Helicobacter typhlonius and Helicobacter rodentium differentially affect the severity of colon inflammation and inflammation-associated neoplasia in IL10-deficient mice.
Helicobacter typhlonius and Helicobacter rodentium differentially affect the severity of colon inflammation and inflammation-associated neoplasia in IL10-deficient mice.
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发表时间：
2008-12
影响因子：
0.8
通讯作者：
M. Chichlowski;Julie M. Sharp;Deborah A. Vanderford;M. Myles;L. Hale
中科院分区：
文献类型：
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作者：
M. Chichlowski;Julie M. Sharp;Deborah A. Vanderford;M. Myles;L. Hale
幽门螺杆菌感染在许多动物设施中是地方性的，并且可以改变炎性肠病（IBD）表型的发病率。然而，关于H. typhlonius、黑腹蛛H.啮齿类和IBD模型中的联合感染。我们用H. typhlonius、黑腹蛛H.啮齿类或两者都是细菌。在有和没有抗螺杆菌治疗的情况下评估IBD的严重程度和炎症相关结肠肿瘤的发生率。感染的IL 10-/-小鼠发展IBD，严重程度为未感染（最小至无炎症）< H。rodentium < H. typhlonius <mixed H. rodentium + H.伤寒（严重炎症）。炎症相关性结肠肿瘤在感染小鼠中很常见，其发生率与IBD严重程度相关。阿莫西林、克拉霉素、甲硝唑和奥美拉唑联合治疗根除了感染小鼠的螺杆菌，并改善了感染和未感染小鼠的IBD。用H. rodentium，鼠尾草H.伤寒沙门氏菌或这两种微生物可引发严重IBD的发展，最终导致结肠肿瘤形成。感染小鼠中肿瘤病变的高发病率和多样性使该模型非常适合未来与炎症相关结肠癌的发展和化学预防相关的研究。抗生素治疗在患有结肠炎的螺杆菌感染和未感染的IL 10-/-小鼠中的相似的抑制作用表明，除了螺杆菌之外，未鉴定的微生物群驱动该模型中的炎症过程。这一发现表明螺杆菌和其他肠道微生物群在这些易感宿主中IBD的发病和持续中起着复杂的作用。
Infection with Helicobacter species is endemic in many animal facilities and may alter the penetrance of inflammatory bowel disease (IBD) phenotypes. However, little is known about the relative pathogenicity of H. typhlonius, H. rodentium, and combined infection in IBD models. We infected adult and neonatal IL10-/- mice with H. typhlonius, H. rodentium, or both bacteria. The severity of IBD and incidence of inflammation-associated colonic neoplasia were assessed in the presence and absence of antiHelicobacter therapy. Infected IL10-/- mice developed IBD with severity of noninfected (minimal to no inflammation) < H. rodentium < H. typhlonius <mixed H. rodentium + H. typhlonius (severe inflammation). Inflammation-associated colonic neoplasia was common in infected mice and its incidence correlated with IBD severity. Combined treatment with amoxicillin, clarithromycin, metronidazole, and omeprazole eradicated Helicobacter in infected mice and ameliorated established IBD in both infected and noninfected mice. Infection of IL10-/- mice with H. rodentium, H. typhlonius, or both organisms can trigger development of severe IBD that eventually leads to colonic neoplasia. The high incidence and multiplicity of neoplastic lesions in infected mice make this model well-suited for future research related to the development and chemoprevention of inflammation-associated colon cancer. The similar antiinflammatory effect of antibiotic therapy in Helicobacter-infected and -noninfected IL10-/- mice with colitis indicates that unidentified microbiota in addition to Helicobacter drive the inflammatory process in this model. This finding suggests a complex role for both Helicobacter and other intestinal microbiota in the onset and perpetuation of IBD in these susceptible hosts.