The hypothesis of how LRRC75A-AS1 functions in immune response is proposed on the base of our findings. Bacteria component, such as LPS, triggers the activation of NF-κB pathway, introducing large secretion of inflammatory factors, which collapsed the TJ structure resulting in more exposes of cell to bacteria and triggering more intensified inflammation (left). Simultaneously, LRRC75A-AS1 is downregulated, then LRRC75A was degraded because of losing the protection of base pairing with LRRC75A-AS1, leading to enhanced TJ and less antigen receptor on the surface of cell, and finally attenuating the activation of inflammation (right). Left part and right part of the mechanism contribute together to an appropriate and sound immune response of bovine mammary epithelial cells to the bacteria stimuli.