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首页> 外文期刊>Infection and immunity >Colonization and Inflammation Deficiencies in Mongolian Gerbils Infected by Helicobacter pylori Chemotaxis Mutants
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Colonization and Inflammation Deficiencies in Mongolian Gerbils Infected by Helicobacter pylori Chemotaxis Mutants

机译：幽门螺杆菌趋化性突变株感染的蒙古沙鼠的定殖和炎症缺乏

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Helicobacter pylori causes disease in the human stomach and in mouse and gerbil stomach models. Previous results have shown that motility is critical for H. pylori to colonize mice, gerbils, and other animal models. The role of chemotaxis, however, in colonization and disease is less well understood. Two genes in the H. pylori chemotaxis pathway, cheY and tlpB, which encode the chemotaxis response regulator and a methyl-accepting chemoreceptor, respectively, were disrupted. The cheY mutation was complemented with a wild-type copy of cheY inserted into the chromosomal rdxA gene. The cheY mutant lost chemotaxis but retained motility, while all other strains were motile and chemotactic in vitro. These strains were inoculated into gerbils either alone or in combination with the wild-type strain, and colonization and inflammation were assessed. While the cheY mutant completely failed to colonize gerbil stomachs, the tlpB mutant colonized at levels similar to those of the wild type. With the tlpB mutant, there was a substantial decrease in inflammation in the gerbil stomach compared to that with the wild type. Furthermore, there were differences in the numbers of each immune cell in the tlpB-mutant-infected stomach: the ratio of lymphocytes to neutrophils was about 8 to 1 in the wild type but only about 1 to 1 in the mutant. These results suggest that the TlpB chemoreceptor plays an important role in the inflammatory response while the CheY chemotaxis regulator plays a critical role in initial colonization. Chemotaxis mutants may provide new insights into the steps involved in H. pylori pathogenesis.
机译：幽门螺杆菌会导致人类胃部疾病以及小鼠和沙鼠胃部疾病。先前的结果表明，运动性对H至关重要。幽门螺杆菌可在小鼠，沙鼠和其他动物模型中定殖。然而，对趋化作用在定植和疾病中的作用了解得很少。 H中的两个基因。幽门螺杆菌的趋化途径，分别编码趋化反应应答调节剂和接受甲基的化学感受器的 cheY 和 tlpB 。 cheY 突变与插入到染色体 rdxA 基因的野生型 cheY 互补。 cheY 突变体失去趋化性但保留了运动能力，而其他所有菌株在体外均具有运动性和趋化性。将这些菌株单独或与野生型菌株组合接种到沙鼠中，并评估定植和炎症。虽然 cheY 突变体完全无法在沙鼠的胃中定植，但 tlpB 突变体的定植水平与野生型相似。与野生型相比，使用 tlpB 突变体，沙鼠胃中的炎症显着减少。此外，在 tlpB 突变体感染的胃中，每个免疫细胞的数量存在差异：在野生型中，淋巴细胞与中性粒细胞的比率约为8：1，而在野生型中，约为1：1。突变体。这些结果表明，TlpB化学感受器在炎症反应中起重要作用，而CheY趋化性调节剂在初始定植中起关键作用。趋化突变体可能为H涉及的步骤提供新的见解。幽门螺杆菌的发病机理

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