@article{HerwegHansmeierOttoetal.2015,
  author    = {Herweg, Jo-Ana and Hansmeier, Nicole and Otto, Andreas and Geffken, Anna C. and Subbarayal, Prema and Prusty, Bhupesh K. and Becher, D{\"o}rte and Hensel, Michael and Schaible, Ulrich E. and Rudel, Thomas and Hilbi, Hubert},
  title     = {Purification and proteomics of pathogen-modified vacuoles and membranes},
  series = {Frontiers in Cellular and Infection Microbiology},
  volume    = {5},
  journal   = {Frontiers in Cellular and Infection Microbiology},
  number    = {48},
  doi       = {10.3389/fcimb.2015.00048},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-151823},
  year      = {2015},
  abstract  = {Certain pathogenic bacteria adopt an intracellular lifestyle and proliferate in eukaryotic host cells. The intracellular niche protects the bacteria from cellular and humoral components of the mammalian immune system, and at the same time, allows the bacteria to gain access to otherwise restricted nutrient sources. Yet, intracellular protection and access to nutrients comes with a price, i.e., the bacteria need to overcome cell-autonomous defense mechanisms, such as the bactericidal endocytic pathway. While a few bacteria rupture the early phagosome and escape into the host cytoplasm, most intracellular pathogens form a distinct, degradation-resistant and replication-permissive membranous compartment. Intracellular bacteria that form unique pathogen vacuoles include Legionella, Mycobacterium, Chlamydia, Simkania, and Salmonella species. In order to understand the formation of these pathogen niches on a global scale and in a comprehensive and quantitative manner, an inventory of compartment-associated host factors is required. To this end, the intact pathogen compartments need to be isolated, purified and biochemically characterized. Here, we review recent progress on the isolation and purification of pathogen-modified vacuoles and membranes, as well as their proteomic characterization by mass spectrometry and different validation approaches. These studies provide the basis for further investigations on the specific mechanisms of pathogen-driven compartment formation.},
  language  = {en}
}
@article{KosterGurumurthyKumaretal.2022,
  author    = {Koster, Stefanie and Gurumurthy, Rajendra Kumar and Kumar, Naveen and Prakash, Pon Ganish and Dhanraj, Jayabhuvaneshwari and Bayer, Sofia and Berger, Hilmar and Kurian, Shilpa Mary and Drabkina, Marina and Mollenkopf, Hans-Joachim and Goosmann, Christian and Brinkmann, Volker and Nagel, Zachary and Mangler, Mandy and Meyer, Thomas F. and Chumduri, Cindrilla},
  title     = {Modelling Chlamydia and HPV co-infection in patient-derived ectocervix organoids reveals distinct cellular reprogramming},
  series = {Nature Communications},
  volume    = {13},
  journal   = {Nature Communications},
  number    = {1},
  doi       = {10.1038/s41467-022-28569-1},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-301349},
  year      = {2022},
  abstract  = {Coinfections with pathogenic microbes continually confront cervical mucosa, yet their implications in pathogenesis remain unclear. Lack of in-vitro models recapitulating cervical epithelium has been a bottleneck to study coinfections. Using patient-derived ectocervical organoids, we systematically modeled individual and coinfection dynamics of Human papillomavirus (HPV)16 E6E7 and Chlamydia, associated with carcinogenesis. The ectocervical stem cells were genetically manipulated to introduce E6E7 oncogenes to mimic HPV16 integration. Organoids from these stem cells develop the characteristics of precancerous lesions while retaining the self-renewal capacity and organize into mature stratified epithelium similar to healthy organoids. HPV16 E6E7 interferes with Chlamydia development and induces persistence. Unique transcriptional and post-translational responses induced by Chlamydia and HPV lead to distinct reprogramming of host cell processes. Strikingly, Chlamydia impedes HPV-induced mechanisms that maintain cellular and genome integrity, including mismatch repair in the stem cells. Together, our study employing organoids demonstrates the hazard of multiple infections and the unique cellular microenvironment they create, potentially contributing to neoplastic progression.},
  language  = {en}
}
@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}
}