Effect of anaerobiosis and sulfide on killing of bacteria by polymorphonuclear leukocytes.
Anaerobic microorganisms in periodontal pockets produce toxic amounts of hydrogen sulfide. The capacity of polymorphonuclear leukocytes to kill a capsulated and a non-capsulated variant of a group B streptococcal strain was studied in presence and absence of sulfide. The killing was equally efficient under aerobic and anaerobic conditions. However, in presence of sulfide the killing of the capsulated variant of the strain was significantly inhibited. Since this strain required higher serum concentrations to be killed by the polymorphonuclear leukocytes, it suggested that sulfide interfered with the opsonization of the bacteria. The capacity of sulfide to split the disulfide bonds of complement factor 3 and immunoglobulin G, deposited on the bacterial surface, was evaluated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. There was no detectable effect of 2 mM sulfide on immunoglobulin G. However, sulfide released from opsonized bacteria the beta-chain of C3b C3bi, and the C-terminal part of the alpha-chain of C3bi. This region of the alpha-chain of C3bi has been suggested to bind to the complement receptor 3 of polymorphonuclear leukocytes. The beta-chain of C3b/C3bi may augment the binding of opsonized bacteria to the complement receptors of polymorphonuclear leukocytes. The formation of sulfide by the microflora of the periodontal pockets may provide conditions for the bacteria to escape important parts of the host immune system.
Granlund-Edstedt
M
M
Department of Oral Microbiology, University of Umeå, Sweden.
Johansson
E
E
Claesson
R
R
Carlsson
J
J
D000693:Anaerobiosis; D001770:Blood Bactericidal Activity / Q000187:drug effects; D003179:Complement C3b / Q000737:chemistry / Q000187:drug effects*; D003180:Complement C3b Inactivator Proteins / Q000494:pharmacology; D004220:Disulfides / Q000737:chemistry; D004591:Electrophoresis, Polyacrylamide Gel; D006801:Humans; D007074:Immunoglobulin G / Q000187:drug effects; D009504:Neutrophils / Q000276:immunology / Q000502:physiology*; D009895:Opsonin Proteins / Q000187:drug effects / Q000502:physiology; D010587:Phagocytosis / Q000187:drug effects*; D013292:Streptococcus agalactiae / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D013440:Sulfides / Q000378:metabolism / Q000494:pharmacology*
D003180:Complement C3b Inactivator Proteins; D004220:Disulfides; D007074:Immunoglobulin G; D009895:Opsonin Proteins; D013440:Sulfides; D003179:Complement C3b