Berg R D
Infect Immun. 1980 Sep;29(3):1073-81. doi: 10.1128/iai.29.3.1073-1081.1980.
Escherichia coli C25 maintained population levels of 10(9) to 10(10) per g of cecum and translocated to 100% of the middle mesenteric lymph nodes in gnotobiotic mice monoassociated with E. coli C25. Intragastric inoculation of these mice with the cecal contents from specific-pathogen-free mice reduced the population levels of E. coli C25 to 10(6) per g of cecum and completely inhibited translocation to the mesenteric lymph nodes. Intragastric inoculation with heat-treated, Formalintreated, or filtered cecal contents did not reduce the population levels of E. coli C25 or reduce the incidence of translocation of E. coli C25 to the mesenteric lymph nodes. Thus, viable bacteria apparently are required in the cecal contents inocula to reduce the population levels and the incidence of translocation of E. coli C25. Treatment with streptomycin plus bacitracin decreased the anaerobic bacterial levels in these gnotobiotic mice, allowing increased population levels of E. coli C25 and increased translocation to the mesenteric lymph nodes. E. coli C25 also translocated to the mesenteric lymph nodes of specific-pathogen-free mice treated with streptomycin and bacitracin before colonization with E. coli C25. The high cecal population levels of E. coli C25 in these antibiotic-decontaminated specific-pathogen-free mice apparently overwhelm any barrier to translocation exerted by the immunologically developed lamina propria of the specific-pathogen-free mice. Inoculation of gnotobiotic mice with a cecal flora also reduced the population levels of an indigenous strain of E. coli with a concomitant inhibition of translocation of the indigenous E. coli to the mesenteric lymph nodes. Thus, bacterial antagonism of the gastrointestinal population levels of certain indigenous bacteria, such as E. coli, by other members of the normal bacterial flora appears to be an important defense mechanism confining bacteria to the gastrointestinal tract.
在与大肠杆菌C25单联的悉生小鼠中，大肠杆菌C25在盲肠中的菌量维持在每克10⁹至10¹⁰个，并转移至100%的肠系膜淋巴结。用无特定病原体小鼠的盲肠内容物对这些小鼠进行胃内接种，可将大肠杆菌C25的菌量降至每克盲肠10⁶个，并完全抑制其向肠系膜淋巴结的转移。用经热处理、甲醛处理或过滤的盲肠内容物进行胃内接种，并未降低大肠杆菌C25的菌量，也未降低大肠杆菌C25向肠系膜淋巴结转移的发生率。因此，接种的盲肠内容物中显然需要有活细菌，才能降低大肠杆菌C25的菌量及其转移发生率。链霉素加杆菌肽处理可降低这些悉生小鼠中的厌氧菌水平，使大肠杆菌C25的菌量增加，并增加其向肠系膜淋巴结的转移。在接种大肠杆菌C25之前，用链霉素和杆菌肽处理的无特定病原体小鼠，大肠杆菌C25也会转移至其肠系膜淋巴结。在这些经抗生素净化的无特定病原体小鼠中，大肠杆菌C25在盲肠中的高菌量显然克服了无特定病原体小鼠免疫发育的固有层所施加的任何转移屏障。用盲肠菌群接种悉生小鼠，也可降低一种本地大肠杆菌菌株的菌量，同时抑制本地大肠杆菌向肠系膜淋巴结转移。因此，正常菌群的其他成员对某些本地细菌（如大肠杆菌）在胃肠道中的菌量进行细菌拮抗作用，似乎是将细菌限制在胃肠道内的一种重要防御机制。
