Open AccessChlamydia trachomatis impairs host base excision repair by downregulating polymerase β
Author(s) -
Gulve Nitish,
Prusty Bhupesh K.,
Rudel Thomas
Publication year - 2019
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12986
Subject(s) - downregulation and upregulation , biology , base excision repair , dna repair , polymerase , chlamydia trachomatis , carcinogenesis , cancer research , microbiology and biotechnology , gene , immunology , genetics
Chlamydia trachomatis infections have been associated with ovarian cancer by several epidemiological studies. Here, we show that C . trachomatis ‐infected primary human ovarian epithelial cells display elevated oxidative DNA damage. Base excision repair, an important cellular mechanism to repair oxidative DNA lesions, was impaired in infected primary ovarian and in several other types of cells. Polymerase β was downregulated in infected cells associated with upregulation of microRNA‐499a (miR‐499a). Stabilising polymerase β by inhibiting miR‐499a significantly improved repair. Moreover, downregulation of tumour suppressor p53 also resulted in attenuated repair in these cells. Thus, our data show that downregulation of polymerase β by direct inhibition through miR‐499a and downregulation of p53 debilitate the host‐cell base excision repair during C . trachomatis infection.