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Isolation of Lamina Propria Mononuclear Cells from Murine Colon Using Collagenase E
Published on: September 26, 2019
Emergency granulopoiesis and innate immune memory in inflammatory bowel disease
Sílvia Pires1, Randy S Longman1
1Department of Medicine, Division of Gastroenterology and Hepatology, Weill Cornell Medicine, New York, NY, USA; Jill Roberts Center for Inflammatory Bowel Disease, Weill Cornell Medicine, New York, NY, USA; Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, New York, NY, USA.
Abstract:
Emerging evidence now points to innate tissue immunity as a critical orchestrator of both local tissue adaptation and long-range hematopoietic reprogramming, including the amplification of emergency granulopoiesis through bone marrow progenitor remodeling. These findings position the intestine as an instructive niche capable of imprinting long-lived changes both locally and systemically. This review synthesizes current findings at the intersection of gut and bone marrow biology, examining how intestinal inflammation shapes granulopoietic output and how bone marrow-derived effectors, in turn, reinforce maladaptive tissue responses that underlie chronic intestinal manifestations, including colitis-associated cancer and extraintestinal inflammatory complications frequently seen in IBD. We delineate the physiological framework governing these regulatory nodes and highlight the translational implications for next-generation therapeutic intervention.
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