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Biomedical subjects

J G Tew

Publications and source records attributed to J G Tew.

At least 37 records · Page 2Linked to original sources
PubMed1999

Antibody reactive with Porphyromonas gingivalis serotypes K1-6 in adult and generalized early-onset periodontitis.

BACKGROUND: Six serotypes of Porphyromonas gingivalis have recently been described. We sought to test the hypothesis that serotype specific carbohydrates from these strains are important antigens that elicit potent immune responses. METHODS: Serum concentrations of IgG reactive with P. gingivalis serotypes K1-K6 were determined for 28 adult (AP) and 28 generalized early-onset (G-EOP) periodontitis patients previously determined to be seropositive for a broken cell preparation of P. gingivalis. To confirm relationships suggested for K1, K2, and K6 in the analysis of initial data, the study population was increased to 133. RESULTS: Frequency of seropositivity for the 6 serotypes ranged from 26 to 54% of subjects. IgG concentrations ranged from 0 to 453 microg/ml with many subjects seropositive to more than one serotype. Concentrations for the subset of patients who was seropositive were high (mean responses ranged from 20 to 105 microg/ml for the 6 serotypes). Significant correlations between seropositivity to serotypes K1 and K5 as well as between K5 and K6 were found. CONCLUSIONS: We examined the relationship of diagnosis, race, gender, smoking, probing depth, attachment loss, and antibody reaction with the P. gingivalis serotypes by analysis of variance. Initial findings suggested potential relationships between diagnosis, smoking, race, gender, and antibody reactive with serotypes K1, K2, and K6. A significant relationship did exist between smoking and decreased antibody reactive with P. gingivalis serotype K2. No other relationships were substantiated. We also examined the IgG subclass distribution and found that responses were almost exclusively IgG2. These data support the concept that antibody responses to all 6 serotypes are common in both AP and G-EOP and that these K serotype carbohydrates elicit potent IgG2 responses.

Adult↗
PubMed1998

Evidence for an important interaction between a complement-derived CD21 ligand on follicular dendritic cells and CD21 on B cells in the initiation of IgG responses.

The addition of Ags to mononuclear leukocyte cultures typically elicits modest Ab responses, implying that cosignals beyond those provided by T cells and macrophages may be needed. Recently, we reported that Ab responses could be dramatically enhanced (10-1000-fold) by the addition of follicular dendritic cells (FDC), suggesting that FDC may provide an important costimulatory signal. This result prompted a study of molecules involved in FDC-mediated enhancement of Ab responses stimulated by specific Ag with memory T and B cells or nonspecifically by the addition of LPS. In this study, we report evidence supporting the concept that FDC bear a ligand that engages complement receptor II (CR2 or CD21) on B cells and provides a critical cosignal for both Ag-specific and polyclonal responses. A blockade of the CR2 ligand on FDC by the use of soluble CR2 or a blockade of CR2 on B cells by use of CR2 knockout mice (or B cells with CR2 blocked) reduced Ab responses from the microg/ml to the ng/ml range (10-1000-fold reductions). FDC from C3 knockout mice, which cannot generate the CR2-binding fragments (iC3b, C3d, and C3dg), were unable to provide costimulatory activity, suggesting the CR2 ligand on FDC consists of C3 fragments. FDC trap complement-activating Ag-Ab complexes, and it appears that FDC present B cells with both specific Ag to engage B cell receptors and a CR2 ligand to engage B cell-CR2. In short, optimal induction of specific Ab responses appears to require the combination of specific Ag and costimulatory molecules from both T cells and FDC.

Animals↗
PubMed1998

Follicular dendritic cell (FDC) precursors in primary lymphoid tissues.

The origin of follicular dendritic cells (FDC) is unresolved, and as such, remains controversial. Based on the migration of Ag-transporting cells (ATC) into lymphoid follicles and the phenotypic similarity between FDC and ATC, one hypothesis is that ATC may represent emigrating FDC precursors. This contrasts with the view that FDC originate from local stromal cells in the secondary lymphoid tissues. Mice homozygous for the severe combined immunodeficiency (prkdc(scid)) mutation (scid) lack FDC. Thus, they provide a powerful tool for assessing de novo generation of FDC. To test whether FDC precursors could be found in bone marrow or fetal liver, scid/scid mice were reconstituted with either: 1) bone marrow cells from (BALB/c x C57BL/6)F1 donors, 2) bone marrow cells from ROSA BL/6 F1 (lacZ-transfected) mice, 3) rat bone marrow cells, or 4) rat fetal liver cells. Six to eight weeks after reconstitution with F1 bone marrow, cells reactive with the FDC-labeling mAb, FDC-M1, also expressed donor class I molecules on their surfaces. Similarly in mice reconstituted with lacZ-transfected bone marrow cells, these cells were also positive for the lacZ gene product. Furthermore, in spleens of animals reconstituted with either rat bone marrow or rat fetal liver, rat FDC were identified using the specifically labeling mAb, ED5. In all cases, host FDC were also present, indicating that scid/scid mice have FDC precursors that will mature in the presence of allogeneic or xenogeneic lymphoid cells. In summary, FDC can be derived from progenitor cells present in primary lymphoid tissues.

Animals↗
PubMed1998

Tingible body macrophages in regulation of germinal center reactions.

Tingible body macrophages (TBM), long thought simply as scavengers of apoptotic lymphocytes, are located in the unique microenvironment of germinal centers in close proximity to antigen-retaining follicular dendritic cells (FDC). Observations that TBM endocytose FDC-iccosomal (immune-complex coated bodies) antigen suggested that TBM might present this antigen and help regulate the germinal center reaction. To test for antigen presentation, the ovalbumin (OVA)-specific T(H) hybridoma, 3DO-54.8, which produces IL-2 on receiving effective presentation of OVA, were used as responders to OVA-bearing TBM. Results showed that OVA-bearing TBM failed to induce IL-2 production. Furthermore, addition of TBM to IL-2-inducing positive controls (B cells) not only failed to augment IL-2 production, but rather TBM significantly (55-90%) reduced B-cell induction of IL-2. We found that TBM were rich in prostaglandin by comparison with other nongerminal center lymph node macrophages and that addition of indomethacin to the cultures reversed the inhibitory effect of TBM. Depletion of TBM from enriched preparations, prior to addition to positive control cultures, also abrogated the inhibitory effect on IL-2 production. These data support the concept that TBM, within the unique microenvironment of germinal centers, may be specialized to downregulate the germinal center reaction.

Animals↗
PubMed1998

The influence of smoking and race on adult periodontitis and serum IgG2 levels.

Smoking is a known risk factor for developing periodontal diseases, but the risk appears to be greater for white smokers than black smokers. Furthermore, it has been reported that young white subjects have significantly lower levels of serum IgG2 than their non-smoking counterparts while young black adult subjects are generally not affected by smoking. These relationships prompted the hypothesis that adult white subjects, including periodontitis subjects, who smoked would have more attachment loss than adult black subjects and that smoking would be associated with lower serum IgG2 levels in adult white subjects but not in adult black subjects. Smoking status was established from serum cotinine levels determined by radioimmunoassay. Serum IgG subclass levels were determined using radial immunodiffusion. White adult periodontitis (AP) and non-periodontitis (NP) subjects who smoked had greater mean attachment loss per site than their non-smoking counterparts. Furthermore, smoking white AP subjects and their age-matched NP controls had substantially less IgG2 in their serum. In marked contrast, we were unable to detect any increase in periodontal destruction or a significant decrease in serum IgG2 levels in smoking black AP subjects or their age-matched controls. However, IgG1 and IgG4 levels were reduced in smoking black AP subjects. IgG3 was the only subclass in adults that was unaffected by smoking. IgG2 can be a good opsonin and may help control periodontitis-associated bacteria in adults. Even though a cause-and-effect relationship has not been established, the association between a smoking-related decrease in serum IgG2 and an increase in periodontal destruction in white subjects is striking.

Adult↗
PubMed1997

Antibody reactive with Actinobacillus actinomycetemcomitans leukotoxin in early-onset periodontitis patients.

The objective of this study was to determine whether a relationship exists between antibody reactive with the Actinobacillus actinomycetemcomitans leukotoxin and the severity of periodontal disease. Serum concentrations of antibody reactive with the leukotoxin were determined for 119 early-onset periodontitis patients and 59 non-periodontitis subjects using limiting dilution analysis on Western blots. Immunoglobulin G (IgG) antibody reactive with the A. actinomycetemcomitans leukotoxin ranged from undetectable to 29 micrograms/ml (mean = 3.13 +/- 0.97 micrograms/ml for the generalized early-onset periodontitis and 2.17 +/- 0.86 micrograms/ml for the localized juvenile periodontitis patients vs 0.32 +/- 0.24 ng/ml for 59 non-periodontitis controls), and the dominant subclass was IgG1. Analysis of the relationship between antibody reactive with A. actinomycetemcomitans sonicate, A. actinomycetemcomitans leukotoxin and attachment loss patterns indicates that seropositive generalized early-onset periodontitis patients had decreased attachment loss compared with patients lacking this antibody. The statistical relationship appeared to be stronger for the sonicate than the purified leukotoxin. These data suggest that antibody reactive with A. actinomycetemcomitans leukotoxin may be protective in early-onset periodontitis, but given that the sonicate appeared better than the leukotoxin alone, it is not likely that leukotoxin is the only antigen of importance to host defense.

Adolescent↗
PubMed1997

Follicular dendritic cells and presentation of antigen and costimulatory signals to B cells.

This review focuses on how immunogens trapped by FDC in the form of Ag-Ab complexes productively signal B cells. In vitro. Ag-Ab complexes are poorly immunogenic but in vivo immune complexes elicit potent recall responses. FDC trap Ag-Ab complexes and make immune complex coated bodies or "iccosomes". B cells endocytose iccosomes, the Ag is processed, and T-cell help is elicited. In vitro, addition of FDC bearing appropriate Ag-Ab complex to memory T and B cells provoke potent recall responses (IgG and IgE). FDC also provide nonspecific costimulatory signals which augment B-cell proliferation and Ab production. B cell-FDC contact is important and interference with ICAM-1-LFA-1 interactions reduces FDC-mediated costimulation. Preliminary data suggest that a costimulatory signal may be delivered via CR2L on FDC binding CR2 on B cells. FDC can also stimulate B cells to become chemotactically active and can protect lymphocytes from apoptosis. FDC also appear to be rich in thiol groups and may replace reducing compounds such as 2 mercaptoethanol in cultures. In short, FDC-Ag specifically signals B cells through BCR, and FDC provide B cells with iccosomal-Ag necessary for processing to elicit T-cell help. In addition, FDC provide nonspecific signals that are important to promote B-cell proliferation, maintain viability, and induce chemotactic responsiveness.

Animals↗
PubMed1997

Follicular dendritic cells (FDC) in retroviral infection: host/pathogen perspectives.

Follicular dendritic cells (FDC) are found in the follicles of virtually all secondary lymphoid tissues. In health, these cells trap and retain antigens (Ag) in the form of immune complexes and preserve them for months in their native conformation. FDC thus serve as a long-term repository of extracellular Ag important for induction and maintenance of memory responses. In retroviral infection, FDC trap and retain large numbers of retroviral particles with profound effects on FDC. FDC-trapped retrovirus induces follicular hyperplasia, and conventional Ag trapped prior to infection are lost and new Ag cannot be trapped. Concomitantly, antibody-forming cells (AFC) specific for Ag lost from FDC decrease followed by loss of specific serum antibody (Ab). Eventually, FDC die and follicular lysis occurs. From the pathogen perspective, binding to FDC is remarkably beneficial, bringing together virus and activated target cells that are highly susceptible to infection. Furthermore, FDC permit HIV to infect surrounding cells even in the presence of a vast excess of neutralizing Ab. Preliminary data suggest that FDC maintain virus infectivity-even when the virus cannot replicate. Thus retrovirus infection monopolizes FDC networks, thereby transforming the FDC Ag repository into a highly infectious retroviral reservoir.

Animals↗
PubMed1997

Polyclonal B cell activators and in vitro induction of auto-antibody reactive with collagen.

Cells producing autoantibodies are known to be present in chronically inflamed periodontal tissues. In sites of chronic inflammation, polyclonal B cell activators (PBA) are known to exhibit adjuvant activity when combined with foreign antigens. These results prompted an examination of PBA in eliciting an antibody response to an autoantigen (i.e. collagen type I). Rat lymphocytes were stimulated with rat collagen (type I), microbial PBA (LPS) or the combination of LPS plus rat collagen in vitro. Anti-collagen antibody-forming cells (AFC) were enumerated using an ELISPOT assay. Collagen or LPS alone elicited few anti-collagen AFC but the addition of LPS to collagen resulted in a substantial adjuvant effect and yielded maximal responses to collagen. Comparisons of anti-collagen AFC from short-term immunized (2-6 wk after booster), non-immunized and long-term immunized (3-4 months after booster) animals were performed. It revealed that cells from recently immunized rats were significantly easier to activate than the other 2 groups. The adjuvant effect of microbial PBA may be important in anti-collagen antibody production and thus the localization of PBA in periodontal pockets may explain why anti-collagen AFC are restricted to the chronically inflamed periodontal tissues.

Adjuvants, Immunologic↗
PubMed1997

Heterogeneity of antibodies reactive with the dominant antigen of Actinobacillus actinomycetemcomitans.

The serotype b-specific carbohydrate antigen (SbAg) of Actinobacillus actinomycetemcomitans Y4 is reported to be the O antigen of lipopolysaccharide, and the highest titers of serum antibody reactive with A. actinomycetemcomitans in early-onset periodontitis (EOP) patients bind SbAg. These high titers of serum antibody reactive with SbAg are associated with a lesser extent and severity of periodontal disease. The aim of this study was to determine if a limited number of genes code for anti-SbAg antibodies as has been shown for immunoglobulin G (IgG) reactive with the type b polysaccharide from Haemophilus influenzae. Serum IgG reactive with the SbAg was prepared from 20 high-titer EOP patients by affinity chromatography. The IgG subclass concentrations were determined, and heterogeneity was analyzed by isoelectric focusing (IEF). IgG2 was the dominant subclass (83% of total IgG) in the anti-SbAg IgG fraction and represented an average of 1.33% of total serum IgG2. The IgG2 reactive with SbAg was isolated from the affinity-purified IgG fraction by affinity chromatography with protein A and subclass-specific monoclonal antibodies. On IEF gels, only 4 to 20 bands were observed in the anti-SbAg IgG fractions, indicating limited heterogeneity. N-terminal amino acid sequence analysis of eight representative anti-SbAg IgG2 preparations indicated that variable heavy and light chains consisted largely of V(H)III and V(kappa)II, respectively. However, a significant fraction of anti-SbAg may use V(H) and V(lambda) genes with blocked N termini. In short, these findings indicate that IgG reactive with SbAg is very much like the antibody reactive with H. influenzae type b polysaccharide. Similarities include IgG2 dominance, limited bands on IEF gels, supporting an oligoclonal response, and use of genes from V(H)III and V(kappa)II regions.

Aggregatibacter actinomycetemcomitans↗
PubMed1997

Tobacco and smoking: environmental factors that modify the host response (immune system) and have an impact on periodontal health.

This review summarizes the current data on the effects of smoking and tobacco on the immune system and its potential impact on periodontal health. Smokers are 2.5-6 times more likely to develop periodontal disease than non-smokers, and there is evidence for a direct correlation between the number of cigarettes smoked and the risk of developing disease. Tobacco users also tend to exhibit increased severity of periodontal disease. Direct correlations between tobacco use and increased attachment loss and pocket depth and reduced bone crest height have been reported. Although the correlation between tobacco use and periodontal disease is quite strong, the role of tobacco in the pathogenesis of periodontal disease is uncertain. Recent studies indicate that one potential mechanism is that tobacco use exacerbates periodontal disease because it alters the immune response to periodontal pathogens. Indeed, smokers exhibit increased numbers of peripheral blood mononuclear phagocytes which appear to be functionally compromised. Inadequate phagocyte activity could reduce the clearance of pathogens from the oral cavity and thereby facilitate the development of periodontal disease. Tobacco-exposed B- and T-lymphocytes exhibit reduced proliferative capacities which could limit the production of protective immunoglobulins against oral pathogens. The risk factors for periodontal disease can be broadly classified as genetic, environmental, host-response factors, and host-related factors such as age. Tobacco, an environmental factor, undermines the host response and may facilitate the development and progression of periodontal disease. This review highlights the inter-relatedness of two of the risk factors associated with periodontal disease.

Alveolar Bone Loss↗
PubMed1997

A comparison of IgG antibody reactive with Bacteroides forsythus and Porphyromonas gingivalis in adult and early-onset periodontitis.

Recent work has indicated that Bacteroides forsythus and Porphyromonas gingivalis are significant local risk factors for periodontitis. Several reports find that both organisms are frequently associated with periodontitis lesions and often are present together. We have previously shown that early-onset periodontitis patients seropositive for P. gingivalis have less attachment loss than seronegative patients. In this study, we determined serum IgG antibody concentrations reactive with B. forsythus in adult and early-onset periodontitis patients using an ELISA and used P. gingivalis in the same populations as a positive control. The results for P. gingivalis were consistent with previous work and indicated that 47%, 36%, and 33% of adult, generalized early-onset, and localized juvenile patients were seropositive, respectively. Mean serum IgG concentrations for the three groups were 5.36 microg/ml, 5.65 microg/ml, and 5.44 microg/ml for adult, generalized early-onset, and localized juvenile patients, respectively. In contrast, for B. forsythus only 11%, 14%, and 10% of adult, generalized early-onset, and localized juvenile patients were seropositive, with mean serum IgG concentrations of 0.46 microg/ml, 0.46 microg/ml, and 0.47 microg/ml, respectively. This suggests that B. forsythus is either poorly immunogenic or less invasive than P. gingivalis. If most patients fail to mount an immune response to B. forsythus and it is invasive, it may explain why this organism is a risk factor for disease.

Adult↗
PubMed1997

The effect of smoking on serum IgG2 reactive with Actinobacillus actinomycetemcomitans in early-onset periodontitis patients.

High titers of serum IgG2 reactive with Actinobacillus actinomycetemcomitans are present in early-onset periodontitis (EOP) patients and it appears that anti-A. actinomycetemcomitans may be protective. Smoking is associated with increased periodontal disease severity in generalized early-onset periodontitis (G-EOP) patients, but is not associated with periodontal disease severity in patients with localized juvenile periodontitis (LJP). Furthermore, smoking is associated with reduced serum IgG2 levels in black patients with G-EOP but not in those with LJP. Based on this selective effect of smoking, we hypothesized that smoking would be associated with a reduction of specific IgG2 reactive with A. actinomycetemcomitans in black G-EOP patients but not black LJP patients. In addition, we examined IgG2 responses to carbohydrate antigens from non-periodontal pathogens including Haemophilus influenzae b oligosaccharide antigen (Hib) and the Streptococcus pneumoniae antigen phosphocholine (PC). Smoking status was assessed from serum cotinine levels, and IgG2 specific for A. actinomycetemcomitans, Hib, and PC was assessed by ELISA. Our study revealed that smoking was correlated with a dramatic reduction in serum IgG2 anti-A. actinomycetemcomitans in G-EOP smokers but not in LJP smokers. In contrast, anti-Hib IgG2 and anti-PC IgG2 were not affected in either G-EOP or LJP patients. In short, these results indicate that smoking is associated with a reduction in serum IgG2 anti-A. actinomycetemcomitans in black G-EOP subjects, but IgG2 reactive with other antigens may not be reduced in G-EOP smokers.

Adolescent↗
PubMed1996

Follicular dendritic cell-derived antigen and accessory activity in initiation of memory IgG responses in vitro.

Follicular dendritic cells (FDC) release Ag in developing germinal centers in the form of immune complex-coated bodies (iccosomes). Iccosomes are endocytosed by B cells, and the B cells process and present the FDC-derived Ag to T cells. By 3 days after Ag challenge, Ab-forming cells producing IgG specific for the iccosomal Ag emerge from the developing germinal centers and home to the bone marrow, where most Ab in a secondary response are produced. In addition to providing Ag, FDC exhibit potent accessory activities that promote B cell proliferation. These observations prompted the hypothesis that both FDC-derived Ag and FDC-derived Ag-independent secondary signal(s) are essential for optimal secondary Ab responses. To test this hypothesis, methods were developed to separate Ag-bearing iccosomes from intact FDC, and we then examined the ability of isolated iccosomes to elicit secondary Ab responses in vitro in the presence and absence of intact FDC. In the absence of FDC, iccosomes bearing the appropriate Ag elicited only minimal levels of specific IgG. Proliferation studies revealed that iccosomes lacked the FDC accessory activity necessary to augment B cell proliferation. When a source of FDC lacking the relevant Ag but exhibiting accessory activity was added to the iccosomal/Ag/lymphocyte mixture, dramatic increases in IgG specific for the iccosomal Ag were obtained (increases were from low ng/ml to microg/ml levels of specific IgG). The results suggest the concept that Ag on FDC or on iccosomes signals B cells through B cell Ag receptor, the iccosome provides these B cells with Ag necessary to process and elicit T cell help, and a secondary signal(s) necessary to optimize the memory response is delivered to B cells by FDC in an Ag-nonspecific fashion.

Animals↗
PubMed1996

Hyper-immunoglobulin G2 production by B cells from patients with localized juvenile periodontitis and its regulation by monocytes.

Localized juvenile periodontitis (LJP) runs in families, and a predisposition to develop disease appears to be inherited in an autosomal dominant fashion. Patients with LJP have elevated levels of serum immunoglobulin G2 (IgG2), and this is most striking in black LJP patients. We hypothesized that the markedly elevated serum IgG2 levels related to LJP status and race may be attributable to a fundamental difference in the response of black LJP leukocytes. To test this possibility, leukocytes from black LJP patients, black non-periodontitis (NP) controls, and white NP controls were cultured with a nonspecific mitogen (pokeweed mitogen) which stimulates immunoglobulin production. The levels of IgG2 produced were measured using an enzyme-linked immunosorbent assay. The results revealed that the serum IgG2 level differences among black LJP patients and white and black NP subjects were reproducible in peripheral blood leukocytes in vitro. Analysis revealed that B cells from the LJP patients appeared to be predisposed to produce high levels of IgG2. Further analysis supported the concept that the high IgG2 responses of B cells from black LJP patients were regulated by monocytes. Replacing the monocytes in cultures from white NP subjects with LJP monocytes from black patients resulted in production of IgG2 at levels that were comparable with those produced by the LJP B cells from black patients. In short, B cells from black LJP patients produce elevated levels of IgG2 in vitro, and at least part of this elevation appears to be attributable to regulation via the LJP monocytes.

Adult↗
PubMed1996

Influence of smoking and race on immunoglobulin G subclass concentrations in early-onset periodontitis patients.

Recent data indicate that smoking is an important risk factor for the development of periodontitis. Smoking is also known to reduce serum immunoglobulin G (IgG) levels. Interestingly, patients with the localized form of early-onset periodontitis (LJP) have elevated levels of serum IgG2, and those who smoke are not clinically different from nonsmoking LJ subjects. In contrast, patients with the generalized form of early-onset periodontitis (G-EOP) who smoke have more extensive destruction than their nonsmoking counterparts. Given the effects of smoking on EOP and the association of IgG2 with less severe disease, we hypothesized that smoking might reduce serum IgG2 and that this might be most apparent in G-EOP. We therefore examined the effects of smoking on serum IgG subclass concentrations in race-matched groups: LJP, G-EOP, and age-matched periodontally healthy controls (NPs). Smoking status was established from serum cotinine levels, and serum IgG subclass concentrations were determined by using radial immunodiffusion. The data indicated that the effects of smoking were remarkably selective with respect to both IgG subclass and race. Smoking did not appear to have any effect on the concentration of IgG1 or IgG3 in either black or white subjects. In contrast, smoking was associated with depressed serum IgG2 concentrations in both white NP and G-EOP subgroups. Serum IgG2 levels in black subjects did not appear to be depressed by smoking, with the single striking exception of the black G-EOP subgroup which also had depressed serum IgG4 levels. The results here confirm that smoking has effects on serum immunoglobulin levels, but the effects were both race and serum IgG subclass specific. Furthermore, the periodontal diagnosis of EOP subjects appeared to be important, as indicated by the fact that IgG2 and IgG4 levels were reduced in smoking black G-EOP subjects whereas the IgG2 and IgG4 levels in black LJP and NP subjects were not reduced by smoking.

Adult↗
PubMed1996

Influence of anti-Actinobacillus actinomycetemcomitans Y4 (serotype b) lipopolysaccharide on severity of generalized early-onset periodontitis.

The objective of this study was to determine if a relationship exists between antibody reactive with the Actinobacillus actinomycetemcomitans serotype b lipopolysaccharide (LPS) and severity of periodontal disease in generalized early-onset periodontitis (G-EOP). The concentration of antibody reactive with A. actinomycetemcomitans serotype b LPS was determined for 102 G-EOP subjects. Analysis of the relationship between antibody reactive with A. actinomycetemcomitans serotype b LPS and measures of periodontal attachment loss indicated that the patients with the highest concentrations of antibody reactive with A. actinomycetemcomitans serotype b LPS had significantly less attachment loss. These high-responder subjects also had anti-A. actinomycetemcomitans serotype b LPS with significantly higher relative avidity. The results suggest that antibody reactive with A. actinomycetemcomitans serotype b LPS is protective in G-EOP patients.

Adult↗