From the results of our present study, we speculate that AVR-48 may act as a feedback modulator as a result of which the binding of AVR-48 with TLR4 enhances resident or anti-inflammatory macrophages M2 over inflammatory macrophages M1 via an alternate pathway activation, as has been shown with chitohexaose in an LPS-induced sepsis model [21]. Here, TLR4 is linked to Sepsis.