GO and KEGG terms analysis files between TLR2-4 and WT cells

<p><em><span>Staphylococcus aureus</span></em><span> infections pose a potential threat to livestock production and public health. A novel strategy is needed to control <em>S. aureus</em> infection due to its adaptive evolution to antibiotics. Autophagy plays a key role in degrading bacteria for innate immune cells.</span> <span>In order to promote <em>S. aureus</em> clearance via TLR induced autophagy pathway, the domain fusion TLR2-4 with the extracellular domain of TLR2, specific recognizing <em>S. aureus</em>, and transmembrane and intracellular domains of TLR4 is assembled, then the goats expressing TLR2-4 is generated. TLR2-4 substantially augments the removal of <em>S. aureus</em> within macrophages by elevating autophagy level. Phosphorylated JNK/ERK1/2 promote LC3-puncta in TLR2-4 macrophages during <em>S. aureus</em>-induced autophagy via MyD88-mediated the TAK1 signaling cascade. Meantime, the TRIF-dependent TBK1-TFEB-OPTN signaling is involved in TLR2-4-triggered autophagy after <em>S. aureus</em> challenge. Moreover, the transcript of <em>ATG5 </em>and <em>ATG12 </em>is significantly increased via cAMP-PKA-NF-</span><span>k</span><span>B signaling, which facilitates <em>S. aureus</em>-induced autophagy in TLR2-4 macrophages. Overall, the novel receptor TLR2-4 enhances the autophagy-dependent clearance of <em>S. aureus</em> in macrophages via TAK1/TBK1-JNK/ERK, TBK1-TFEB-OPTN and cAMP-PKA-NF-</span><span>k</span><span>B-ATGs signaling pathways, which provide an alternative </span><span>approach to resistant against <em>S. aureus</em> infection.</span></p>