Supplementary Figure 7: Model of dual TREM1 amplification of immune responses after cerebral ischemia.
From: Peripheral TREM1 responses to brain and intestinal immunogens amplify stroke severity
(Left side) Cerebral injury activates the sympathetic nervous system (SNS) within hours of MCAo, leading to early disruption of the gut barrier and translocation of bacterial PAMPs across the epithelial barrier. There, PAMPs induce and activate TREM1 signaling in lamina propria Mo/MΦ subsets, amplifying the innate immune response and further disrupting gut barrier integrity and facilitating translocation of bacteria to the periphery. (Right side): Cerebral infarction induces the release of sterile DAMPs that activate TREM1 on circulating peripheral and splenic myeloid cells. Thus, TREM1 is induced in myeloid cells in two spatially distinct processes after MCAo. Dual brain-derived and intestinal-derived TREM1 responses converge and amplify the post-stroke innate immune response, increasing cerebral injury.
