MPI时HAI与H. pylori感染的小鼠H.与H.幽门螺杆菌感染小鼠（P < 0.01）。与H. hepaticus对H.幽门螺杆菌诱导的胃Th 1细胞因子IFN-γ和TNF-α升高（P < 0.0001），但在6 MPI时增加了Th 17细胞因子mRNA水平（P = 0.028）。IL-17 A mRNA表达水平与幽门螺杆菌胃粘膜病变程度呈正相关（HhHp>H. pylori>HmHp）（6 MPI时r（2）= 0.92，P < 0.0001; 11 MPI时r（2）= 0.82，P < 0.002）。尽管对胃炎有不同的影响，但胃H。pylori的表达在HhHp小鼠（在6 MPI）和HmHp小鼠（在两个时间点）中比在mono-H. pylori感染的小鼠这些数据表明，尽管持续下调Th 1反应，EHS共感染或减弱或促进H。C57 BL/6小鼠中幽门螺杆菌诱导的胃病理学。这种调节与EHS对胃对H.幽门感染
To investigate how different enterohepatic Helicobacter species (EHS) influence Helicobacter pylori gastric pathology, C57BL/6 mice were infected with Helicobacter hepaticus or Helicobacter muridarum, followed by H. pylori infection 2 weeks later. Compared to H. pylori-infected mice, mice infected with H. muridarum and H. pylori (HmHp mice) developed significantly lower histopathologic activity index (HAI) scores (P < 0.0001) at 6 and 11 months postinoculation (MPI). However, mice infected with H. hepaticus and H. pylori (HhHp mice) developed more severe gastric pathology at 6 MPI (P = 0.01), with a HAI at 11 MPI (P = 0.8) similar to that of H. pylori-infected mice. H. muridarum-mediated attenuation of gastritis in coinfected mice was associated with significant downregulation of proinflammatory Th1 (interlukin-1beta [Il-1 beta], gamma interferon [Ifn-gamma], and tumor necrosis factor-alpha [Tnf-alpha]) cytokines at both time points and Th17 (Il-17A) cytokine mRNA levels at 6 MPI in murine stomachs compared to those of H. pylori-infected mice (P < 0.01). Coinfection with H. hepaticus also suppressed H. pylori-induced elevation of gastric Th1 cytokines Ifn-gamma and Tnf-alpha (P < 0.0001) but increased Th17 cytokine mRNA levels (P = 0.028) at 6 MPI. Furthermore, mRNA levels of Il-17A were positively correlated with the severity of helicobacter-induced gastric pathology (HhHp>H. pylori>HmHp) (at 6 MPI, r(2) = 0.92, P < 0.0001; at 11 MPI, r(2) = 0.82, P < 0.002). Despite disparate effects on gastritis, colonization levels of gastric H. pylori were increased in HhHp mice (at 6 MPI) and HmHp mice (at both time points) compared to those in mono-H. pylori-infected mice. These data suggest that despite consistent downregulation of Th1 responses, EHS coinfection either attenuated or promoted the severity of H. pylori-induced gastric pathology in C57BL/6 mice. This modulation was related to the variable effects of EHS on gastric interleukin 17 (IL-17) responses to H. pylori infection.