Wells C L
Department of Laboratory Medicine, University of Minnesota, Minneapolis 55455.
Antonie Van Leeuwenhoek. 1990 Aug;58(2):87-93. doi: 10.1007/BF00422722.
It is now well known that endogenous bacteria can translocate from the intestinal tract and cause many of the complicating infections seen in severely ill, hospitalized patients. Of the hundreds of bacterial species in the intestinal tract, relatively few aerobic/facultative species appear to translocate with any frequency. Van der Waaij and colleagues (1971, 1972a, 1972b) originally proposed that, by a process termed 'colonization resistance', strictly anaerobic bacteria prevented the intestinal overgrowth and subsequent translocation of these potentially pathogenic aerobic/facultative bacteria. Selective antimicrobial decontamination, designed to maintain colonization resistance, has been effective in reducing the incidence of infectious morbidity in high risk patients. However, the mechanisms controlling bacterial translocation remain unclear, but appear to depend on host factors, as well as on factors inherent in the microbe itself. There is both clinical and experimental evidence supporting the concept that strictly anaerobic bacteria do not readily translocate. Bacteria that are able to survive within macrophages (e.g., Salmonella species and Listeria monocytogenes) translocate easier than others, and there is recent experimental evidence that normal intestinal bacteria may translocate to the draining mesenteric lymph node within host phagocytes. There is also evidence that anaerobic bacteria translocate along with facultative species in situations associated with intestinal epithelial damage, i.e., burn trauma, oral ricinoleic acid, and acute mesenteric ischemia. In contrast, recent experimental evidence demonstrates that facultative bacteria can translocate across a histologically intact intestinal epithelium, and that the ileal absorptive cell may be at least one portal of entry prior to transport into deeper tissues. It is anticipated that further clarification of the routes and mechanisms involved in bacterial translocation will provide new insights into the treatment and prevention of a significant proportion of the infectious morbidity seen in severely ill, hospitalized patients.
现在已经清楚地知道，内源性细菌可从肠道移位，并导致重症住院患者出现许多并发症感染。在肠道中的数百种细菌中，相对较少的需氧/兼性菌种似乎会频繁移位。范德瓦伊及其同事（1971年、1972年a、1972年b）最初提出，通过一种称为“定植抗性”的过程，严格厌氧菌可防止这些潜在致病性需氧/兼性细菌在肠道过度生长及随后的移位。旨在维持定植抗性的选择性抗菌去污已有效降低了高危患者感染性发病的发生率。然而，控制细菌移位的机制仍不清楚，但似乎取决于宿主因素以及微生物自身固有的因素。有临床和实验证据支持严格厌氧菌不易移位这一概念。能够在巨噬细胞内存活的细菌（如沙门氏菌属和单核细胞增生李斯特菌）比其他细菌更容易移位，并且最近有实验证据表明正常肠道细菌可能在宿主吞噬细胞内移位至引流的肠系膜淋巴结。也有证据表明，在与肠道上皮损伤相关的情况下，即烧伤创伤、口服蓖麻油酸和急性肠系膜缺血时，厌氧菌会与兼性菌种一起移位。相比之下，最近的实验证据表明，兼性细菌可穿过组织学上完整的肠道上皮移位，并且回肠吸收细胞在转运至更深层组织之前可能至少是一个进入门户。预计进一步阐明细菌移位所涉及的途径和机制将为治疗和预防重症住院患者中很大一部分感染性发病提供新的见解。
