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1 Intestinal Diseases Research Program and 3 Gastrointestinal Division and Department of Medicine, Health Sciences Center, McMaster University, Hamilton, Ontario, Canada L8N 3Z5; and 2 Department of Surgical and Gastroenterological Science, Section of Gastroenterology, University of Padua, 35131 Padua, Italy
Intestinal
inflammation due to nematode infection impairs enteric cholinergic
nerve function and induces hypercontractility of intestinal muscle.
Macrophages have been implicated in the neural changes, but the
subpopulation and mechanism involved are unknown. We examined whether
macrophages alter nerves by virtue of their ability to activate
lymphocytes via major histocompatibility complex (MHC) II-restricted
antigen presentation. We also attempted to evaluate the role of
macrophage subsets using op/op mice deficient in macrophage
colony-stimulating factor (M-CSF). ACh release from the myenteric
plexus was measured in MHC II- and M-CSF-deficient (op/op)
mice infected with Trichinella spiralis. F4/80-positive macrophages and interleukin-1
were constitutively present in op/op and op/? mice but increased only in
op/? mice postinfection. After infection, a marked
suppression of ACh release occurred only in infected MHC II-deficient
and op/? mice. Muscle hypercontractility remained evident in
infected op/? mice. Treatment with M-CSF restored macrophage
number, and this was accompanied by suppression of cholinergic nerve
function during infection. Thus M-CSF plays a critical role in this
model by recruiting a subset of macrophages that selectively suppresses
enteric neural function.
macrophage colony-stimulating factor; op/op mice; nematode; enteric nerves; inflammatory bowel disease
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