Transforming activities of Chlamydia pneumoniae in human mesothelial cells Autors/ores Antonietta Rizzo Department of Experimental Medicine, Second University of Naples, Naples. Caterina Romano Carratelli Department of Experimental Medicine, Second University of Naples. Anna De Filippis Department of Experimental Medicine, Second University of Naples. Nazario Bevilacqua Department of Clinical Pathology, A. Cardarelli Hospital, Naples. Maria Antonietta Tufano Department of Experimental Medicine, Second University of Naples. Elisabetta Buommino Department of Experimental Medicine, Second University of Naples. Paraules clau: Chlamydia pneumoniae, cytotoxicity, human mesothelial cells, cellular transformation, tumoral markers Resum Knowledge in viral oncology has made considerable progress in the field of cancer fight. However, the role of bacteria as mediators of oncogenesis has not yet been elucidated. As cancer still is the leading cause of death in developed countries, understanding the long-term effects of bacteria has become of great importance as a possible means of cancer prevention. This study reports that Chlamydia pneumoniae infection induce transformation of human mesothelial cells. Mes1 cells infected with C. pneumoniae at a multiplicity of infection of 4 inclusion-forming units/cell showed many intracellular inclusion bodies. After a 7-day infection an increased proliferative activity was also observed. Real-time PCR analysis revealed a strong induction of calretinin, Wilms’ tumour gene 1, osteopontin, matrix metalloproteinases-2, and membrane-type 1 metalloproteinases gene expression in Mes1 cell, infected for a longer period (14 days). The results were confirmed by western blot analysis. Zymography analysis showed that C. pneumoniae modulated the in-vitro secretion of MMP-2 in Mes1 cells both at 7 and 14 days. Cell invasion, as measured by matrigel-coated filter, increased after 7 and 14 days infection with C. pneumoniae, compared with uninfected Mes1 cells. The results of this study suggest that C. pneumoniae infection might support cellular transformation, thus increasing lung cancer risk. [Int Microbiol 2014; 17(4):185-193]Keywords: Chlamydia pneumoniae · cytotoxicity · human mesothelial cells · cellular transformation · tumoral markers Descàrregues PDF (English) Número Vol. 17 Núm. 4 (2014) Secció Articles Llicència Submission of a manuscript to International Microbiology implies: that the work described has not been published before, including publication in the World Wide Web (except in the form of an Abstract or as part of a published lecture, review, or thesis); that it is not under consideration for publication elsewhere; that all the coauthors have agreed to its publication. The corresponding author signs for and accepts responsability for releasing this material and will act on behalf of any and all coauthors regarding the editorial review and publication process.If an article is accepted for publication in International Microbiology, the authors (or other copyright holder) must transfer to the journal the right–not exclusive–to reproduce and distribute the article including reprints, translations, photographic reproductions, microform, electronic form (offline, online) or any other reproductions of similar nature. Nevertheless, all article in International Microbiology will be available on the Internet to any reader at no cost. The journal allows users to freely download, copy, print, distribute, search, and link to the full text of any article, provided the authorship and source of the published article is cited. The copyright owner's consent does not include copying for new works, or resale. In these cases, the specific written permission of International Microbiology must first be obtained.Authors are requested to create a link to the published article on the journal's website. The link must be accompanied by the following text: "The original publication is available on LINK at <http://www.im.microbios.org>. Please use the appropiate URL for the article in LINK. Articles disseminated via LINK are indexed, abstracted, and referenced by many abstracting and information services, bibliographic networks, subscription agencies, library networks, and consortia.
