人类微生物群与IL-10-/-小鼠相关:一个有价值的小肠结肠炎模型,用于解剖空肠弯曲杆菌与宿主免疫和肠道微生物群的相互作用。

Nizar W Shayya, Minnja S Foote, Luis Q Langfeld, Ke Du, Rasmus Bandick, Soraya Mousavi, Stefan Bereswill, Markus M Heimesaat
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引用次数: 4

摘要

继发性非生物(SAB) IL-10-/-小鼠构成了有价值的肠弯曲杆菌诱导的小肠结肠炎模型。鉴于宿主特异性肠道微生物群在脊椎动物宿主对肠致病性感染的易感性或抗性中起关键作用,我们调查了人类微生物群相关(hma)和SAB IL-10-/-小鼠中空肠梭菌感染的免疫病理后遗症。在口腔攻击后,空肠梭菌很容易在hma和SAB小鼠的胃肠道中定植,但前者的数量低于后者。尽管hma小鼠的临床损害程度较轻,但在感染后第6天,IL-10-/-小鼠结肠中存在和不存在人类肠道微生物群时,空肠梭菌感染的宏观和微观炎症后遗症(包括组织病理学和凋亡细胞反应)都相当明显。此外,hma和SAB小鼠的空肠梭菌感染导致结肠免疫细胞反应和肠道促炎介质分泌的差异类似地增强,这也适用于肠外包括全身隔间。值得注意的是,人乳头状瘤病毒感染小鼠与不同的肠道菌群变化有关。总之,hma IL-10-/-小鼠是一种可靠的空肠梭菌诱导的小肠结肠炎模型,用于解剖肠道病原体、脊椎动物宿主免疫和人类肠道微生物群的相互作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Human microbiota associated IL-10-/- mice: A valuable enterocolitis model to dissect the interactions of Campylobacter jejuni with host immunity and gut microbiota.

Human microbiota associated IL-10-/- mice: A valuable enterocolitis model to dissect the interactions of Campylobacter jejuni with host immunity and gut microbiota.

Human microbiota associated IL-10-/- mice: A valuable enterocolitis model to dissect the interactions of Campylobacter jejuni with host immunity and gut microbiota.

Human microbiota associated IL-10-/- mice: A valuable enterocolitis model to dissect the interactions of Campylobacter jejuni with host immunity and gut microbiota.

Secondary abiotic (SAB) IL-10-/- mice constitute a valuable Campylobacter jejuni-induced enterocolitis model. Given that the host-specific gut microbiota plays a key role in susceptibility of the vertebrate host towards or resistance against enteropathogenic infection, we surveyed immunopathological sequelae of C. jejuni infection in human microbiota associated (hma) and SAB IL-10-/- mice. Following oral challenge, C. jejuni readily colonized the gastrointestinal tract of hma and SAB mice, but with lower numbers in the former versus the latter. Whereas hma mice were clinically less severely compromised, both, macroscopic and microscopic inflammatory sequelae of C. jejuni infection including histopathological and apoptotic cell responses in the colon of IL-10-/- mice were comparably pronounced in the presence and absence of a human gut microbiota at day 6 post-infection. Furthermore, C. jejuni infection of hma and SAB mice resulted in similarly enhanced immune cell responses in the colon and in differential pro-inflammatory mediator secretion in the intestinal tract, which also held true for extra-intestinal including systemic compartments. Notably, C. jeuni infection of hma mice was associated with distinct gut microbiota shifts. In conclusion, hma IL-10-/- mice represent a reliable C. jejuni-induced enterocolitis model to dissect the interactions of the enteropathogen, vertebrate host immunity and human gut microbiota.

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