Bacterial extracellular vesicles modulate epithelial antiviral responses via macrophage-mediated immunomodulation.

The observed cellular responses to conditioned supernatants from bEV Kp - and bEV Ec -stimulated macrophages showed a trend of reduction, in case of OASL and ISG20 (Fig. 3 A) or significantly blocked for Mx1 and IFIT1 (Fig. 3 B) when Calu-3 cells were pre-treated with the Janus kinase inhibitor Ruxolitinib, which blocks the pathway activated by the interferon-α/β receptor (IFNAR).

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