Immune reactions to Bacteroides fragilis populations with three different types of capsule in a model of infection.
The survival and growth of populations of the obligately anaerobic pathogenic bacterium Bacteroides fragilis enriched for large capsules (LCs), small capsules (SCs) or an electron-dense layer (EDL; non-capsulate by light microscopy) were examined in a mouse model of infection over a minimum period of 20 d. Chambers which allowed the influx of leukocytes, but not the efflux of bacteria, were implanted in the mouse peritoneal cavity. The LC and EDL populations consistently attained viable cell densities of the order of 10(8)-10(9) c.f.u. ml-1 within 24 h, whereas the SC population did not. However, after 3 d, all three bacterial populations maintained total viable numbers of 10(8)-10(9) c.f.u. ml-1 within the chambers. LC expression was selected against within 24 h in the model, the populations becoming non-capsulate by light microscopy, whereas in the SC population expression of the SC was retained by approximately 90% of the population. The EDL population remained non-capsulate by light microscopy throughout. Lymphocytes infiltrated the chambers to an equal extent for all three B. fragilis populations and at approximately 1000 times higher concentration than chambers which contained only quarter-strength Ringer's solution. The presence of neutrophils within the chambers did not cause a decrease in the total viable bacterial count. Each population elicited antibodies specific for outer-membrane proteins and polysaccharide, as detected by immunoblotting, which cross-reacted with the other populations. Differences were observed in the immunogenicity of the outer-membrane proteins within the three populations. Neutrophils were initially the predominant cell type in the chambers, but as the total leukocyte count increased with incubation time, neutrophils were outnumbered by other leukocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
Patrick
Sheila
S
Department of Microbiology and Immunobiology, School of Clinical Medicine, Queen's University of Belfast Royal Victoria Hospital Site, Grosvenor Road, Belfast BT12 6BN, UK.
Lutton
Deborah A
DA
Department of Microbiology and Immunobiology, School of Clinical Medicine, Queen's University of Belfast Royal Victoria Hospital Site, Grosvenor Road, Belfast BT12 6BN, UK.
Crockard
Alistair D
AD
Regional Immunology Laboratory, Royal Victoria Hospital Site, Grosvenor Road, Belfast BT12 6BN, UK.
D000818:Animals; D000907:Antibodies, Bacterial / Q000096:biosynthesis*; D001402:B-Lymphocytes / Q000276:immunology; D016667:Bacterial Capsules / Q000737:chemistry / Q000276:immunology*; D001425:Bacterial Outer Membrane Proteins / Q000276:immunology; D016866:Bacteroidaceae Infections / Q000276:immunology*; D001441:Bacteroides fragilis / Q000235:genetics / Q000254:growth & development / Q000276:immunology* / Q000378:metabolism; D000939:Epitopes / Q000276:immunology; D007106:Immune Sera / Q000276:immunology; D007111:Immunity, Cellular; D015151:Immunoblotting; D007958:Leukocyte Count; D051379:Mice; D009504:Neutrophils / Q000276:immunology; D011135:Polysaccharides, Bacterial / Q000276:immunology; D013997:Time Factors
D000907:Antibodies, Bacterial; D001425:Bacterial Outer Membrane Proteins; D000939:Epitopes; D007106:Immune Sera; D011135:Polysaccharides, Bacterial