Differences in mucosal gene expression in the colon of two inbred mouse strains after colonization with commensal gut bacteria.
Differences in mucosal gene expression in the colon of two inbred mouse strains after colonization with commensal gut bacteria.
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DOI：
10.1371/journal.pone.0072317
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Loh G
中科院分区：
文献类型：
--
作者：
Brodziak F;Meharg C;Blaut M;Loh G
宿主基因型被认为有助于肠道中单独组成的细菌群落。为了更深入地了解肠道细菌与宿主之间的相互作用，我们将无菌C3H和C57BL/10小鼠与来自C57BL/10供体小鼠的肠道细菌进行了关联。用变性梯度凝胶电泳分析动物之间的微生物群相似性，揭示了小鼠菌株特异性微生物群的发展。基于微阵列的结肠粘膜基因表达分析鉴定出202个基因，其表达差异大于2个因子。生物信息学工具的应用表明，包括信号/分泌、脂质降解/分解代谢、鸟嘌呤核苷酸/鸟苷结合和免疫应答在内的功能术语在差异表达基因中显著富集。我们仔细观察了56个表达差异大于4的基因，发现编码Tlr1和Ang4的基因在C57BL/10小鼠中表达更高，这两个基因参与了对肠道细菌的识别和反应。在C3H小鼠中检测到较高的Pla2g2a表达。此外，许多干扰素诱导基因在C3H中的表达高于C57BL/10小鼠，包括Gbp1、Mal、Oasl2、Ifi202b、Rtp4、Ly6g6c、Ifi27l2a、Usp18、Ifit1、Ifi44和Ly6g，这表明干扰素可能在微生物群调节中发挥重要作用。然而，编码干扰素的基因、受体、参与干扰素表达调控或信号通路的因子在两种小鼠品系之间的表达没有差异。综上所述，我们的研究证实了宿主基因型参与了肠道中宿主特异性细菌群落的建立。基于相同细菌接种定殖后的表达差异，我们提出Pla2g2a和干扰素依赖基因可能促成了这一现象。
The host genotype has been proposed to contribute to individually composed bacterial communities in the gut. To provide deeper insight into interactions between gut bacteria and host, we associated germ-free C3H and C57BL/10 mice with intestinal bacteria from a C57BL/10 donor mouse. Analysis of microbiota similarity between the animals with denaturing gradient gel electrophoresis revealed the development of a mouse strain-specific microbiota. Microarray-based gene expression analysis in the colonic mucosa identified 202 genes whose expression differed significantly by a factor of more than 2. Application of bioinformatics tools demonstrated that functional terms including signaling/secretion, lipid degradation/catabolism, guanine nucleotide/guanylate binding and immune response were significantly enriched in differentially expressed genes. We had a closer look at the 56 genes with expression differences of more than 4 and observed a higher expression in C57BL/10 mice of the genes coding for Tlr1 and Ang4 which are involved in the recognition and response to gut bacteria. A higher expression of Pla2g2a was detected in C3H mice. In addition, a number of interferon-inducible genes were higher expressed in C3H than in C57BL/10 mice including Gbp1, Mal, Oasl2, Ifi202b, Rtp4, Ly6g6c, Ifi27l2a, Usp18, Ifit1, Ifi44, and Ly6g indicating that interferons may play an essential role in microbiota regulation. However, genes coding for interferons, their receptors, factors involved in interferon expression regulation or signaling pathways were not differentially expressed between the two mouse strains. Taken together, our study confirms that the host genotype is involved in the establishment of host-specific bacterial communities in the gut. Based on expression differences after colonization with the same bacterial inoculum, we propose that Pla2g2a and interferon-dependent genes may contribute to this phenomenon.
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影响因子：
64.8
作者：
通讯作者：
--
影响因子：
64.8
作者：
Arumugam, Manimozhiyan;Raes, Jeroen;Pelletier, Eric;Le Paslier, Denis;Yamada, Takuji;Mende, Daniel R.;Fernandes, Gabriel R.;Tap, Julien;Bruls, Thomas;Batto, Jean-Michel;Bertalan, Marcelo;Borruel, Natalia;Casellas, Francesc;Fernandez, Leyden;Gautier, Laurent;Hansen, Torben;Hattori, Masahira;Hayashi, Tetsuya;Kleerebezem, Michiel;Kurokawa, Ken;Leclerc, Marion;Levenez, Florence;Manichanh, Chaysavanh;Nielsen, H. Bjorn;Nielsen, Trine;Pons, Nicolas;Poulain, Julie;Qin, Junjie;Sicheritz-Ponten, Thomas;Tims, Sebastian;Torrents, David;Ugarte, Edgardo;Zoetendal, Erwin G.;Wang, Jun;Guarner, Francisco;Pedersen, Oluf;de Vos, Willem M.;Brunak, Soren;Dore, Joel;Weissenbach, Jean;Ehrlich, S. Dusko;Bork, Peer
通讯作者：
Bork, Peer
影响因子：
12.3
作者：
Gentleman RC;Carey VJ;Bates DM;Bolstad B;Dettling M;Dudoit S;Ellis B;Gautier L;Ge Y;Gentry J;Hornik K;Hothorn T;Huber W;Iacus S;Irizarry R;Leisch F;Li C;Maechler M;Rossini AJ;Sawitzki G;Smith C;Smyth G;Tierney L;Yang JY;Zhang J
通讯作者：
Zhang J
DOI：
10.1073/pnas.0907722106
发表时间：
2009-09-15
影响因子：
11.1
作者：
Petnicki-Ocwieja, Tanja;Hrncir, Tomas;Kobayashi, Koichi S.
通讯作者：
Kobayashi, Koichi S.
影响因子：
8
作者：
Markova, M;Koratkar, RA;Farber, SA
通讯作者：
Farber, SA