ABSTRACT
Porcine skin (PS) gelatin suppressed proliferation of a murine hepatic cell carcinoma cell line, MH134, a murine fibrosarcoma cell line, Meth A and a murine T cell lymphoma cell line, RL Male 1. The magnitude of suppression of the proliferation by cold water fish skin (CWFS) or bovine bone (BB) gelatin was lower than that by PS gelatin. On the other hand, BB gelatin stimulated proliferation of murine spleen cells. The magnitude of stimulation of the proliferation by CWFS gelatin was lower than that by BB gelatin. PS gelatin slightly suppressed proliferation of murine spleen cells. PS gelatin induced apoptosis but not necrosis of MH134 tumor cells. CWFS gelatin induced weaker apoptosis of the cells than PS gelatin. DNA histogram indicated that PS and CWFS gelatins acted on MH134 tumor cells to increase ratios of G2 + M-phase.
Subject(s)
Cell Division/drug effects , Gelatin/pharmacology , Animals , Apoptosis/drug effects , Bone and Bones/chemistry , Cattle , Female , Fibrosarcoma/pathology , Fishes , G2 Phase/drug effects , Gelatin/isolation & purification , Liver Neoplasms, Experimental/pathology , Lymphoma, T-Cell/pathology , Male , Metaphase/drug effects , Mice , Mice, Inbred BALB C , Skin/chemistry , Species Specificity , Spleen/cytology , Swine , Tumor Cells, Cultured/cytology , Tumor Cells, Cultured/drug effectsABSTRACT
An experimental model for autoimmune enterocolitis was produced in mice by repeated immunization of homologous colon extract together with Klebsiella 03 lipopolysaccharide (KO3 LPS) as an immunological adjuvant. Histological changes in the intestinal lesions were characterized by infiltration with polymorphonuclear leukocytes in the lamina propria, muscularis mucosae and submucosa of repeatedly immunized mice. No such intestinal lesions were produced in mice receiving injections of colon extract alone or KO3 LPS alone. Development of the autoantibody and delayed-type hypersensitivity against colon extract were found in mice immunized with the mixture of colon extract and KO3 LPS. Distinct positive staining was detected specifically on the columnar epithelium of villi. Sera from hyperimmunized mice defined organ-specific antigens present in the intestine. Therefore, it was suggested that the intestinal lesions might be caused by an autoimmune mechanism.
Subject(s)
Autoimmune Diseases/immunology , Disease Models, Animal , Enterocolitis/immunology , Klebsiella pneumoniae/immunology , Lipopolysaccharides/immunology , Adjuvants, Immunologic , Animals , Autoantibodies/blood , Autoantigens/analysis , Colon/immunology , Female , Hypersensitivity, Delayed , Intestines/pathology , Klebsiella pneumoniae/chemistry , Male , MiceABSTRACT
Intraperitoneal administration of lipopolysaccharide to mice induced a marked reduction of CD5+ B cells in the peritoneal cavity. The reduction was not induced by intravenous, subcutaneous, or oral administration of lipopolysaccharide. The reduction continued for about 10 days after the injection, and the CD5+ B-cell count recovered to the normal state about 14 days after the injection. The reduction of peritoneal CD5+ B cells might be caused by apoptotic cell death. Injection of lipopolysaccharide did not result in production of antibody to lipopolysaccharide. On the other hand, intraperitoneal injection of heat-killed bacteria did not induce a reduction of peritoneal CD5+ B cells and elicited the definite production of antibody to lipopolysaccharide.
Subject(s)
B-Lymphocyte Subsets/immunology , CD5 Antigens , Klebsiella pneumoniae/immunology , Lipopolysaccharides/immunology , Peritoneal Cavity/cytology , Animals , Apoptosis , Drug Administration Routes , Female , Immunoglobulin M/analysis , Lipopolysaccharides/pharmacology , Mice , Mice, Inbred BALB C , Receptors, Antigen, B-Cell/analysisABSTRACT
A monoclonal antibody (mAb) with a unique antigenic specificity against Escherichia coli O9 was produced. The O9a mAb was reactive with a part of the strains in E. coli O9. The O9a mAb did not react with LPS from the E. coli O9 test strain Bi316-42. The distribution of the antigen defined by the O9a mAb in E. coli O9 was consistent with that of E. coli O9a present in E. coli O9 strains. The chemical structure of the repeating unit of the O-specific polysaccharide detected by the mAb was demonstrated to be a mannotetraose by two-dimensional nuclear magnetic resonance spectroscopy. It was confirmed that the mAb recognized E. coli O9a serotype in E. coli O9 serotype strains, suggesting that E. coli O9a serotype might be a dominant strain in E. coli O9.
Subject(s)
Antibodies, Monoclonal/biosynthesis , Escherichia coli/classification , O Antigens/analysis , Animals , Antibody Specificity , Binding Sites, Antibody , Epitopes/analysis , Epitopes/chemistry , Escherichia coli/immunology , Immunoblotting , Magnetic Resonance Spectroscopy , Mice , Mice, Inbred BALB C , RabbitsABSTRACT
Recombinant lipopolysaccharide possessing the mannose homopolymer as the O-specific polysaccharide was manufactured genetically by transforming Escherichia coli K-12 with various rfb genes capable of synthesizing the mannose homopolymer. Recombinant lipopolysaccharide exhibited levels of anticomplement activity, adjuvant activity, and regional lymph node-enlarging activity much higher than those exhibited by the original rough-type lipopolysaccharide from E. coli K-12 or lipopolysaccharide possessing the heteropolysaccharide from E. coli O111. Immunological activities of recombinant lipopolysaccharide were as strong as those of wild-type lipopolysaccharide possessing the mannose homopolymer. Characteristic activities of wild-type lipolysaccharide possessing the mannose homopolymer were exhibited by recombinant lipopolysaccharide. The abilities of lipopolysaccharide to activate B cells polyclonally and to produce cytokines did not seem to be related to the presence of the mannose homopolymer. Therefore, it was suggested that the mannose homopolymer in the O-specific polysaccharide might exclusively enhance anticomplement activity, adjuvant activity, and regional lymph node-enlarging activity among various lipid A activities.
