Virulence factors of Porphyromonas gingivalis.
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Animals↗
Biomedical subjects
S C Holt
Publications and source records attributed to S C Holt.
Systemic manifestations of periodontitis in the non-human primate.
This report describes our findings regarding the potential contribution of periodontitis to atherosclerotic processes using a nonhuman primate model. The goal of the investigations was to target general mechanisms which could describe the association of these disease processes, including: (i) systemic translocation of bacteria/products during periodontitis; (ii) alterations in systemic inflammatory biomarkers during periodontitis; and (iii) the relationship of periodontitis to serum lipids/lipoproteins. Increases in serum endotoxin (e.g. LPS) during ligature-induced periodontitis were observed in these animals. We determined serum levels of various acute phase reactants and chemokines (e.g. CRP, alpha 1-antitrypsin, haptoglobin, fibrinogen, IL-8). A number of these host factors were significantly increased during gingivitis and/or periodontitis. Finally, we observed specific changes in serum lipid levels (cholesterol, triglycerides, HDL, LDL) and lipoproteins (apoA-I) during periodontitis, which were exacerbated by exposure of the animals to a diet with elevated fat content. Thus, we have described systemic manifestations of periodontitis that include detection of bacterial products, inflammatory biomarkers, and dyslipoproteinemia consistent with an increased atherogenic risk.
Animals↗
Lack of humoral immune protection against Treponema denticola virulence in a murine model.
This study investigated the characteristics of humoral immune responses to Treponema denticola following primary infection, reinfection, and active immunization, as well as immune protection in mice. Primary infection with T. denticola induced a significant (400-fold) serum immunoglobulin G (IgG) response compared to that in control uninfected mice. The IgG response to reinfection was 20, 000-fold higher than that for control mice and 10-fold higher than that for primary infection. Mice actively immunized with formalin-killed treponemes developed serum antibody levels seven- to eightfold greater than those in animals after primary infection. Nevertheless, mice with this acquired antibody following primary infection or active immunization demonstrated no significant alterations of lesion induction or decreased size of the abscesses following a challenge infection. Mice with primary infection developed increased levels of IgG3, IgG2b, and IgG2a antibodies, with IgG1 being lower than the other subclasses. Reinfected mice developed enhanced IgG2b, IgG2a, and IgG3 and less IgG1. In contrast, immunized mice developed higher IgG1 and lower IgG3 antibody responses to infection. These IgG subclass distributions indicate a stimulation of both Th1 and Th2 activities in development of the humoral immune response to infection and immunization. Our findings also demonstrated a broad antigen reactivity of the serum antibody, which was significantly increased with reinfection and active immunization. Furthermore, serum antibody was effective in vitro in immobilizing and clumping the bacteria but did not inhibit growth or passively prevent the treponemal infection. These observations suggest that humoral immune responses, as manifested by antibody levels, isotype, and antigenic specificity, were not capable of resolving a T. denticola infection.
Animals↗
Environmental modulation of oral treponeme virulence in a murine model.
This investigation examined the effects of environmental alteration on the virulence of the oral treponemes Treponema denticola and Treponema pectinovorum. The environmental effects were assessed by using a model of localized inflammatory abscesses in mice. In vitro growth of T. denticola and T. pectinovorum as a function of modification of the cysteine concentration significantly enhanced abscess formation and size. In contrast, growth of T. denticola or T. pectinovorum under iron-limiting conditions (e.g., dipyridyl chelation) had no effect on abscess induction in comparison to that when the strains were grown under normal iron conditions. In vivo modulation of the microenvironment at the focus of infection with Cytodex beads demonstrated that increasing the local inflammation had no effect on lesion induction or size. In vivo studies involved the determination of the effects of increased systemic iron availability (e.g., iron dextran or phenylhydrazine) on the induction, kinetics, and size of lesions. T. denticola induced significantly larger lesions in mice with iron pretreatment and demonstrated systemic manifestations of the infectious challenge and an accompanying spreading lesion with phenylhydrazine pretreatment (e.g., increases in circulating free hemoglobin). In contrast, T. pectinovorum virulence was minimally affected by this in vivo treatment to increase iron availability. T. denticola virulence, as evaluated by lesion size, was increased additively by in vivo iron availability, and cysteine modified growth of the microorganism. Additionally, galactosamine sensitized mice to a lethal outcome following infection with both T. denticola and T. pectinovorum, suggesting an endotoxin-like activity in these treponemes. These findings demonstrated the ability to modify the virulence capacity of T. denticola and T. pectinovorum by environmental conditions which can be evaluated by using in vivo murine models.
Abscess↗
Virulence of a polymicrobic complex, Treponema denticola and Porphyromonas gingivalis, in a murine model.
The effect of a polymicrobic infection employing Treponema denticola and Porphyromonas gingivalis in the murine lesion model was used to determine the synergistic virulence of these two periodontopathic bacteria. At high doses of P. gingivalis W50, addition of T. denticola in the infection mixture had no effect on the formation and size of the spreading lesion caused by this microorganism. However, at low P. gingivalis challenge doses, T. denticola significantly enhanced the virulence of P. gingivalis compared with monoinfection of this microorganism. A potential role of the trypsin-like protease enzyme activity of P. gingivalis in this synergistic virulence was tested using P. gingivalis mutants deficient (i.e., BEI) or devoid (i.e., NG4B19) of this protease activity. These findings demonstrated that T. denticola-P. gingivalis complexes exhibit enhanced virulence in this model and that even using a polymicrobic challenge infection, the trypsin-like protease activity was important to P. gingivalis virulence expression.
Abscess↗
Bone resorption caused by three periodontal pathogens in vivo in mice is mediated in part by prostaglandin.
Gingival inflammation, bacterial infection, alveolar bone destruction, and subsequent tooth loss are characteristic features of periodontal disease, but the precise mechanisms of bone loss are poorly understood. Most animal models of the disease require injury to gingival tissues or teeth, and the effects of microorganisms are thus complicated by host responses to tissue destruction. To determine whether three putative periodontal pathogens, Porphyromonas gingivalis, Campylobacter rectus, and Fusobacterium nucleatum, could cause localized bone resorption in vivo in the absence of tissue injury, we injected live or heat-killed preparations of these microorganisms into the subcutaneous tissues overlying the calvaria of normal mice once daily for 6 days and then examined the bones histologically. We found that all three microorganisms (both live and heat killed) stimulated bone resorption and that the strain of F. nucleatum used appeared to be the strongest inducer of osteoclast activity. Treatment of the mice concomitantly with indomethacin reduced but did not completely inhibit bone resorption by these microorganisms, suggesting that their effects were mediated, in part, by arachidonic acid metabolites (e.g., prostaglandins). Our findings indicate that these potential pathogens can stimulate bone resorption locally when placed beside a bone surface in vivo in the absence of prior tissue injury and support a role for them in the pathogenesis of bone loss around teeth in periodontitis.
Alveolar Bone Loss↗
Immunization with Porphyromonas gingivalis cysteine protease: effects on experimental gingivitis and ligature-induced periodontitis in Macaca fascicularis.
Targeting bacterial virulence factors such as proteases for immunization may hold the key to limiting or preventing loss of attachment and alveolar bone in periodontal disease. This study examined the clinical, microbiological, and immununological responses following active immunization with a purified Porphyromonas gingivalis cysteine protease (porphypain-2) in the nonhuman primate (Nhp) Macaca fascicularis. One group of Nhp was immunized with porphypain-2 antigen while control Nhp received placebo injections. All Nhp were subjected to experimental gingivitis followed by ligature-induced periodontitis in a split-mouth design. An enzyme-linked immunosorbent assay demonstrated that immunization elicited a significantly elevated and specific IgG antibody response to both whole cell P. gingivalis (36-fold) and to porphypain-2 (194-fold). Checkerboard hybridization DNA analysis of subgingival plaque from ligated sextants demonstrated that 25% more Gram-negative anaerobic species became significantly elevated from baseline and at earlier timepoints in the control group than in the immununized group. Immunization with this protease did not suppress the emergence of P. gingivalis. Clinical indices showed few changes related to immunization. Alveolar bone density changes demonstrated a highly significant loss in ligated sextants compared to non-ligated sextants within the control group (P < 0.001), and a smaller but significant difference within the immunized group (P = 0.043). Comparison of ligated sextants only demonstrated more bone loss in the control group versus the immunized group (-13.07+/-9.51 versus -9.41+/-6.18; computer-assisted densitometric image analysis units +/- SD); the difference approached, but did not reach, significance. The results suggest that porphypain-2 may contribute to the pathogenic potential of the subgingival plaque microbiota in the Nhp model of ligature-induced periodontitis, and that active immunization with porphypain-2 appeared capable of altering this pathogenic response.
Absorptiometry, Photon↗
Host modulation of tissue destruction caused by periodontopathogens: effects on a mixed microbial infection composed of Porphyromonas gingivalis and Fusobacterium nucleatum.
These studies determined the ability of selected periodontopathogens to synergistically initiate soft tissue destruction in a murine abscess model. The development of immunity following recovery from infection or by active immunization was also examined. Mice were infected with P. gingivalis W50, F. nucleatum T18, or a combination of the two microorganisms. F. nucleatum caused only a localized lesion in contrast to P. gingivalis which caused a spreading suppurative inflammatory lesion of the skin and subcutaneous tissues, which, depending upon the dose, could result in death. Infection of mice with a combination of P. gingivalis and F. nucleatum elicited a significantly greater lesion size (P<0.001) and lethality compared with P. gingivalis alone. Mice infected with a subclinical dose (no visible lesion) of P. gingivalis failed to develop protective immunity to a secondary P. gingivalis challenge. Mice that had recovered from P. gingivalis lesions demonstrated partial protection against subsequent P. gingivalis challenge; however, the immunity was less protective against the mixed F. nucleatum + P. gingivalis infection. Active immunization with P. gingivalis protected against both the P. gingivalis and F. nucleatum + P. gingivalis challenges and this protection was correlated with the levels of specific serum immunoglobulin G (IgG) antibody. The results indicated that the murine model is ideally suited to examine bacterially-mediated mixed infections that result in soft tissue destruction. This destruction can be minimized, but not abrogated, with development of immunity. Challenge with sufficient numbers of the pathogens can overwhelm the acquired immunity.
Animals↗
Porphyromonas gingivalis virulence in a murine lesion model: effects of immune alterations.
This study utilized various mouse strains with documented alterations in immune system components to assess their contribution to modify the virulence of Porphyromonas gingivalis. P. gingivalis W50 was cultivated on blood agar plates, harvested and used to challenge mice by subcutaneous injection on the dorsolateral surface of the back. Soft tissue lesion development was estimated by measuring the area of the spreading lesion formed by this microorganism over a period of 15 days. Challenge of various normal inbred and outbred mouse strains including: BALB/cN, BALB/cJ, BALB/c nu/+, ICR, B10.A(4R), B10.MBR, A/J, C57BL/6J, CBA/CaH, C.B-17/Icv Tacf DF and C3H/HeN with 2 x 10(10) bacteria showed similar lesion size among these strains (approximately 400 mm2). Genetically deficient mouse strains [C.B-17/Icr Tac (SCID); DBA/2 (C5 deficient); BALB/c nu/nu (T cell deficient); CBA/CaHN-XID/J (B cell deficient) and C3H/HeJ (LPS hyporesponsive)] demonstrated a lesion size which was similar to normal animals. C57BL/6J-BgJ (NK cell deficient) mice exhibited a significantly more severe lesion than the other strains tested. Following healing of the lesions, we initiated a secondary infection of the surviving animals to estimate the acquisition of protective immunity following recovery from the primary infection. Normal mice demonstrated a delayed onset and decrease in lesion size of 15 to 30% compared with the primary infection. In contrast, each of the immunodeficient strains appeared unable to develop immune protection to the secondary challenge. The findings suggest that protection against primary infections with P. gingivalis are mediated by innate immune mechanisms (PMN. NK cells). Additionally, it appears that T-cell-dependent humoral responses are critical to developing immunity to subsequent P. gingivalis infection.
Animals↗
Oral bone loss is increased in ovariectomized rats.
Alveolar bone loss associated with periodontal disease occurs frequently in postmenopausal females, the same group that is predisposed to osteoporosis. To determine if the estrogen-deficient state enhances oral bone loss, we studied ovariectomized rats administered the potent bone-resorbing cytokine interleukin-1 or the periodontal pathogen Campylobacter rectus lipopolysaccharide (LPS). Distal root canals of first mandibular molars were instrumented with endodontic files, and bone resorbing factors were deposited and sealed into the root canal. Radiographs of periapical bone loss were evaluated using computer assisted image analysis to determine lesion size. Both interleukin-1 and C. rectus LPS caused a significant increase in lesion area in both ovariectomized and normal rats when compared with controls and a significant increase in ovariectomized animals compared to nonovariectomized animals receiving LPS. Using this endodontic model, we have demonstrated that estrogen deficiency results in increased oral bone loss in rats.
Alveolar Bone Loss↗
Characteristics of systemic antibody responses of nonhuman primates to cell envelope and cell wall antigens from periodontal pathogens.
The immune response of the primate, Macaca fascicularis, to cell envelope (CEA) or cell wall (CWA) antigens of several periodontal pathogens was examined to develop a strategy to interfere with ligature-induced periodontitis. Animals were parenterally immunized with CEA of either Porphyromonas gingivalis, Prevotella intermedia or a combination of CEA/CWA of Campylobacter rectus, Fusobacterium nucleatum and Actinomyces viscosus. Serum samples were taken every 2-4 weeks over a 4-month period, which included a 13-week interval with molar teeth ligated. All of the nonhuman primates in the study exhibited baseline levels of IgG, IgM and IgA antibody to formalinized whole cells of the bacteria. These levels increased significantly following immunization and were elevated above baseline throughout the remainder of the experiment. The largest change in antibody responses was seen in IgA antibody levels of P. gingivalis and C. rectus (42-fold above baseline), IgM antibody to P. intermedia, (41-fold increase) and IgG antibody to F. nucleatum and A. viscosus (32 and 63-fold increases). Moreover, the nonhuman primates exhibited differences in isotype response levels to whole microorganisms compared with the cell envelope antigens. These findings demonstrate the capacity of these nonhuman primates to produce an active immune response to microorganisms chronically colonizing the subgingival microbiota. Additionally, it appears that the bacteria may exhibit some unique differences in their immunogenicity as detected by the nonhuman primate and may contribute to the ability of the immune responses to effectively interact with these pathogens.
Actinomyces viscosus↗
Virulence characteristics of oral treponemes in a murine model.
This study was designed to investigate the virulence characteristics of Treponema denticola, T. socranskii, T. pectinovorum, and T. vincentii following challenge infection of mice. These microorganisms induced well-demarcated, dose-dependent, raised subcutaneous (s.c.) abscesses which were similar in time of onset, lesion progression, and duration of healing. Only viable cells were capable of inducing these characteristic s.c. abscesses. Histological examination of the skin lesion 3 and 5 days postinfection revealed abscess formation in the s.c. tissues, and abundant spiral organisms were demonstrated to be present in the abscess. Host resistance modulation by dexamethasone (neutrophil alteration) and cyclophosphamide (neutrophil depletion) pretreatment had a minimal effect on the virulence expression by any of these treponemes. The T. denticola isolates demonstrated significant trypsin-like protease (TLPase) activity, while both T. socranskii and T. vincentii were devoid of this activity. Interestingly, T. pectinovorum strains were heterogeneous with respect to TLPase as high producers, low producers, and nonproducers. However, no differences in lesion formation were noted regardless of whether the species expressed this proteolytic activity or whether treatment with N alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK) and dithiothreitol was performed. These results showed that (i) a murine model may be used to evaluate virulence expression by oral treponemes; (ii) while TLPase activity varies among the oral treponemes, this protease does not appear to participate in abscess induction in the mouse model; and (iii) T. pectinovorum strains show variation in TLPase activity.
Animals↗
Purification and characterization of Campylobacter rectus surface layer proteins.
Campylobacter rectus is a putative periodontopathogen which expresses a proteinaceous surface layer (S-layer) external to the outer membrane. S-layers are considered to play a protective role for the microorganism in hostile environments. The S-layer proteins from six different C. rectus strains (five human isolates and a nonhuman primate [NHP] isolate) were isolated, purified, and characterized. The S-layer proteins of these strains varied in molecular mass (ca. 150 to 166 kDa) as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. They all reacted with monospecific rabbit antiserum to the purified S-layer of C. rectus 314, but a quantitative enzyme-linked immunosorbent assay demonstrated a strong antigenic relationship among the five human strains, while the NHP strain, 6250, showed weaker reactivity. Amino acid composition analysis showed that the S-layers of four C. rectus strains contained large proportions of acidic amino acids (13 to 27%) and that >34% of the amino acid residues were hydrophobic. Amino acid sequence analysis of six S-layer proteins revealed that the first 15 amino-terminal amino acids were identical and showed seven residues of identity with the amino-terminal sequence of the Campylobacter fetus S-layer protein SapA1. CNBr peptide profiles of the S-layer proteins from C. rectus 314, ATCC 33238, and 6250 confirmed that the S-layer proteins from the human strains were similar to each other and somewhat different from that of the NHP isolate (strain 6250). However, the S-layer proteins from the two human isolates do show some structural heterogeneity. For example, there was a 17-kDa fragment unique to the C. rectus 314 S-layer. The amino-terminal sequence of this peptide had homology with the C. rectus 51-kDa porin and was composed of nearly 50% hydrophobic residues. Thus, the S-layer protein from C. rectus has structural heterogeneity among different human strains and immunoheterogeneity with the NHP strain.
Amino Acid Sequence↗
Cystalysin, a 46-kilodalton cysteine desulfhydrase from Treponema denticola, with hemolytic and hemoxidative activities.
A 46-kDa hemolytic protein, referred to as cystalysin, from Treponema denticola ATCC 35404 was overexpressed in Escherichia coli LC-67. Both the native and recombinant 46-kDa proteins were purified to homogeneity. Both proteins expressed identical biological and functional characteristics. In addition to its biological function of lysing erythrocytes and hemoxidizing the hemoglobin to methemoglobin, cystalysin was also capable of removing the sulfhydryl and amino groups from selected S-containing compounds (e.g., cysteine) producing H2S, NH3, and pyruvate. This cysteine desulfhydrase resulted in the following Michaelis-Menten kinetics: Km = 3.6 mM and k(cat) = 12 s(-1). Cystathionine and S-aminoethyl-L-cysteine were also substrates for the protein. Gas chromatography-mass spectrometry and high-performance liquid chromatography analysis of the end products revealed NH3, pyruvate, homocysteine (from cystathionine), and cysteamine (from S-aminoethyl-L-cysteine). The enzyme was active over a broad pH range, with highest activity at pH 7.8 to 8.0. The enzymatic activity was increased by beta-mercaptoethanol. It was not inhibited by the proteinase inhibitor TLCK (N alpha-p-tosyl-L-lysine chloromethyl ketone), pronase, or proteinase K, suggesting that the functional site was physically protected or located in a small fragment of the polypeptide. We hypothesize that cystalysin is a pyridoxal-5-phosphate-containing enzyme, with activity of an alphaC-N and betaC-S lyase (cystathionase) type. Since large amounts of H2S have been reported in deep periodontal pockets, cystalysin may also function in vivo as an important virulence molecule.
Cystathionine gamma-Lyase↗
Identification, isolation, and characterization of the 42-kilodalton major outer membrane protein (MompA) from Treponema pectinovorum ATCC 33768.
The major protein present in the isolated outer membrane of Treponema pectinovorum ATCC 33768, MompA, was identified, purified, and characterized. Immuno-gold electron microscopy, using anti-MompA serum, and cell fractionation experiments confirmed the localization of MompA to the outer membrane. MompA was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis to have a molecular mass of 42 kDa when heat denatured, whereas native MompA formed a number of detergent-stable forms with molecular masses of 71, 76, and 83 kDa. A temperature of 60 degrees C was required to convert the native protein to the 42-kDa form. A number of detergents and chemical agents that are capable of breaking ionic and hydrogen bonds of proteins did not convert native MompA to the 42-kDa species. The native forms of the protein were resistant to the combined action of proteinase K, trypsin, and chymotrypsin, whereas the 42-kDa form of MompA was not. The N-terminal amino acid sequence of MompA was determined to be DVTVNINSRVRPVLYTT, and database searches did not identify any homology with known protein sequences. Amino acid compositional analysis showed the protein to be rich in proline and glycine, with these amino acids accounting for 28 and 13%, respectively, of the total amino acids. Antiserum raised against the major outer membrane protein of T. denticola GM-1 and ATCC 35405 did not cross-react with MompA, and antiserum raised against MompA did not react with any cellular components of Treponema denticola, Treponema vincentii, or Treponema socranskii. A major outer membrane protein similar in molecular mass to MompA was identified in eight clinical isolates of T. pectinovorum. The major outer membrane protein produced by four of the clinical isolates reacted strongly, by Western blotting, with anti-MompA serum, whereas proteins of the other strains did not.
Amino Acid Sequence↗
Trypsin-like protease activity of Porphyromonas gingivalis as a potential virulence factor in a murine lesion model.
Porphyromonas gingivalis possesses a large number of enzymatic activities which might be important in the virulence of this putative periodontopathogen. The purpose of this study was to examine these enzymatic activities in vivo in a murine model to assess their role in soft tissue destruction. Whole cells of P. gingivalis strains whether grown on blood agar plates or in broth exhibited high levels of alkaline phosphatase (ALPase), a trypsin-like protease (TLPase), acid phosphatase (ACPase), N-acetyl beta-glucosaminidase (Na beta-Gase) enzymes and collagenolytic activities. P. gingivalis W50 treated with 2 mM Na-P-tosyl-L-lysine chloromethyl ketone (TLCK)/phenylmethylsulfonyl fluoride (PMSF) prior to subcutaneous infection of mice failed to induce a phlegmonous abscess and lethality characteristic of animals challenged with untreated P. gingivalis. Comparison of wild type P. gingivalis strain 3079.03 with its protease-deficient (TLPase-negative) mutant NG4B19 revealed the mutant to be avirulent (no lesion and no death) in this model. P. gingivalis BEI and SW5 mutants (parent W50), which partially lacked TLPase enzyme activity produced only localized lesions, and no death. Thus, the TLPase enzyme appears to be correlated with the lesion type (spreading or localized), lesion size, and death in this mouse abscess model. Therefore, the enzymatic activities of P. gingivalis and specifically the TLPase enzyme could play an important role in periodontal disease by enhancing bacterial spread and degrading gingival tissues.
Acetylglucosaminidase↗
Isolation and characterization of a hemin-binding cell envelope protein from Porphyromonas gingivalis.
A 30 kDa (heated 24 kDa) hemin-binding protein whose expression is both hemin and iron regulated was identified and purified in Porphyromonas gingivalis 381. A strong hemin-binding function was found by LDS-PAGE and TMBZ staining when cells were grown under hemin (iron)-limited conditions. N-terminal amino acid sequence analysis of CNBr-digested 24 kDa hemin binding protein revealed that this protein belongs to a new, so far undescribed hemin-binding class of proteins.
Amino Acid Sequence↗
Lipopolysaccharide isolated from Porphyromonas gingivalis grown in hemin-limited chemostat conditions has a reduced capacity for human neutrophil priming.
One way prokaryotes respond to environmental stresses is by modifying selected outer membrane components. Iron, in the form of hemin, has been shown to be a significant regulator of Porphyromonas gingivalis growth and virulence and of the expression of outer membrane proteins and lipopoly saccharide. Since lipopoly saccharide has profound effects on host immune cells, this study compared the effect of hemin-restricted and hemin-normal P. gingivalis growth conditions on lipopolysaccharide priming of N-formylmethionyl-leucyl-phenylalanine-induced superoxide generation by human neutrophils. P. gingivalis was grown in a chemostat under normal (5 micrograms hemin/ml) and hemin-restricted (0.08 microgram hemin/ml) conditions. Purified lipopolysaccharide from both P. gingivalis normal and hemin-limited environments increased N-formylmethionyl-leucyl-phenylalanine-induced superoxide release by neutrophils in a dose-dependent manner. Lipopolysaccharide isolated from the hemin-normal conditions was a significantly more potent neutrophil priming agent than the lipopolysaccharide isolated from hemin-restricted conditions. Addition of normal human serum enhanced the priming effect of both lipopolysaccharide preparations; this effect, however, was more evident with the hemin-normal lipopolysaccharide. Further, this enhancing effect of serum was partly reduced in the presence of antibodies raised against the serum lipopolysaccharide-binding protein. The differences in the biological activity of the two lipopolysaccharide preparations could be associated with structural differences detected by sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis. These results indicate that hemin availability affects regulation of an aspect of P. gingivalis virulence, lipopolysaccharide-human neutrophils priming. The reduced capacity for neutrophil priming by hemin-restricted lipopolysaccharide appears to be related to lipopolysaccharide-neutrophil interactions and not to serum factors Targeting bacterial cell-surface components involved in hemin transport might be effective therapy for P. gingivalis-associated periodontal diseases.
Culture Media, Serum-Free↗