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

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