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1 mptomatic carrier state similar to bacterial commensalism.
2 nisms other than altering lipid A to support commensalism.
3 acquiring branched-chain amino acids during commensalism.
4 ear to be a determinant for C. jejuni during commensalism.
5 ic host cells to promote pathogenesis and/or commensalism.
6 cues the inability of mutants to compete for commensalism.
7 uestion of how these molecules contribute to commensalism.
8 ion to the changing intestinal milieu during commensalism.
10 is likely to play an important role in both commensalism and dissemination to cause invasive disease
15 Our findings indicate that many aspects of commensalism and pathogenicity are intertwined and that
18 tory IgA immunity, the regulation of mucosal commensalism, and defense of the barrier against enterop
20 omal cell interaction in itself is a form of commensalism, because it has been demonstrated that thes
21 enforcing mucosal tolerance and maintaining commensalism by promoting intestinal Treg cell formation
26 EtN by EptC is key to its ability to promote commensalism in an avian host and to survive in the mamm
34 mutualism is likely in P-limited systems and commensalism or parasitism is likely in N-limited system
42 review, we will discuss the transition from commensalism to pathogenesis, the key players of the fun
43 obligatory endosymbiosis and from restricted commensalism to semi-parasitism, with the specialisation
44 investigate E. faecalis factors required for commensalism, we identified E. faecalis genes that are u
45 To understand how the bacterium promotes commensalism, we used signature-tagged transposon mutage
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