Chlamydia psittaci-infected dendritic cells communicate with NK cells via exosomes to activate anti-bacterial immunity
Dendritic cells (DCs) and Natural killer (NK) cells are critically involved in the early response against various bacterial microbes. Functional activation of infected DCs and NK cell-mediated IFN-γ secretion essentially contributes to the protective immunity against Chlamydia. How DCs and NK cells cooperate during the anti-chlamydial response is not fully understood. Therefore, in our present study, we investigated the functional interplay between Chlamydia-infected DCs and NK cells. Our biochemical and cell biological experiments show that Chlamydia (C.) psittaci-infected dendritic cells (DCs) display enhanced exosome release. We find that such extracellular vesicles (referred to as dexosomes) do not contain infectious bacterial material but strongly induce IFN-γ production by NK cells. This directly affects C. psittaci growth in infected target cells. Furthermore, NK cell-released IFN-γ in cooperation with TNF-α and/or dexosomes augments apoptosis of non-infected as well as infected epithelial cells. Thus, the combined effect of dexosomes and pro-inflammatory cytokines restricts C. psittaci growth and attenuates bacterial subversion of apoptotic host cell death. In conclusion, this provides new insights into the functional cooperation between DCs, dexosomes and NK cells in the early steps of anti-chlamydial defense.
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