Figure 8.

Schematic representation of the outcome of this study. (A): 1) MAP induces Notch-1 signaling and downstream influence on IL-6 to hijack MCL-1 dependent inhibition of apoptosis, which allow its chronic intracellular persistence, and subsequent inflammation. 2) Notch-1 and IL-6 reciprocal modulation to amplify MCL-1 expression, suggesting the critical role of Notch-1 signaling and its downstream effect in intensifying MAP-mediated effect in macrophages. 3) MAP promoting M1 versus M2 polarization through Notch-1 signaling. (B): Targeting Notch signaling in MAP-infected macrophages enhanced macrophage apoptosis, decreased MAP burden, and promoted M2 polarization and anti-inflammatory cytokines production. TLRs: Toll-like receptors, NICD: Notch intracellular domain.