Taken together, our results indicate that the absence of RsmY in Lp-EVs resulted in an up-regulation of IFN-ß in the supernatant, whereas the transfection of RsmY-RNA lead to a reduced IFN-ß secretion compared to the control RNA, in agreement with our model that RsmY contained within the Lp-EVs is biological active in the host cell and plays a role in dampening the immune response of host cells to infection. The gene discussed is IFNA1; the disease is infection.