Die Translokation von Bakterien der Normalflora aus dem Gastrointestinal-Trakt zu Mesenterialen Lymphknoten und anderen Organen

Journal/Book: Mikroökologie und Therapie. 1981; 11: 27-34.

Abstract: Bacterial translocation is defined as the passage of viable bacteria from the gastrointestinal tract to the mesenteric lymph nodes and other organs. Normal flora bacteria are not found in the mesenteric lymph nodes, spleens, livers, or kidneys of healthy specific pathogen-free mice. These bacteria either do not pass through the gastrointestinal mucosa, are killed in transit, or are killed in organs such as the mesenteric lymph nodes. Two mechanisms operating to inhibit bacterial translocation from the gastrointestinal tract are: (a) the control of population levels of certain bacteria by other antagonistic members of the normal flora and (b) the host's immune system. Various normal flora bacteria translocate readily to the mesenteric lymph nodes of gnotobiotic mice monoassociated with these bacteria. For example, Escherichia coli translocates to 96 % of the mesenteric lymph nodes of gnotobiotic mice monoassociated with E. coli. Subsequent colonization of these monoassociated mice with the entire cecal flora obtained from specific pathogen-free mice reducers the cecal population levels of E. coli by 1,000-fold and translocation of E. coli to the mesenteric lymph nodes ceases. E. coli also maintains high population levels in the ceca of antibiotic-decontaminated mice subsequently inoculated with E. coli and L. coli translocates to 100 % of the mesenteric lymph nodes. Intragastric inoculation of these mice with a whole cecal flora reduces the cecal populations of E. coli and inhibits its translocation to the mesenteric lymph nodes. Enteric bacteria, such as E. coli, also translocate to the mesenteric lymph nodes of specific pathogen-free mice given oral penicillin, clindamycin, or metronidazole for only 4 days in their drinking water. These oral antibiotics disrupt the normal flora ecology in the gastrointestinaI tract allowing bacteria such as E. coli to obtain abnormally high population level, in the ceca and translocate to the mesenteric lymph nodes. Therefore, bacterial antagonism of the gastrointestinal population levels of certain enteric bacilli by other members of the normal flora is one mechanism inhibiting bacterial translocation and confining these bacteria to the gastrointestinal tract. The immune system also operates to inhibit bacterial translocation from the gastrointestinal tract. Immunosuppressive chemotherapeutic agents such as prednisone, cyclophosphamide, methotrexate, 5-fluorouracil, and cytosine arabinoside injected once intraperitoneally into specific pathogen-free mice promote the translocation of enteric bacilli to the mesenteric lymph nodes, spleens, livers, and kidneys. Viable aerobic and anaerobic bacteria also are present in 50 % of the mesenterc lymph nodes, spleens, liver, and kidneys of athymic (nu/nu) mice, whereas only 5.2 % of these organs contain viable bacteria in heterozygous (nu/+) mice with thymuses. Grafting thymuses to nu/nu mice reduces the incidence of bacterial translocation to 7.8 % of the mesenteric lymph nodes and other organs. Furthermore, neonatal thymectomy of specific pathogen-free mice increases the incidence of bacterial translocation to 29.3 % of these organs compared with only a 2.5 % translocation incidence in shamoperated control mice. Thus, the host's immune system, especially T-cell mediated immunity, is a defense mechanism inhibiting bacterial translocation from the gastrointestinal tract. Treatment of specific pathogen-free mice with the combination of an oral antibiotic, such as penicillin or clindamycin, and an immunosuppressive agent, such as prednisone or cyclophosphamide, synergistically promoted the translocation of bacteria from the gastrointestinal tract to the peritoneal cavity as compared to treatment with only an antibiotic or only an immunosuppressive agent. Bacterial translocation from the gastrointestinal tract may be the first step in the pathogenesis of infection by normal flora bacteria in debilitated human patients, especially those receiving immunosuppressive drugs and/ or oral antibiotics.

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