Mechanisms Mediating<i>Porphyromonas gingivalis</i>Gingipain RgpA-Induced Oral Mucosa Inflammation In Vivo

Rubinstein, Israel; Potempa, Jan; Travis, James; Gao, Xiaopei

doi:10.1128/iai.69.2.1199-1201.2001

Cited by 19 publications

(30 citation statements)

References 33 publications

(38 reference statements)

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“…Although the mechanism responsible for endogenous release of kinins by systemically administered carrageenin was not examined in the present study, it is likely to reflect contact phase activation of plasma kallikrein (14). In other settings, e.g., infection, DC may respond to B 2 R agonists that are released from kininogens by tissue kallikrein or by unique microbial cysteine proteases (15)(16)(17)(18).…”

Section: Lbk Induces Il-12-dependent Th1 Priming For Ova Ag In Vivo Amentioning

confidence: 99%

Cutting Edge: Bradykinin Induces IL-12 Production by Dendritic Cells: A Danger Signal That Drives Th1 Polarization

Aliberti

Viola

Vieira‐de‐Abreu

et al. 2003

The Journal of Immunology

104

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Dendritic cells play a major role in the induction of both innate and acquired immune responses against pathogenic invaders. These cells are also able to sense endogenous activation signals liberated by injured tissues even in the absence of infection. In the present work, we demonstrate that kinins mobilize dendritic cells to produce IL-12 through activation of the B2 bradykinin receptor subtype and that bradykinin-induced IL-12 responses are tightly regulated both by angiotensin-converting enzyme, a kinin-degrading peptidase, and by endogenous IL-10. Using a mouse model of allergic inflammation, we further show that addition of bradykinin to OVA during immunization results in decreased eosinophil infiltration on Ag challenge. The latter effect was demonstrated to be due to IL-12-driven skewing of Ag-specific T cell responses to a type 1 cytokine profile. Our data thus indicate that kinin peptides can serve as danger signals that trigger dendritic cells to produce IL-12 through activation of B2 bradykinin receptors.

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Section: Lbk Induces Il-12-dependent Th1 Priming For Ova Ag In Vivo Amentioning

confidence: 99%

Cutting Edge: Bradykinin Induces IL-12 Production by Dendritic Cells: A Danger Signal That Drives Th1 Polarization

Aliberti

Viola

Vieira‐de‐Abreu

et al. 2003

The Journal of Immunology

104

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“…It is conceivable that Bacillus spores could contaminate chewing tobacco processed for human use and germinate when placed onto the oral mucosa. These bacteria could then elaborate potent virulence factors, such as proteinases, that activate oral keratinocytes and the kallikrein/ kinin metabolic pathway in the oral mucosa, leading to plasma exudation and tissue injury (2,9,14,16,19,20).…”

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confidence: 99%

“…The clearance of FITC-dextran was determined before the application of the supernatant and every 5 min after for 60 min. In another group of animals, 1 M Hoe140 or 1 M NPC 17647, both structurally distinct selective bradykinin B 2 receptor antagonists (2,5,(19)(20)(21), was suffused over the check pouch for 30 min before the check pouch was suffused with the Bacillus supernatant (1:1,000 dilution in bicarbonate buffer, pH 7.4) for 20 min. The observer of the cheek pouch microcirculation was unaware which hamster belonged in which treatment group.…”

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confidence: 99%

“…With a spectrophotofluorometer, the concentration of FITC-dextran in the plasma and suffusate was determined based on a standard curve of FITC-dextran concentration versus percent emission. The clearance of FITC-dextran was determined by calculating the ratio of the concentration of FITC-dextran in suffusate (nanograms per milliliter) to that in plasma (milligrams per milliliter) and multiplying this ratio by the suffusate flow rate (2 ml/min).The experimental design has been used previously in our laboratory (5,6,(18)(19)(20)25). After the buffer was suffused for 30 min (the equilibration period), FITC-dextran was injected intravenously and the number of leaky sites and the clearance of FITC-dextran were determined for 30 min.…”

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confidence: 99%

“…Macromolecular leakage was determined by extravasation of fluorescein isothiocyanate-labeled dextran (FITC-dextran; molecular mass, 70 kDa), the intravascular tracer, which appeared as fluorescent spots or leaky sites around postcapillary venules. The number of leaky sites in three random microscopic fields was counted, averaged, and expressed as the number of leaky sites per 0.11 cm 2 of cheek pouch, which corresponds to the area of one microscopic field (5,6,13,(18)(19)(20)25). With a spectrophotofluorometer, the concentration of FITC-dextran in the plasma and suffusate was determined based on a standard curve of FITC-dextran concentration versus percent emission.…”

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confidence: 99%

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BacillusSpecies Are Present in Chewing Tobacco Sold in the United States and Evoke Plasma Exudation from the Oral Mucosa

Rubinstein

Pedersen

2002

Clin Vaccine Immunol

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Five Bacillus species, predominantly Bacillus megaterium and Bacillus pumilus, were isolated from two popular brands of commercially available chewing tobacco [(5.0 ؎ 1) ؋ 10 6 CFU/ml of supernatant; results for four experiments]. Moreover, the supernatant of the Bacillus culture evoked plasma exudation from postcapillary venules in the intact hamster cheek pouch, exudation that was mediated by the kallikrein/kinin metabolic pathway. Taken together, these data indicate that Bacillus species contaminate chewing tobacco commercially available in the United States and elaborate a potent exogenous virulence factor(s) that injures the oral mucosa.Habitual use of chewing tobacco is on the rise in the United States (4). This practice may be associated with oral mucosa inflammation and injury in susceptible individuals and may predispose chewing tobacco users to oral epithelial cell dysplasia and cancer (7,15,23). Previous studies from our laboratory showed that chewing tobacco elicits plasma exudation from the oral mucosa by activating oral keratinocytes and the kallikrein/ kinin metabolic pathway (2,5,6,18,25). However, the toxic constituent(s) of chewing tobacco that accounts for these responses has not been characterized (8,17).A physiological disorder of the tobacco plant, termed "frenching," has been known to the tobacco industry since colonial times (22). Although the etiology of this condition is uncertain, so-called organic toxins produced by Bacillus species and found in the soil where tobacco plants are grown have been implicated (22). It is conceivable that Bacillus spores could contaminate chewing tobacco processed for human use and germinate when placed onto the oral mucosa. These bacteria could then elaborate potent virulence factors, such as proteinases, that activate oral keratinocytes and the kallikrein/ kinin metabolic pathway in the oral mucosa, leading to plasma exudation and tissue injury (2,9,14,16,19,20).The purpose of this study was to begin to address this issue by determining whether Bacillus species contaminate commercially available chewing tobacco and, if so, whether they evoke plasma exudation from the intact oral mucosa. MATERIALS AND METHODSCulture of chewing tobacco. One box each of two popular chewing tobacco brands (moist snuff; Skoal Cherry and Skoal Spearmint [U.S. Tobacco Co., Richmond, Va.]) were purchased at a local grocery store in Chicago, Ill. One-half gram of chewing tobacco from each box was mixed with 50 ml of sterile, doubledistilled water for 5 min. Then samples of the mixture were transferred onto blood, mannitol salt, and MacConkey agar plates by sterile cotton swabs and streaked for isolated colonies (13). The blood and mannitol salt agar plates were incubated under aerobic, anaerobic, and 10% CO 2 conditions. MacConkey agar plates were incubated aerobically at 37°C. After 48 h, the cultures were examined and a Gram stain of the isolated colonies was performed (11,12,16). After an additional 48 h of incubation 13 biochemical tests were conducted to identify the isolate...

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E. coli lipopolysaccharide attenuates adenosine A1 receptor-mediated increase in plasma exudation from the hamster cheek pouch

Gao

Rubinstein

2010

Inflamm. Res.

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Objective and design To determine whether exposure to E. coli lipopolysaccharide (LPS) modulates adenosine A1 receptor-induced increase in plasma exudation from the intact hamster cheek pouch microcirculation. Methods and results Using intravital microscopy, we found that suffusion of R(−)-N6-(2-phenylisopropyl)-adenosine (R(−)-PIA) (1.0 and 10.0 nM), a selective adenosine A1 receptor agonist, onto the intact cheek pouch elicited significant, concentration-dependent leaky site formation and increase in clearance of fluorescein thioisocyanate-dextran (mol mass, 70 kDa) from post-capillary venules (p < 0.05). These responses were significantly attenuated by pre-treatment of hamsters with LPS (p < 0.05). By contrast, LPS had no significant effects on CGS-21680-, a selective adenosine A2A receptor agonist, bradykinin- and substance P-induced increases in plasma exudation from the cheek pouch. Conclusion These data indicate that LPS attenuates adenosine A1 receptor-induced increase in plasma exudation in vivo in a specific fashion. We suggest that this phenomenon represents an endogenous anti-inflammatory cue to avoid excessive inflammation during Gram-negative bacterial infections.

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Mechanisms MediatingPorphyromonas gingivalisGingipain RgpA-Induced Oral Mucosa Inflammation In Vivo

Cited by 19 publications

References 33 publications

Cutting Edge: Bradykinin Induces IL-12 Production by Dendritic Cells: A Danger Signal That Drives Th1 Polarization

Cutting Edge: Bradykinin Induces IL-12 Production by Dendritic Cells: A Danger Signal That Drives Th1 Polarization

BacillusSpecies Are Present in Chewing Tobacco Sold in the United States and Evoke Plasma Exudation from the Oral Mucosa

E. coli lipopolysaccharide attenuates adenosine A1 receptor-mediated increase in plasma exudation from the hamster cheek pouch

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