Anticardiolipin in porphyromonas gingivalis antisera causes fetal loss in mice.

β2-glycoprotein I (β2GPI)-dependent anticardiolipin autoantibodies (aCl) are associated with thrombosis and fetal loss. Some microbial pathogens can induce pathogenic antibodies cross-reactive with β2GPI. Sera from a significant percentage of periodontitis patients contain aCl, and some periodontal pathogens contain antigens with peptide sequences having homology to β2GPI.

Anti-cardiolipin from periodontitis patients induces MCP-1 production by human umbilical vein endothelial cells.

Aim: Periodontal diseases are associated with a variety of systemic diseases, including cardiovascular disease and stroke, and patients with periodontitis demonstrate elevated levels of anti-cardiolipin antibodies. We sought to determine if anti-cardiolipin antibodies from periodontitis patients induced monocyte chemotactic protein-1 production by human vascular endothelial cells.

Materials And Methods: IgG was purified from sera from 53 subjects, including chronic and aggressive periodontitis patients and periodontally healthy controls, with elevated or normal IgG anti-cardiolipin levels.

Anti-phosphorylcholine-opsonized low-density lipoprotein promotes rapid production of proinflammatory cytokines by dendritic cells and natural killer cells.

Background And Objective: Epidemiological and animal studies suggest that periodontal infections increase atherosclerosis risk. Periodontitis patients have elevated levels of anti-phosphorylcholine (anti-PC) reactive not only with numerous periodontal organisms but also with minimally modified low-density lipoprotein (mmLDL). Dendritic cells (DCs) reside in arterial walls and accumulate in atherosclerotic lesions.

IL-17 in sera from patients with aggressive periodontitis.

Interleukin-17 (IL-17), the prototype cytokine produced by the Th17 subset of T-helper cells, plays a role in inflammatory responses, autoimmunity, and antimicrobial responses in a variety of infectious and inflammatory diseases. In view of the inflammatory nature and severity of aggressive periodontitis, we hypothesized that IL-17 might be detected in sera from patients with aggressive periodontitis. We used ELISA to measure IL-17 serum concentrations from 67 periodontally healthy (NP) individuals and from 53 patients with localized (LAgP) and 49 patients with generalized (GAgP) aggressive periodontitis.

Dendritic-NK cell interactions in P. gingivalis-specific responses.

Patients with localized aggressive periodontitis have type-1 cytokines in gingival crevicular fluid and high titers of IFN-gamma-dependent IgG2 reactive with P. gingivalis in gingival crevicular fluid and serum. Localized aggressive periodontitis monocytes spontaneously differentiate into dendritic cells that can stimulate IFN-gamma production by NK cells.

Opsonization of Actinobacillus actinomycetemcomitans by immunoglobulin G antibody reactive with phosphorylcholine.

We used two strains of Actinobacillus actinomycetemcomitans, one bearing phosphorylcholine (PC) (strain D045D-40) and one devoid of PC antigens (strain DB03A-42), as well as a nonencapsulated strain of Streptococcus pneumoniae (strain 39937), to examine the opsonic properties of physiological concentrations ( View Article and Find Full Text PDF

Phosphorylcholine-dependent cross-reactivity between dental plaque bacteria and oxidized low-density lipoproteins.

Antibodies reactive with phosphorylcholine (PC) are ubiquitous in human sera, but the antigens stimulating their production and their function are not clear. Previous studies have shown that a significant proportion of dental plaque bacteria contain PC as determined by reactivity with PC-specific mouse myeloma proteins and monoclonal antibodies. Additionally, serum antibody concentrations of immunoglobulin (IgG) G anti-PC are higher in sera of individuals who have experienced periodontal attachment loss than those who are periodontally healthy.

Neutrophil chemotaxis and superoxide production are induced by cross-linking FcgammaRII receptors.

Neutrophils express two types of receptor for the Fc region of IgG, FcgammaRII and FcgammaRIIIB. Via these receptors, neutrophils bind IgG complexes that contain more than one IgG molecule. This binding activates functional processes, such as the respiratory burst and chemotaxis.

Effect of allotype on activation of neutrophils by FcgammaRIIIB cross-linking.

Human neutrophils constitutively synthesize two receptors for the constant region of IgG, FcgammaRII, and FcgammaRIIIB. Fluo-3-loaded neutrophils were treated with biotinylated Fab fragments of anti-FcgammaR antibodies and cross-linked with streptavidin, and intracellular calcium ([Ca2+](i)) was monitored by flow cytometry. Polymerization of filamentous actin was quantitated by NBD-phallacidin using flow cytometry.

Myelinated dorsal root ganglion cultures activate both the alternative and classical pathways of complement.

We used rat myelinated dorsal root ganglion (MDRG) cultures to study antibody and complement-mediated mechanisms of peripheral demyelinating diseases. Heat inactivated serum from a patient (LT) with peripheral neuropathy and a monoclonal IgM reactive with myelin-associated glycoprotein (anti-MAG) and sulfated glucuronosyl glycolipids (anti-SGGL) was used as an antibody source. Incubation of whole human serum (WHS) or WHS and anti-SGGL with MDRGs resulted in reduction of classical and alternative pathway hemolytic activities and the development of abnormal myelin sheaths.

Effects of thrombospondin purified by heparin affinity or ion-exchange chromatography on the alternative complement pathway.

Thrombospondin (TSP), a platelet glycoprotein, was purified from platelet supernatants applied sequentially to Sepharose 4B and heparin-agarose affinity columns. This TSP inhibited alternative pathway activity in serum as assessed by lysis of rabbit erythrocytes and contained bound heparin, a substance which is known to inhibit the alternative pathway. TSP purified by anion exchange chromatography did not contain heparin and was not inhibitory.

Covalent linkage of C3 to properdin during complement activation.

Activation of the alternative complement pathway of serum produces complexes of properdin (P) and C3 as measured in a double antibody enzyme-linked immunosorbent assay. When purified from serum, these complexes decrease factor B hemolytic activity in serum and do not restore the alternative pathway hemolytic activity of serum deficient in P. Sodium dodecylsulfate-polyacrylamide gel electrophoresis (SDS-PAGE) of activated serum containing biotinylated P, followed by blotting to nitrocellulose and development with streptavidin-alkaline phosphatase revealed a band at 53 kDa for monomeric P and an additional band at 160 kDa.

Association of activated properdin with complexes of properdin with C3.

An ELISA using antibody to properdin (P), followed by antibody to C3 to detect complexes of P with C3 (P-C3), detected low levels of P-C3 complexes in human serum and plasma samples. Incubating serum for 1 h at 37 degrees C increased the amount of P-C3 and diminished factor B hemolytic activity without altering total alternative pathway activity or C3 activity in serum. When P and C3 in incubated serum were analyzed by size exclusion HPLC, complexes of P-C3 were detected at retention times corresponding to molecular mass measuring in excess of 2 x 10(6) Da.

Inherited deficiency of properdin and C2 in a patient with recurrent bacteremia.

A nine-year-old white boy with recurrent pneumococcal bacteremia is described. His serum had no hemolytic activity in either the classic or alternative complement pathways. Absence of classic pathway activity was secondary to a homozygous deficiency of C2.