Inflammation-induced impairment of enteric nerve function in nematode-infected mice is macrophage dependent.

Trichinella spiralis infection in rodents is associated with suppression of ACh release from myenteric plexus that can be mimicked by macrophage-derived cytokines. We verified the presence of a macrophage infiltrate in the intestine during T. spiralis infection and determined the extent to which this cell type is responsible for the neural changes. C57BL/6 mice were infected with 375 T. spiralis larvae by gavage, and the presence of macrophages (F4/80 positive) in the jejunum was determined immunohistochemically. In another experiment, infected mice were treated intravenously with liposomes containing dichloromethylene diphosphonate (clodronate, Cl(2)MDP), which causes apoptosis of macrophages, and killed at postinfection day 6, and jejunal tissues were evaluated for the presence of F4/80-positive cells and for [(3)H]ACh release from the myenteric plexus. Infection caused an infiltration of F4/80-positive cells into the intestinal mucosa, muscle layers, and myenteric plexus region and a significant suppression of ACh release (50%). Depletion of F4/80-positive macrophages using Cl(2)MDP-containing liposomes prevented the suppression in [(3)H]ACh release, identifying macrophages as the cell type involved in the functional impairment of enteric cholinergic nerves.

[1]  S. Collins,et al.  Inflamation-induced impairment of cholinergic nerve function is CD-4 independent in nematode-infected mice , 1998 .

[2]  S. Collins,et al.  Increased intestinal muscle contractility and worm expulsion in nematode-infected mice. , 1997, The American journal of physiology.

[3]  Y. Takei,et al.  Liposome‐encapsulated dichloromethylene diphosphonate induces macrophage apoptosis in vivo and in vitro , 1996, Journal of leukocyte biology.

[4]  T. K. van den Berg,et al.  Apoptosis of macrophages induced by liposome-mediated intracellular delivery of clodronate and propamidine. , 1996, Journal of immunological methods.

[5]  S. Collins,et al.  Involvement of eicosanoids and macrophage-like cells in cytokine-mediated changes in rat myenteric nerves. , 1995, Gastroenterology.

[6]  K. Mchugh,et al.  Experimental colitis alters myenteric nerve function at inflamed and noninflamed sites in the rat. , 1995, Gastroenterology.

[7]  K. Driscoll.  Macrophage inflammatory proteins: biology and role in pulmonary inflammation. , 1994, Experimental lung research.

[8]  S. Collins,et al.  Synergism between interleukins 1 beta and 6 on noradrenergic nerves in rat myenteric plexus. , 1994, Gastroenterology.

[9]  N. Van Rooijen,et al.  Liposome mediated depletion of macrophages: mechanism of action, preparation of liposomes and applications. , 1994, Journal of immunological methods.

[10]  S. Collins,et al.  Expression of cytokines in the longitudinal muscle myenteric plexus of the inflamed intestine of rat. , 1994, Gastroenterology.

[11]  S. Collins,et al.  Mechanism underlying tumor necrosis factor-alpha suppression of norepinephrine release from rat myenteric plexus. , 1994, The American journal of physiology.

[12]  S. Collins,et al.  Human recombinant interleukin 1 beta suppresses acetylcholine release from rat myenteric plexus. , 1993, Gastroenterology.

[13]  W. Hsueh,et al.  Cellular localization of tumor necrosis factor (TNF)-alpha transcripts in normal bowel and in necrotizing enterocolitis. TNF gene expression by Paneth cells, intestinal eosinophils, and macrophages. , 1993, The American journal of pathology.

[14]  J. Vilček,et al.  Tumor necrosis factor. New insights into the molecular mechanisms of its multiple actions. , 1991, The Journal of biological chemistry.

[15]  C. Dinarello.  Interleukin-1 and interleukin-1 antagonism. , 1991, Blood.

[16]  S. Collins,et al.  Impaired acetylcholine release from the myenteric plexus of Trichinella-infected rats. , 1989, The American journal of physiology.

[17]  N. Rooijen.  The liposome-mediated macrophage ‘suicide’ technique , 1989 .

[18]  Y. Mahida,et al.  Enhanced production of interleukin 1-beta by mononuclear cells isolated from mucosa with active ulcerative colitis of Crohn's disease. , 1989, Gut.

[19]  N. Read,et al.  Studies on the mechanism of bowel disturbance in ulcerative colitis. , 1987, Gastroenterology.

[20]  W. Weems,et al.  Intrinsic jejunal propulsion in the guinea pig during parasitism with Trichinella spiralis. , 1987, Gastroenterology.

[21]  L. Old,et al.  Tumor necrosis factor (TNF). , 1985, Science.

[22]  D. Priebat,et al.  Measurement of cutaneous inflammation: estimation of neutrophil content with an enzyme marker. , 1982, The Journal of investigative dermatology.

[23]  C. Ottaway,et al.  Regional blood flow and the localization of lymphoblasts in the small intestine of the mouse. II. The effects of a primary enteric infection with Trichinella spiralis. , 1980, Immunology.

[24]  A. Dvorak,et al.  Crohn's disease: transmission electron microscopic studies. III. Target tissues. Proliferation of and injury to smooth muscle and the autonomic nervous system. , 1980, Human pathology.

[25]  A. Dvorak,et al.  Crohn's disease: transmission electron microscopic studies. II. Immunologic inflammatory response. Alterations of mast cells, basophils, eosinophils, and the microvasculature. , 1980, Human pathology.

[26]  H. Mikkelsen.  Invited Re vie W Histology and Histo pathology Macrophages in the external muscle layers of mammalian intestines , 2010 .

[27]  J. Snick,et al.  Interleukin-6: an overview. , 1990, Annual review of immunology.

[28]  S. Gordon,et al.  F4/80, a monoclonal antibody directed specifically against the mouse macrophage , 1981, European journal of immunology.