@article{RudelMehlitz2013,
  author    = {Rudel, Thomas and Mehlitz, Adrian},
  title     = {Modulation of host signaling and cellular responses by Chlamydia},
  series = {Cell Communication and Signaling},
  journal   = {Cell Communication and Signaling},
  doi       = {10.1186/1478-811X-11-90},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-97225},
  year      = {2013},
  abstract  = {Modulation of host cell signaling and cellular functions is key to intracellular survival of pathogenic bacteria. Intracellular growth has several advantages e.g. escape from the humoral immune response and access to a stable nutrient rich environment. Growth in such a preferred niche comes at the price of an ongoing competition between the bacteria and the host as well as other microbes that compete for the very same host resources. This requires specialization and constant evolution of dedicated systems for adhesion, invasion and accommodation. Interestingly, obligate intracellular bacteria of the order Chlamydiales have evolved an impressive degree of control over several important host cell functions. In this review we summarize how Chlamydia controls its host cell with a special focus on signal transduction and cellular modulation.},
  language  = {en}
}
@article{PrustyBoehmeBergmannetal.2012,
  author    = {Prusty, Bhupesh K. and B{\"o}hme, Linda and Bergmann, Birgit and Siegl, Christine and Krause, Eva and Mehlitz, Adrian and Rudel, Thomas},
  title     = {Imbalanced oxidative stress causes chlamydial persistence during non-productive Human Herpes Virus co-infection},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-76215},
  year      = {2012},
  abstract  = {Both human herpes viruses and Chlamydia are highly prevalent in the human population and are detected together in different human disorders. Here, we demonstrate that co-infection with human herpes virus 6 (HHV6) interferes with the developmental cycle of C. trachomatis and induces persistence. Induction of chlamydial persistence by HHV6 is independent of productive virus infection, but requires the interaction and uptake of the virus by the host cell. On the other hand, viral uptake is strongly promoted under co-infection conditions. Host cell glutathione reductase activity was suppressed by HHV6 causing NADPH accumulation, decreased formation of reduced glutathione and increased oxidative stress. Prevention of oxidative stress restored infectivity of Chlamydia after HHV6-induced persistence. We show that co-infection with Herpes simplex virus 1 or human Cytomegalovirus also induces chlamydial persistence by a similar mechanism suggesting that Chlamydia -human herpes virus co-infections are evolutionary shaped interactions with a thus far unrecognized broad significance.},
  subject      = {Biologie},
  language  = {en}
}
@article{KarunakaranMehlitzRudel2011,
  author    = {Karunakaran, Karthika and Mehlitz, Adrian and Rudel, Thomas},
  title     = {Evolutionary conservation of infection-induced cell death inhibition among Chlamydiales},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-68978},
  year      = {2011},
  abstract  = {Control of host cell death is of paramount importance for the survival and replication of obligate intracellular bacteria. Among these, human pathogenic Chlamydia induces the inhibition of apoptosis in a variety of different host cells by directly interfering with cell death signaling. However, the evolutionary conservation of cell death regulation has not been investigated in the order Chlamydiales, which also includes Chlamydia-like organisms with a broader host spectrum. Here, we investigated the apoptotic response of human cells infected with the Chlamydia-like organism Simkania negevensis (Sn). Simkania infected cells exhibited strong resistance to apoptosis induced by intrinsic stress or by the activation of cell death receptors. Apoptotic signaling was blocked upstream of mitochondria since Bax translocation, Bax and Bak oligomerisation and cytochrome c release were absent in these cells. Infected cells turned on pro-survival pathways like cellular Inhibitor of Apoptosis Protein 2 (cIAP-2) and the Akt/PI3K pathway. Blocking any of these inhibitory pathways sensitized infected host cell towards apoptosis induction, demonstrating their role in infection-induced apoptosis resistance. Our data support the hypothesis of evolutionary conserved signaling pathways to apoptosis resistance as common denominators in the order Chlamydiales.},
  subject      = {Chlamydiales},
  language  = {en}
}