Biomedical subjects

S Hanazawa

Publications and source records attributed to S Hanazawa.

At least 55 records · Page 3Linked to original sources

PubMed1994

The effect of pentoxifylline on ischemia and reperfusion injury in the rat cremaster muscle.

The accumulation of leukocytes is believed to contribute to reperfusion injury following ischemia. The purpose of this study was to determine if pentoxifylline (PTX) would ameliorate reperfusion injury by preventing activation of leukocytes. Male Wistar rats received 40 mg/kg of PTX orally in water for 6 days, and a single dose of PTX (30 mg/kg) intraarterially before experiments. Control measurements of red-cell velocity and inside diameter were made in first-through-third-order arterioles (1A-3A) of the cremaster muscle, along with the number of rolling and sticking leukocytes (WBC) in venules and the density of flowing capillaries, by intravital microscopy. The muscles were then subjected to total ischemia for 2 hr by arterial clamping, followed by a repeat of the measurements during reperfusion. The number of both rolling and sticking WBCs was not different between the two groups during the control period but, following reperfusion, there were significantly fewer WBCs rolling and sticking in the venules of the PTX group at the measured times (immediately, 1, 2, and 3 hr after reperfusion). Arteriolar blood flow was lower than initial values during the first hour of reperfusion in both groups. But while blood flow decreased further in the untreated group, it significantly improved in the PTX group. There were no significant differences in arteriolar diameter or density of flowing capillaries between the two groups at any time. Treatment with PTX prevented accumulation of rolling and sticking leukocytes following reperfusion. This may contribute to the improved arteriolar blood flow following 2 hr of ischemia.

Animals↗

PubMed1994

Anti-bacterial antibodies in Epstein-Barr virus (EBV)-transformed oligoclonal B-cell lines established from normal persons and autoimmune disease patients.

We have established 950 and 430 oligoclonal B-lymphoblastoid cell lines (LCL) from two normal persons and eight autoimmune disease patients, respectively by using Epstein-Barr virus (EBV)-induced transformation. To re-evaluate the EBV technique for production of human monoclonal antibodies (mAb) related to infectious disease, we screened these oligoclonal LCLs for antibodies against 31 bacterial strains systematically. A total of 74 cultures out of 1380 were reactive to a total of 18 strains out of 31. Among these, eight cultures showed 10(-3) antibody (Ab) titers to Pseudomonas aeruginosa serotypes C, E, F and I, Staphylococcus aureus, Serratia marcescens and Bacillus cereus. Ten cultures showed 10(-2) Ab titers to Ps. aeruginosa serotypes D, E, F and I, Ps. maltophilia, Staph. epidermidis, Klebsiella ozaenae, Ser. marcescens and B. subtilis. The results reveal the further possibilities for the EBV technique to produce various infectious disease-related human mAbs.

Adolescent↗

PubMed1994

Porphyromonas gingivalis fimbriae induce a 68-kilodalton phosphorylated protein in macrophages.

The present study was performed to examine whether Porphyromonas gingivalis fimbriae induce specifically a protein kinase-mediated phosphorylated protein that is involved in the mechanism of signal transduction. The fimbriae induced a 68-kDa phosphorylated protein (pp68) in a dose-dependent manner in mouse peritoneal macrophages. A marked appearance of pp68 was observed 20 min after the initiation of fimbrial treatment. The fimbria-induced pp68 was inhibited dramatically by staurosporine, a potent inhibitor of protein kinase C. pp68 induction was also inhibited by H-7, a potent inhibitor of several types of protein kinase. However, the induction was not inhibited by HA-1004 and H-8, relatively high-affinity inhibitors of protein kinase A. Phorbol myristate acetate and 1-oleoyl-2-acetyl-sn-glycerol, activators of protein kinase C, were able to induce pp68 in mouse peritoneal macrophages. This protein was localized in the cytosolic fraction of fimbria-treated macrophages. pp68 also was induced in fimbria-treated human monocyte-like cells. Finally, we observed that gene expression of the fimbria-induced neutrophil chemoattractant KC was inhibited markedly by staurosporine.

Alkaloids↗

PubMed1994

Porphyromonas gingivalis fimbriae stimulate bone resorption in vitro.

Our previous study demonstrated that Porphyromonas gingivalis fimbriae induce the expression of interleukin-1, a potent bone-resorbing cytokine, in macrophages. This demonstration suggested to use the possibility that the fimbriae may stimulate bone resorption via the generation of an inflammatory cytokine(s). The present study was performed to test this suggestion. The bone-resorbing activity was evaluated by measuring the area of resorption lacunae on bone slices incubated with calvarial bone cells taken from 14-day-old mouse embryos. Fimbriae at 0.5 micrograms of protein per ml stimulated the bone-resorbing activity significantly, and the effect was dose and treatment time dependent. Since it is well known that interleukin-1 and granulocyte macrophage colony-stimulating factor induce differentiation of osteoclast lineage cells, we examined the involvement of these cytokines in fimbria-stimulated bone resorption. Fimbria-stimulated bone resorption was abolished significantly by antisera against both cytokines. We observed by Northern (RNA) blot assay that both cytokine genes were markedly expressed in the fimbria-treated calvarial bone cells. Our present data demonstrate that P. gingivalis fimbriae stimulate bone resorption in vitro.

Animals↗

PubMed1994

Anti-glycolipid antibodies produced by Epstein-Barr virus (EBV)-transformed oligoclonal B cell lines obtained from normal persons and autoimmune disease patients.

Oligoclonal B-lymphoblastoid cell lines (LCL) were blindly established by nonimmunized protocol from natural populations of two normal persons and 8 autoimmune disease patients using Epstein-Barr virus (EBV)-induced transformation. We systematically screened these LCLs on antibodies against a panel of glycolipids using liposome immune lysis assay (LILA). Eventually we found antibodies to 12 out of 15 compounds containing CTH, globoside, Forssman, paragloboside, CPH, sulfatide, NAGM3, NGGM3, i active glycolipid, GM1, GA1 and GA2 in 81 out of 950 LCLs from normal PBL, and antibodies to 2 out of 15 compounds containing sulfatide and CPH were also detected in 11 out of 430 LCLs from autoimmune disease patients. Unexpectedly, the antibody repertoire of LCLs from autoimmune disease patients was impoverished. The possibility of the EBV technique for production of various kinds of human monoclonal antibodies (MAbs) to glycolipid was shown.

Antibodies, Monoclonal↗

PubMed1993

Tumor necrosis factor-alpha induces expression of monocyte chemoattractant JE via fos and jun genes in clonal osteoblastic MC3T3-E1 cells.

The mechanism by which circulating monocytes are attracted to sites of bone remodeling is unknown. We now report that tumor necrosis factor-alpha (TNF-alpha), a potent osteotrophic cytokine, was stimulatory for expression of the monocyte chemoattractant JE gene in osteoblastic MC3T3-E1 cells. TNF-alpha stimulated this JE gene expression transcriptionally. The presence of JE gene product in conditioned medium of the cytokine-treated cells was evidenced by an immunoprecipitation assay with antiserum specific for JE/MCP-1. The stimulated JE gene expression was markedly inhibited by H-7, a potent inhibitor of protein kinase C. Phorbol 12-myristate 13-acetate induced the JE gene expression, and the cytokine-induced JE gene expression was down-regulated by the phorbol ester pretreatment. TNF-alpha induced expression of both early protooncogenes, c-fos and c-jun, in the cells. Antisense oligonucleotides to these oncogenes significantly inhibited the cytokine-induced monocyte chemotactic activity. Furthermore, curcumin, a specific inhibitor of c-jun/AP-1, markedly inhibited JE gene expression and monocyte chemotactic activity induced by the cytokine. These results suggest that TNF-alpha may contribute to the regulation of remodeling and inflammation of bone tissues through the JE gene product.

3T3 Cells↗

PubMed1993

N-acetyl-D-galactosamine inhibits TNF-alpha gene expression induced in mouse peritoneal macrophages by fimbriae of Porphyromonas (Bacteroides) gingivalis, an oral anaerobe.

Adherence to host cells is an essential step in the initiation of most infectious diseases. It is well known that bacterial fimbriae may be involved in the adherence. Porphyromonas (Bacteroides) gingivalis is a pathogenic organism of adult periodontitis which is a chronic inflammatory disease. Using an experimental system for fimbria-induced TNF-alpha gene expression in mouse peritoneal macrophages, we examined the role of sugar moieties in the adhesion of P. gingivalis fimbriae to these cells. The fimbriae strongly induced TNF-alpha gene expression in the macrophages, and marked TNF activity toward fibroblasts was observed in culture supernatants of the fimbria-treated cells. The potent expression of TNF-alpha was inhibited by N-acetyl-D-galactosamine, but not inhibited by D-mannose, alpha-lactose, and alpha-L-rhamnose, D-galactose, and N-acetyl-D-glucosamine.

Acetylgalactosamine↗

PubMed1993

IL-1 induces expression of monocyte chemoattractant JE in clonal mouse osteoblastic cell line MC3T3-E1.

Recent studies demonstrated that platelet-derived growth factor-inducible JE is an inflammatory cytokine that directs chemotaxis of monocytes, and is a homolog of monocyte chemoattractant protein-1, which is a human monocyte chemotactic factor. Migration and accumulation of monocyte lineage cells in bone tissue sites are very important for the recruitment of multinucleate osteoclasts, because the origin of osteoclasts is derived from monocyte lineage cells in hemopoietic cells. Because IL-1 is a potent regulator in bone remodeling, we examined whether IL-1 beta induces JE expression in a clonal mouse osteoblastic cell line, MC3T3-E1. Significant chemotactic activity for human monocytes was detected in conditioned medium of the cells at 6 h after initiation of IL-1 beta treatment, and the chemotactic activity increased in both a culture time- and dose-dependent manner. The peak of the chemotactic activity in the conditioned medium was observed in fractions corresponding to a m.w. of 26 kDa when the conditioned medium was fractionated by gel filtration. The chemotactic activity in the peak fraction was completely neutralized by antiserum specific for JE protein. And the JE gene product in the conditioned medium was detected as a microheterogeneous protein with a m.w. of 21 to 33 kDa by immunoprecipitation with the specific antiserum. IL-1 beta induced a maximal JE gene expression in the cells at 3 h after initiation of the cytokine treatment. This significant expression was observed when IL-1 beta was used at a concentration of 10 U/ml, and the expression was dose dependent. The run-on assay showed that the cytokine-induced JE gene expression increased at the transcriptional level. IL-1 beta and TNF-alpha acted synergistically to stimulate JE gene expression in the cells. Expression and product of the JE gene were also observed in an osteoblast-enriched cell population prepared from mouse calvariae. These results suggest the possibility that osteoblastic cells can participate in osteoclast recruitment via the JE gene product.

Animals↗

PubMed1993

Expression of monocyte chemoattractant protein 1 (MCP-1) in adult periodontal disease: increased monocyte chemotactic activity in crevicular fluids and induction of MCP-1 expression in gingival tissues.

The present study shows that monocyte chemotactic activity in crevicular fluids increases with severity of the disease and that a monocyte chemoattractant, monocyte chemoattractant protein 1 (MCP-1), is expressed as the predominant cytokine of gingival tissues and their fibroblasts treated with Porphyromonas (Bacteroides) gingivalis lipopolysaccharide (P-LPS). High monocyte chemotactic activity in the crevicular fluids was neutralized significantly by antiserum specific for the JE/MCP-1 protein. Marked expression of the MCP-1 gene was observed in the gingival tissues of all adult periodontal patients tested, but not in those of healthy subjects. Monocyte chemotactic activity was observed in culture supernatants of human normal gingival tissues treated with P-LPS, and the chemotactic activity increased in a dose-related manner. Expression of MCP-1 in P-LPS-treated human gingival fibroblasts was further examined. P-LPS induced the MCP-1 gene expression in a dose- and treatment time-dependent manner. The MCP-1 gene product in the culture supernatant was detected as two forms with molecular masses of 11,000 and 15,000 Da by immunoprecipitation with the specific antiserum. The MCP-1 gene expression was induced in the fibroblasts treated with interleukin-1 beta and tumor necrosis factor alpha, but not with interleukin-6. These results suggest that gingival fibroblasts can participate in monocyte recruitment in gingival tissues of adult periodontal patients via the MCP-1 gene product and that MCP-1 plays an important role in the inflammatory reaction in the disease.

Adult↗

PubMed1992

An assay system utilizing devitalized bone for assessment of differentiation of osteoclast progenitors.

The present study provides a novel assay system to examine the differentiation of osteoclast progenitors on devitalized bone slices. We used the population of bone cells liberated enzymatically from 14-day-old mouse embryonal calvariae as a source of osteoclast progenitors. The analysis of differentiation of osteoclast progenitors into preosteoclasts and mature osteoclasts was assessed in terms of the formation of TRAP-positive cells and pits or resorption lacunae, respectively, on devitalized bone slices. Osteoclasts having bone-resorbing activity appeared when the calvarial cell population was cultured in the presence of 1 alpha,25-(OH)2D3 on devitalized bone slices. The resorbing activity increased in a 1 alpha,25-(OH)2D3 dose-related manner. However, calcitonin, a potent inhibitor of differentiation and activation of osteoclast lineage cells, reduced the area of the resorption lacunae in a dose-dependent fashion. The bone-resorbing cells on the bone slices expressed an obvious ruffled border and clear zone, structures specific to mature osteoclasts. These results suggest that osteoclast progenitors in the mouse calvarial population examined differentiated into mature osteoclasts in the presence of 1 alpha,25-(OH)2D3 on devitalized bone slices. Further, using this assay system we assessed the effect of some other osteotropic factors on the differentiation of osteoclast progenitors to mature osteoclasts. IL-1, IL-6, and PTH increased the formation of TRAP-positive cells and pits and the area of resorption lacunae in a dose-dependent fashion. However, prostaglandin E2 was unable to induce the formation of resorption lacunae, although a significant appearance of TRAP-positive cells was observed at a concentration of 200 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid Phosphatase↗

PubMed1992

Effect of interleukin-1 beta on gene expressions and functions of fibroblastic cells derived from human periodontal ligament.

The present study shows the effect of interleukin-1 beta (IL-1 beta) on some gene expressions and functions of fibroblastic cells (HPLF) derived from human periodontal ligament. HPLF were used at passages number 5 to 10. IL-1 beta increased DNA synthesis in both a dose- and an incubation time-dependent manner. IL-1 beta in combination with tumor-necrosis factor alpha or transforming growth factor beta synergistically stimulated the DNA synthesis in the cells. Since many studies have shown that the c-myc oncogene is involved in cell proliferation and differentiation, the effect of IL-1 beta on c-myc messenger RNA (mRNA) level in HPLF was examined. IL-1 beta induced a marked c-myc mRNA level in the cells at 90 minutes after initiation of the cytokine treatment. On the other hand, IL-1 beta significantly inhibited alkaline phosphatase (ALP) activity of the cells in a dose-dependent manner. Also an inhibitory effect was observed on the liver/bone/kidney ALP mRNA level of the cells, and this inhibition by IL-1 beta was dose- and incubation time-dependent. These results suggest that IL-1 beta is a regulatory cytokine involved in the regeneration of the human periodontal ligament.

Alkaline Phosphatase↗

PubMed1992

Porphyromonas gingivalis fimbriae induce expression of the neutrophil chemotactic factor KC gene of mouse peritoneal macrophages: role of protein kinase C.

To account for infiltration of the periodontal tissues by neutrophils, the present study was undertaken to examine whether Porphyromonas gingivalis fimbriae, important structures involved in attachment of the bacteria to periodontal tissues, induce gene expression of the neutrophil chemoattractant KC in macrophages. The fimbriae induced expression of the KC gene of mouse peritoneal macrophages in a dose-dependent fashion. The peak of KC gene expression was observed as early as 1 h after initiation of the treatment. However, the gene expression was short lived, with the expression decreasing gradually after 6 h. A nuclear transcriptional assay showed that the fimbriae regulated the KC gene expression at a posttranscriptional level. We observed that the fimbria-induced KC gene expression was not regulated by endogenous or exogenous prostaglandin. Furthermore, forskolin, a potent activator of adenyl cyclase, and dibutyryl cyclic AMP were incapable of inducing KC gene expression of the peritoneal macrophages. H-8 and HA 1004, inhibitors of cyclic nucleotide-dependent protein kinases, had little effect on the fimbria-induced KC gene expression. On the other hand, the fimbria-induced KC gene expression was inhibited markedly by treatment with H-7, a potent inhibitor of protein kinase C. We also observed that phorbol 12-myristate 13-acetate, a specific activator of protein kinase C, induced KC gene expression of peritoneal macrophages in a dose-dependent fashion. In addition, the fimbria-induced KC gene expression was suppressed in the peritoneal macrophages pretreated for 24 h with phorbol 12-myristate 13-acetate. These results suggest that the KC gene expression was mediated through activation of protein kinase C and not through that of cyclic nucleotide-dependent protein kinases. The present study indicates that P. gingivalis fimbriae can induce gene expression of the neutrophil chemotactic factor KC by macrophages via protein kinase C and suggests that this factor may be involved in infiltration of neutrophils into the periodontal tissues of adult periodontal patients.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1991

Transforming growth factor-beta-induced gene expression of monocyte chemoattractant JE in mouse osteoblastic cells, MC3T3-E1.

A recent study demonstrated that PDGF-inducible JE is an inflammatory cytokine that directs chemotactic activity of monocytes. Accumulation of monocyte/macrophage lineage cells at site of bone tissue sites is very important for formation of multinucleate osteoclasts, which mediate bone resorption. Since transforming growth factor-beta (TGF-beta) is a potent regulator in bone remodeling, we examined whether TGF-beta induced JE gene expression in mouse osteoblastic cells, MC3T3-E1. TGF-beta induced a maximum JE mRNA expression at 3 hr after initiation of the cytokine treatment. This maximal expression was observed in when TGF-beta was used at a concentration of 1 ng/ml. The chemotactic activity for human monocytes was detected in conditioned medium of TGF-beta-treated cells, and the chemotactic activity was neutralized by anti-JE serum treatment.

Animals↗

PubMed1991

Bacteroides (Porphyromonas) gingivalis fimbriae activate mouse peritoneal macrophages and induce gene expression and production of interleukin-1.

The purpose of this study was to examine whether Bacteroides (Porphyromonas) gingivalis fimbriae, an important structure involved in attachment of the bacteria to periodontal tissues, activate macrophages and subsequently induce gene expression and production of interleukin-1 (IL-1) in the cells. The fimbriae increased glucose consumption and lysozyme activity in BALB/c macrophages, both criteria of macrophage activation of peritoneal macrophages, in a dose-dependent fashion. A marked increase in the mRNA level of the c-myc gene, an oncogene, in the cells was observed after a 1-h treatment with the fimbriae, and the level decreased rapidly after 3 h. The fimbriae (4 micrograms of protein per ml) markedly induced IL-1 alpha and IL-1 beta gene expression in the cells and IL-1 production. The expression of IL-1 alpha and IL-1 beta genes measured in terms of specific mRNA increased 1 h after the start of treatment and peaked at 6 h. Such increased expression of IL-1 beta was also observed in C3H/HeJ mice, a lipopolysaccharide low-responder strain. The fimbriae stimulated transcriptional activity of IL-1 beta in the cells, but not that of IL-1 alpha. We also observed that fimbriae-induced IL-1 gene expression was not regulated by endogenous prostaglandin triggered by the fimbriae. Therefore, these observations suggest that B. gingivalis fimbriae may be involved in the pathogenesis of adult periodontal disease via triggering of IL-1 production by monocytes/macrophages in periodontal diseases.

Animals↗

PubMed1991

Monoclonal antibody against Porphyromonas (Bacteroides) endodontalis lipopolysaccharide and application of the antibody for direct identification of the species.

The aim of the present study was to develop a monoclonal antibody that recognizes the shared antigen of Porphyromonas endodontalis so that we could use the antibody in direct identification and detection of P. endodontalis in infectious material from apical periodontal patients. We established a hybridoma cell line producing monoclonal antibody (BEB5) specific for P. endodontalis. BEB5 antibody reacted with all of the P. endodontalis strains tested, but not with any of the other black-pigmented Porphyromonas and Bacteroides spp. The antibody reacted specifically with the lipopolysaccharide (LPS) of three P. endodontalis strains of different serotypes (O1K1, O1K2, and O1K-). Western blotting (immunoblotting) analysis confirmed the specificity of the antibody to these LPSs, because the antibody recognized the typical "repetitive ladder" pattern characteristic of LPS on sodium dodecyl sulfate-polyacrylamide electrophoretic gels. These observations demonstrate that P. endodontalis LPS is the shared antigen of this species. The antibody can specifically identify P. endodontalis on nitrocellulose membrane blots of bacterial colonies grown on agar. The antibody is also capable of directly detecting the presence of P. endodontalis in infectious material by immunoslot blot assay. These results indicate that LPS is the shared antigen of P. endodontalis and that BEB5 antibody against LPS is a useful one for direct identification and detection of the organisms in samples from apical periodontal patients.

Animals↗

PubMed1990

Effects of transforming growth factor-beta and epidermal growth factor on clonal rat pulp cells.

These factors influence proliferation and differentiation in various cell types. Their effects on a clonal cell line (RPC-C2A) having high ALPase activity were examined by assay of [3H]-thymidine incorporation and ALPase activity. Neither factor (at a dose of 0.5 ng/ml) altered the shape of the pulp cells. DNA synthesis was not affected by transforming growth factor-beta either in growing cells or in those nearly confluent, but epidermal growth factor, in doses ranging from 0.5 to 10 ng/ml, stimulated the incorporation of [3H]-thymidine in nearly confluent cells. Both factors inhibited ALPase activity in a dose-dependent manner. Indomethacin did not affect this inhibition, suggesting that this effect of growth factors may not be mediated by prostaglandin synthesis. Inhibitory effects of ALPase antagonists (L-phenylalanine, L-homoarginine, levamisole) were not affected by transforming growth factor-beta. Thus epidermal growth factor stimulates DNA synthesis and both transforming growth factor-beta and epidermal growth factor inhibit ALPase activity of clonal rat pulp cells, suggesting that both factors may act as regulators of biological function, including cell differentiation, in pulp cells.

Alkaline Phosphatase↗

PubMed1990

Monoclonal antibody against a serotype antigen of Porphyromonas (Bacteroides) endodontalis and characteristics of the antigen.

Recent studies have demonstrated the presence of three serotypes (O1K1, O1K2, and O1K-) of Porphyromonas (Bacteroides) endodontalis. In the present study, a hybridoma cell line producing monoclonal antibody (BEE11) specific for serotype O1K1 of P. endodontalis was established. The specificity of the antibody was evaluated by enzyme-linked immunosorbent assay and immunoslot blot analysis. BEE11 antibody reacted with strains ATCC 35406, HG 400, and HG 421 of the bacterium. However, it did not react with HG 422 or HG 948. Also, the antibody did not react with any of the black-pigmented Bacteroides strains tested. Although the antibody reacted with total cell envelope and capsule materials, it did not do so with lipopolysaccharide. The antibody reacted with antigen material having a molecular mass of 110 kilodaltons (kDa), as judged from fractionation by Superose 12 prep gel chromatography. When the peak fraction from the Superose 12 column was subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot (immunoblot) analysis, the reactivity was detected as a single band at an apparent molecular mass of about 52 kDa. The antigen material purified partially by high-performance liquid chromatography was sensitive to trypsin, V8 protease, and heating to 80 degrees C but not to neuraminidase. Therefore, the present study shows that BEE11 antibody recognizes a serotype antigen of P. endodontalis which may be a dimer consisting of monomers having molecular masses of approximately 52 kDa and sensitivity to proteases and heat.

Animals↗

PubMed1990

Application of monoclonal antibodies to the detection of black-pigmented Bacteroides spp. in subgingival plaques by immunoslot blot assay.

The aim of the present study was to assess the application of monoclonal antibodies to the detection of black-pigmented Bacteroides spp. in subgingival plaques by immunoslot blot assay. Subgingival plaque samples from adult periodontal patients were examined by immunoslot blot assay with monoclonal antibodies that specifically recognize Bacteroides gingivalis, Bacteroides intermedius serogroups I and II, and Bacteroides melaninogenicus. The assay can detect specifically these Bacteroides spp. in the subgingival plaques. Therefore, we investigated the distribution of these Bacteroides spp. in the subgingival plaques of patients classified by Russell's periodontal index. Reactivities of their plaques with monoclonal antibodies toward B. gingivalis and B. intermedius serogroup I were clearly related to the severity of the periodontal disease, but this was not the case with B. intermedius serogroup II and B. melaninogenicus. These results indicate that this immunoslot blot assay using monoclonal antibodies toward these Bacteroides spp. provides simple detection and monitoring of these organisms in periodontal patients.

Adult↗