Abstract
Proinflammatory macrophages are essential drivers of colitis and express the growth factor receptor ErbB4. This study tested the role of ErbB4 and its specific ligand, NRG4, in regulating macrophage function. We show that endogenous NRG4-ErbB4 signaling limits macrophage production of proinflammatory cytokines in vitro and limits colitis severity in vivo and thus is a potential target for therapeutic intervention.
Highlights
Inflammatory bowel disease (IBD) is a chronic illness affecting the gastrointestinal tract that presents with relapsing inflammatory injury
As inflammatory injury is a prominent feature of IBD and macrophages are central to potentiating disease severity, identifying ways to limit cytokine production in these cells may allow for the development of macrophage-specific targets to treat IBD
Inflammatory bowel disease (IBD) is characterized by elevated levels of proinflammatory cytokines in the gastrointestinal tract, and excessive cytokine production in intestinal macrophages is a likely contributor to the pathogenesis of IBD [44, 45]
Summary
Inflammatory bowel disease (IBD) is a chronic illness affecting the gastrointestinal tract that presents with relapsing inflammatory injury. Macrophages, for example, are recruited to sites of tissue injury where they release cytokines and chemokines that target potential pathogens while concurrently amplifying further immune activity [5] These cells exist along a continuum of functional states spanning from one extreme of anti-inflammatory activity that can promote repair and tissue maintenance, to proinflammatory activation that mediates pathogen clearance [6]. Activity of these cells, including cytokine production, at sites of injury is essential for preventing infection. As inflammatory injury is a prominent feature of IBD and macrophages are central to potentiating disease severity, identifying ways to limit cytokine production in these cells may allow for the development of macrophage-specific targets to treat IBD
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