Studying neurological impairment in IL-10 gene deficiency-induced mouse colitis

Abstract

Inflammatory Bowel Disease (IBD) is a group of diseases associated with chronic inflammation and mucosal immune responses within the gut. Elevated pro-inflammatory cytokines and chemokines drive this disease state, with loss of regulatory cytokines such as IL-10 exacerbating this response. The IL-10 Knockout (KO) mouse model replicates key pathological features of human IBD and provides an effective in vivo model for the study of intestinal inflammation and its systemic effects. Current research in the field highlights the link between IBD-associated inflammation and neurocognitive decline. CCL11 (eotaxin-1) is an age-related chemokine that has been linked to IBD and is an emerging biomarker and mediator in neurocognitive decline due to its stimulation of reactive oxygen species (ROS). Experimental evidence shows that CCL11 easily crosses the blood-brain barrier (BBB), accumulates in regions associated with memory formation and retention, and consequently enhances ROS production via the interaction with microglial cells. This study investigates how intestinal inflammation amplifies ROS production in the brain through CCL11 signaling, using IL-10 KO mice, and highlights a link between IBD and neurocognitive decline.