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Effect of anaerobiosis and sulfide on killing of bacteria by polymorphonuclear leukocytes
Author(s) -
GranlundEdstedt Margareta,
Johansson Eva,
Claesson Rolf,
Carlsson Jan
Publication year - 1993
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1993.tb01078.x
Subject(s) - antibody opsonization , microbiology and biotechnology , opsonin , sulfide , bacteria , biology , antibody , chemistry , biochemistry , phagocytosis , immunology , genetics , organic chemistry
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 electrophorests. There was no detectable effect of 2mM sulfide on immunoglobulin G. However, sulfide released from opsonized bacteria the β‐chain of C3b C 3 bi, and the C‐terminal part of the α‐chain of C3bi. This region of the α‐chain of C3bi has been suggested to bind to the complement receptor 3 of polymorphonuclear leukocytes. The β‐chain of C 3 b/C 3 bi 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.