Berg R D
Jikken Dobutsu. 1985 Jan;34(1):1-16. doi: 10.1538/expanim1978.34.1_1.
Bacterial translocation is defined as the passage of viable bacteria from the gastrointestinal (GI) tract through the mucosal epithelium to other sites, such as the mesenteric lymph nodes, spleen, liver and blood. This paper reviews results from animal models utilized to obtain information concerning the defense mechanisms operating in the healthy host to confine bacteria to the GI tract. Gnotobiotic and antibiotic-decontaminated mice colonized with particular bacteria demonstrated that the indigenous GI flora maintains an ecologic equilibrium to prevent intestinal bacterial overgrowth and translocation from the GI tract. Studies with athymic (nu/nu) mice, thymus-grafted (nu/nu) mice, neonatally thymectomized mice, and mice injected with immunosuppressive agents demonstrated that the host immune system is another defense mechanism inhibiting bacterial translocation from the GI tract. Ricinoleic acid given orally to mice disrupted the intestinal epithelial barrier allowing indigenous bacteria to translocate from the GI tract. Thus, bacterial translocation from the GI tract of healthy adult mice is inhibited by: (a) an intact intestinal epithelial barrier, (b) the host immune defense system, and (c) an indigenous GI flora maintaining ecological equilibrium to prevent bacterial overgrowth. Deficiencies in host defense mechanisms act synergistically to promote bacterial translocation from the GI tract as demonstrated by animal models with multiple alterations in host defenses. Bacterial translocation occurred to a greater degree in mice with streptozotocin-induced diabetes, mice receiving nonlethal thermal injury, and mice receiving the combination of an immunosuppressive agent plus an oral antibiotic than in mice with only a primary alteration in host defenses. The study of bacterial translocation in these complex models suggests that opportunistic infections from the GI tract occur in discrete stages. In the healthy adult animal, bacterial translocation from the GI tract either does not occur or occurs at a very low level and the host immune defenses eliminate the translocating bacteria. Bacterial translocation does take place if one of the host defense mechanisms is compromised, such as a deficiency in the immune response, bacterial overgrowth in the intestines, or an increase in the permeability of the intestinal barrier. In this first stage, the bacteria usually translocate in low numbers to the mesenteric lymph node, and sometimes spleen or liver, but do not multiply and spread systemically.(ABSTRACT TRUNCATED AT 400 WORDS)
细菌易位被定义为活细菌从胃肠道穿过黏膜上皮到达其他部位,如肠系膜淋巴结、脾脏、肝脏和血液。本文综述了利用动物模型所获得的结果,这些模型用于获取有关健康宿主中发挥作用以将细菌限制在胃肠道内的防御机制的信息。用特定细菌定殖的无菌和抗生素去污小鼠表明,肠道内的固有菌群维持着一种生态平衡,以防止肠道细菌过度生长和从胃肠道易位。对无胸腺(nu/nu)小鼠、胸腺移植(nu/nu)小鼠、新生期胸腺切除小鼠以及注射免疫抑制剂的小鼠的研究表明,宿主免疫系统是另一种抑制细菌从胃肠道易位的防御机制。给小鼠口服蓖麻油酸会破坏肠道上皮屏障,使固有细菌从胃肠道易位。因此,健康成年小鼠胃肠道的细菌易位受到以下因素抑制:(a)完整的肠道上皮屏障;(b)宿主免疫防御系统;(c)维持生态平衡以防止细菌过度生长的肠道固有菌群。如具有多种宿主防御改变的动物模型所示,宿主防御机制的缺陷会协同作用促进细菌从胃肠道易位。与仅存在宿主防御原发性改变的小鼠相比,链脲佐菌素诱导的糖尿病小鼠、接受非致死性热损伤的小鼠以及接受免疫抑制剂加口服抗生素联合治疗的小鼠中,细菌易位的程度更高。对这些复杂模型中细菌易位的研究表明,胃肠道的机会性感染分不同阶段发生。在健康成年动物中,胃肠道细菌易位要么不发生,要么发生率极低,宿主免疫防御会清除易位的细菌。如果宿主防御机制之一受损,如免疫反应缺陷、肠道细菌过度生长或肠道屏障通透性增加,细菌易位就会发生。在第一阶段,细菌通常少量易位至肠系膜淋巴结,有时也会到达脾脏或肝脏,但不会增殖并全身性扩散。(摘要截取自400词)