NFKB1 and peritonitis: Later, Choi and colleagues suggested another potential approach by which BM-MSCs re-treat macrophage phenotype in a zymosan (a TLR-2 agonist)-induced peritonitis model, where they found that the activation of NF-κB signalling from macrophages triggered by zymosan led to the BM-MSC production of TNF-α and TNF-α-stimulated gene-6 (TSG-6), which then interacted with CD44 on the surface of macrophages to initiate a negative feedback loop that inhibited NFκB signalling and associated inflammatory responses [59].