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      1. Author :
        Schwandt, T.; Juengerkes, F.; Schumak, B.; Holzmann, B.; Layland, L.; Limmer, A.
      2. Title :
        Long-term effects of sepsis: The influence of bacteremia and bacterial translocation on systemic adaptive immune responses
      3. Type :
        Journal Article
      4. Year :
      5. Publication :
        Inflammation Research
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      11. Keywords :
        toll like receptor 4, interferon, tumor necrosis factor alpha, interleukin 10, cytokine, noscapine, antigen, Europe, bacteremia, adaptive immunity, sepsis, bacterial translocation, inflammation, surgical infection, injury, mouse, Escherichia coli, bacterium, liver, spleen, infection, lung, intestine, septic shock, abdominal surgery, cytotoxic T lymphocyte, Adenovirus, injection, portal vein, Kupffer cell, filter, immunity, risk, patient, opportunistic infection, model, ascending colon, stent, peritonitis, imaging, microbiology, Listeria monocytogenes IVIS, Xenogen
      12. Abstract :
        Objective: Bacterial translocation is a possible risk of abdominal surgery and may cause life-threatening consequences such as organ failure and septic shock. Patients surviving septic shock often suffer from opportunistic infections as well as defects in adaptive immunity. Methods: Here we investigated the influence of bacteremia and bac-terial translocation on systemic adaptive immune responses using murine models. To mimic abdominal surgery, mice were subjected to intestinal manipulation (IM). To study septic conditions, mice underwent colon ascendens stent peritonitis (CASP) or received E. coli intravenously or intraportally. We monitored the distribution of gut-derived bacteria by in vivo imaging (Xenogen) and additional microbiological assays and determined antigen-specific cytotoxic T lymphocyte (CTL) responses towards subsequent infection with recombinant adenoviruses (rAV) or Listeria monocytogenes. Results: We identified a strong correlation between the presence of bacteria in the spleen and a suppression of the CTL response, which was observed in mice that underwent CASP or were injected i.v. with E. coli. In contrast, the CTL response was not impaired in mice that were subjected to IM, or received E. coli by injection into the hepatic portal vein. Here, bacteria were detected in lung and liver but not in the spleens of mice. Depletion experiments implied that Kupffer cells as well as soluble mediators such as tumor necrosis factor alpha played an important role in trapping and clearance of translocated bacteria in liver and lung. Importantly, we figured out, that mice deficient in TLR-4 or in both MyD88 and TRIF showed no impaired CTL response after systemic E. coli infection. Astonishingly, IL-10-known as an immunosuppres-sive cytokine-did not play any role in E. coli-induced suppression of CTL response but rather type I IFN were shown to represent essential effector molecules as in mice deficient in IFNAR or IRF3/7 generated normal CTL responses after E. coli infection. Conclusion: We suggest that liver and lung fulfill a filter function to prevent systemic distribution of gut-derived bacteria. Failure of or bypassing these barriers might enable bacteria to access the spleen and thus cause systemic suppression of adaptive immunity, whereas the induction of local immunity was not affected. Suppression of CTL responses was strongly dependent on TLR-4 and mediated by downstream signaling of TRIF and MyD88 such as type I interferons.
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