Biomedical subjects

M Granlund-Edstedt

Publications and source records attributed to M Granlund-Edstedt.

5 recordsLinked to original sources

PubMed1993

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.

Anaerobiosis↗

PubMed1993

Adherence and surface properties of buoyant density subpopulations of group B streptococci, type III.

From clinical isolates of group B streptococci, buoyant density subpopulations with variable amounts of type-specific polysaccharide can be derived. The ability of these subpopulations to adhere to vaginal epithelial cells and to glass was assessed by using [3H]-labeled bacteria. Subpopulations with no or minute amounts of capsule showed good adherence capacity and a hydrophobic cell surface. In contrast, a large capsule made the bacteria less adherent and rendered their surface hydrophilic. A negative cell surface charge, judged by determination of the z-potential, was directly related to the amount of capsule. Proteinase K treatment of less encapsulated variants significantly decreased the cell hydrophobicity. The ability of a GBS strain to express different surface characteristics may be a mechanism for adaptation to environmental changes, and may thereby contribute to the pathogenicity of GBS.

Bacterial Adhesion↗

PubMed1991

Effect of sulfide ions on complement factor C3.

In infected sites such as the gingival pockets of patients with periodontal disease, sulfide levels up to 1 mmol/liter may be reached. There is little information, however, on how sulfide may interact with the host defense. In a previous study (R. Claesson, M. Granlund-Edstedt, S. Persson, and J. Carlsson, Infect. Immun. 57:2776-2781, 1989), it was shown that polymorphonuclear leukocytes were able to kill bacteria in the presence of 1 mM sulfide. However, sulfide seemed to interfere with the opsonization of the bacteria. It has been claimed that sulfide may be toxic by splitting disulfide bonds of proteins. In the present study, serum was exposed to 2 mM sulfide under anaerobic conditions, and the capacity of sulfide to split disulfide bonds of 10 serum proteins involved in opsonization was evaluated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunodetection of the proteins after blotting. Sulfide had a low capacity to split the disulfide bonds of most proteins. Sulfide had, however, a pronounced effect on the complement component C3 in the form of C3bi. Sulfide released the C-terminal region of the alpha chain from C3bi. When C3 opsonizes bacteria, it is this region of C3bi which binds to complement receptor 3 (CR3) of the polymorphonuclear leukocytes. If sulfide has the same effect on C3bi deposited on the bacterial surface as it has on C3bi in solution, it will annihilate the very important contribution of C3bi to opsonization.

Complement C3↗

PubMed1990

Demonstration and characterization of buoyant-density subpopulations of group B Streptococcus type III.

Group B Streptococcus (GBS) type III (18 strains) was investigated for the presence of buoyant-density subpopulations; 10 strains originated from invasive isolates causing early-onset septicemia, and 8 were colonizing isolates from pregnant women. By repeated processing in hypotonic density gradients of Percoll, high- (HD) and low-density (LD) subpopulations were recovered from all strains. Synthesis of type-specific polysaccharide (TPS) was increased in the invasive isolates and their respective LD variants compared with the colonizing strains and their LD subpopulations. Production of capsular TPS correlated directly with synthesis of soluble TPS; there was an inverse exponential relationship between soluble TPS production and buoyant density. LD variants were more resistant to phagocytic killing by human polymorphonuclear leukocytes (PMNL) than were the original strains and HD variants. In a luminol-enhanced chemoluminescence assay, LD variants elicited a weak, slow response. In contrast, the HD subpopulations evoked a prompt, strong respiratory burst in the PMNL.

Centrifugation, Density Gradient↗

PubMed1989

Activity of polymorphonuclear leukocytes in the presence of sulfide.

Polymorphonuclear leukocytes (PMN) isolated from human blood were exposed to various levels of hydrogen sulfide. The effect on respiratory burst, myeloperoxidase activity, and capacity to phagocytose and kill bacteria were studied. A 1-h exposure of the PMN to 1 mM sulfide did not decrease their myeloperoxidase activity or their capacity to initiate a respiratory burst. Actually the products of the respiratory burst rapidly oxidized sulfide. The phagocytosis and killing of bacteria in the presence of 1 mM sulfide was only decreased to a minor extent. Myeloperoxidase in cell extract was, however, almost completely inhibited by 1 microM sulfide. These results indicate that hydrogen sulfide does not easily permeate PMN. PMN may be able to function in infected sites with high sulfide levels such as in the gingival pockets of periodontal disease. In the oxygenated areas of these sites the PMN may actually help in the detoxification of sulfide.

Blood Bactericidal Activity↗