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DNA-release by Streptococcus pneumoniae autolysin LytA induced Krueppel-like factor 4 expression in macrophages

AuthorsHerta, Toni; Bhattacharyya, Aritra; Bollensdorf, Christian; Kabus, Christin; García, Pedro ; Suttorp, Norbert; Hippenstiel, Stefan; Zahlten, Janine
Issue Date1-Dec-2018
PublisherNature Publishing Group
CitationScientific Reports 8 (1) 5723 (2018)
AbstractThe recruitment of myeloid cells to the lung is of utmost importance for the elimination of invading pathogens. We investigated the Streptococcus pneumoniae-dependent induction mechanism of KLF4 in macrophages as a potential regulator of the macrophage immune response. We demonstrated that only viable pneumococci, which have direct contact to the host cells and release LytA-dependent DNA, induced KLF4. Exogenous supplementation of pneumococcal, other bacterial, eukaryotic foreign (human) or self (mouse) DNA to autolysis-deficient pneumococci restored (at least in part) pneumococci-related KLF4 induction. Experiments using TLR9, TRIF and MyD88 knockout macrophages revealed that TLR9, TRIF and MyD88 were partly involved in the S. pneumoniae-induced KLF4 expression. BMMs missing important DNA receptor related molecules (ASC-/-, STING-/-) showed no differences in pneumococci-related KLF4 expression. Similar results were observed with IFNAR-/- BMMs and Type I IFN stimulated cells. LyzMcre mediated knockdown of KLF4 in BMMs resulted in a decreased secretion of proinflammatory cytokines and enhanced IL-10 release. In summary, we showed that pneumococci-related KLF4 induction in macrophages is mediated via a PAMP-DAMP induction mechanism involving a hitherto unknown host cell DNA sensor leading to a more proinflammatory macrophage phenotype.
Description14 p.-8 fig.
Publisher version (URL)http://dx.doi.org/10.1038/s41598-018-24152-1
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