title: [Pathologic findings of mouse air-pouches injected with Escherichia coli O: 14, lipopolysaccharide, or interleukin-1 beta].
abstract: Inflammation of the facsimile synovium was induced by injecting 4 mg of heat-killed Escherichia coli (E. coli) O: 14, 1 mg of lipopolysaccharide (LPS), or 100 U of recombinant interleukin-1 beta (IL-1 beta) into a 7-day-old subcutaneous air-pouch in C 57 Black mice. Saline was used for control animals. A total of 150 mice were used. Hyperplasia in the lining cells (lining greater than 5 cells thick) was induced in the inner layer of 18 of 20 air-pouches (in 9 of 10 mice) at 7 days after injection of E. coli or LPS. The results at 7 days after were significantly higher than those at 3 days after injection of E. coli (11/20 mice) or LPS (5/10). The number of lining layers with neutrophil infiltration reached a maximum 3 days after injection of E. coli (3 days: 10/20, 7 days: 2/20, p < 0.01) or LPS (3 days: 7/10, 7 days: 2/10, p < 0.01). There was a greater number of mononuclear cells in the sublining layers 7 days after injection of E. coli (9/20 mice) or LPS (7/10) than at 3 days (2/20, 3/10), (p < 0.01). There was a higher incidence of mononuclear cells around the post-capillary venules (PCV) at 7 days after injection of E. coli (9/20 mice) or LPS (7/10) than at 1 day (0/20, 0/10), (p < 0.01). There were significantly more mast cells around the PCV at 1 day after injection of E. coli (6.0 +/- 2.1) or LPS (5.0 +/- 1.8) than in the saline controls (1.0 +/- 0.4), (p < 0.01). Immunohistochemical stains for IgG showed more positive cells at 7 days after injection of E. coli (4.0 +/- 1.7) or LPS (4.0 +/- 1.4) than in controls (0.5 +/- 0.2), (p < 0.05). Significantly more exudate (0.5 +/- 0.3 mls) was found in the air-pouch at 1 day after injection with IL-1 beta than at 1 day after in the other groups. In conclusion, these results suggest that the air-pouch model may be very useful for investigating possible roles of arthritogenic agents or cytokines on the acute and/or chronic phases of inflammation in connective tissue.
authors.affiliation: Department of Orthopedic Surgery, Yokohama City University School of Medicine, Kanagawa, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Hirakawa
mesh_terms: D000818:Animals; D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000473:pathology; D004195:Disease Models, Animal; D004926:Escherichia coli / Q000276:immunology*; D005260:Female; D007074:Immunoglobulin G / Q000032:analysis; D007150:Immunohistochemistry; D007249:Inflammation / Q000473:pathology; D007375:Interleukin-1 / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000276:immunology*; D008407:Mast Cells / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D011994:Recombinant Proteins / Q000494:pharmacology; D013583:Synovial Membrane / Q000187:drug effects / Q000276:immunology / Q000473:pathology*
chemical_list: D007074:Immunoglobulin G; D007375:Interleukin-1; D008070:Lipopolysaccharides; D011994:Recombinant Proteins