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A lack of role for antibodies in regulating Helicobacter pylori colonization and associated gastritis.

缺乏调节幽门螺杆菌定植和相关性胃炎的抗体作用。

  • 影响因子:3.27
  • DOI:10.1111/hel.12681
  • 作者列表:"Arshad U","Sarkar S","Alipour Talesh G","Sutton P
  • 发表时间:2020-02-23
Abstract

BACKGROUND:Helicobacter pylori occupy a unique niche, located within the mucus layer lining the stomach, and attached to the apical surface of the gastric epithelium. As such, antibodies would be expected to play a major role in regulating infection and/or pathogenesis. However, experiments using antibody-deficient mice to study gastric helicobacter infection have yielded inconsistent results, although some pointed toward antibodies increasing colonization levels and decreasing gastritis severity. The variability in these studies is possibly due to their use of nonmatched wild-type controls. This current study presents the first evaluation of the role of antibodies in H pylori infection by comparing antibody-deficient mice with matched wild-type siblings. METHODS:Matched wild-type and antibody-deficient μMT mice were generated by heterozygous crossings. In two separate experiments, appropriately genotyped sibling littermates were infected with H pylori for 4 months and then sera and stomachs were collected. RESULTS:There was no difference in H pylori colonization levels between infected μMT mice and sibling wild-type controls. Similarly, there was no significant difference in the severity of gastritis between these groups of mice, although there was a trend toward less severe gastritis in μMT mice which was supported by a significantly lower IFNγ (Th1) gastric cytokine response. CONCLUSIONS:Comparing matched antibody-deficient and antibody-competent mice indicates that an antibody response does not influence H pylori colonization levels. Contrary to previous studies, these results suggest antibodies might have a minor pro-inflammatory effect by promoting gastric Th1 cytokines, although this did not translate to a significant effect on gastritis severity.

摘要

背景: 幽门螺杆菌占据了一个独特的位置,位于胃粘膜层内,并附着在胃上皮的顶端表面。因此,抗体有望在调节感染和/或发病机制中发挥主要作用。然而,使用抗体缺陷小鼠研究胃幽门螺杆菌感染的实验得出了不一致的结果,尽管一些实验指出抗体增加定植水平和降低胃炎严重程度。这些研究的变异性可能是由于它们使用了不匹配的野生型对照。本研究通过比较抗体缺陷小鼠与匹配的野生型兄弟姐妹,首次评价了抗体在 H.pylori 感染中的作用。 方法: 通过杂合交叉产生匹配的野生型和抗体缺陷型 μ mt 小鼠。在两个单独的实验中,适当基因分型的同胞同窝被 H.pylori 感染 4 个月,然后收集血清和胃。 结果: 感染 μ mt 小鼠和同胞野生型对照组的 H.pylori 定植水平无差异。同样,这些组小鼠之间胃炎的严重程度没有显著差异, 尽管 μ mt 小鼠存在轻度胃炎的趋势,但 ifn γ (Th1) 胃细胞因子反应显著降低支持了这一趋势。 结论: 比较匹配的抗体缺陷小鼠和抗体感受态小鼠表明抗体反应不影响幽门螺杆菌定植水平。与以前的研究相反,这些结果表明抗体可能通过促进胃 Th1 细胞因子产生轻微的促炎作用,尽管这并没有转化为对胃炎严重程度的显著影响。

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