Effect of an essential oil mouthrinse, with and without fluoride, on plaque metabolic acid production and pH after a sucrose challenge.

This clinical study evaluated the effect of rinsing with an essential oil-containing antiseptic mouthrinse, with or without 100 mg/kg fluoride ion, on the plaque metabolic acid production and plaque pH response after a sucrose challenge. This observer-blind, randomized study used a three-way crossover design. Twenty-four subjects rinsed with 20 ml of one of the following rinses: (1) essential oil (EO) mouthrinse, (2) essential oil mouthrinse plus 100 mg/kg fluoride, or (3) negative control, for 30 s, twice daily for 16 days. On day 17, 1 h after the last mouthrinse, subjects rinsed with 20 ml of mass fraction 10% sucrose solution for 1 min. Seven minutes after the sucrose challenge, supragingival plaque was collected from molar and premolar teeth. Plaque pH and metabolic acid ions were analyzed using a micro pH electrode and capillary electrophoresis, respectively. The results showed that after EO mouthrinse dental plaque produced 36% less lactate, 36% less acetate and 44% less propionate than after the negative control rinse. The dental plaque also exhibited a pH 0.42 unit higher after EO rinse than after the negative control rinse. These results were not affected by the addition of 100 mg/kg fluoride to the EO mouthrinse. From these results we concluded that this EO antiseptic mouthrinse, with or without fluoride ion, is effective in reduction of plaque acidogenicity after a sucrose challenge.

The remineralizing effect of an essential oil fluoride mouthrinse in an intraoral caries test.

BACKGROUND: The authors conducted a two-week clinical study to determine the remineralizing effect of an experimental mouthrinse containing both fluoride and essential oils in an intraoral caries test model. METHODS: The study used an observer-blinded, randomized, controlled, 3 x 3 crossover design. The authors enrolled in the study 153 subjects, each of whom had a mandibular removable partial denture. Two partially demineralized human enamel specimens were mounted on each subject's removable partial denture. Subjects used either a fluoride mouthrinse with essential oils (the test mouthrinse), a fluoride nonessential oils mouthrinse (the positive control) or an essential oil nonfluoride mouthrinse (the negative control) twice daily for 14 days. The researchers assessed specimens for mineral content change and fluoride uptake using surface microhardness, or SMH, testing and enamel fluoride analysis, respectively. RESULTS: Of the 153 subjects enrolled in the study, 125 subjects were evaluable at the study endpoint. The results after two weeks showed that percentage of SMH recovery was 42 percent in the test group, 36 percent in the positive control group and 16 percent in the negative control group. The fluoride uptake was 19 micrograms per square centimeter, 16 microg/cm2 and 3 microg/cm2 for the test mouthrinse, positive control and negative control groups, respectively. In terms of both percentage of SMH and fluoride uptake, the test mouthrinse and positive control mouthrinse were statistically higher than the negative control mouthrinse, and the test mouthrinse was "at least as good as" the positive control mouthrinse. CONCLUSIONS: This study provides evidence that an essential oil mouthrinse with 100 parts per million fluoride is effective in promoting enamel remineralization and fluoride uptake. CLINICAL IMPLICATIONS: The combination of fluoride and essential oils in a mouthrinse may provide anticaries efficacy, in addition to essential oils' previously established antigingivitis efficacy.

Tobacco hypersensitivity and environmental tobacco smoke exposure in a pediatric population.

BACKGROUND: Skin testing and RAST have verified the existence of tobacco-specific IgE. However, published studies report conflicting results concerning the clinical significance of tobacco IgE. Previous studies have not focused on the role of environmental tobacco smoke (ETS) as it relates to tobacco hypersensitivity (TH) in nonsmoking children. OBJECTIVE: We used nonsmoking pediatric patients to investigate the relationship between ETS and TH. METHODS: Children, ages 4 to 10 years, were prospectively enrolled. ETS exposure and smoke-triggered symptoms were recorded by questionnaire and physician history. Patients were given a skin test (ST) with a panel of aeroallergens plus tobacco extract. A ST reaction to at least one aeroallergen classified a patient as atopic; a ST reaction to tobacco classified a patient as TH. RESULTS: We enrolled 170 patients, mean age 7.2 years. We found 58 (34%) patients reported routine exposure to ETS and 78 (46%) patients reported ETS-induced symptoms. We found 121 (71%) atopic patients and 61 (36%) TH patients. TH was more common in atopic patients (P < .0001) and those routinely exposed to ETS (P < .05). However, TH failed to predict ETS-induced symptoms in either atopic or non-atopic patients (PPV = 0.40, NPV = 0.69). CONCLUSIONS: We evaluated the clinical significance of TH in a nonsmoking patient population related to ETS exposure. We concluded that although TH is statistically related to atopy and ETS exposure, the low predictive values of skin testing for TH limit its clinical usefulness.

Caries inhibition efficacy of an antiplaque/antigingivitis dentifrice.

PURPOSE: To evaluate the efficacy of a fluoride dentifrice containing a fixed combination of essential oils (Thymol, Menthol, Eucalyptol, and Methyl Salicylate) in preventing caries in Sprague Dawley rats. MATERIALS AND METHODS: The dentifrice contains 0.76% sodium monofluorophosphate (SMFP) as the fluoride source and a silica abrasive system. A fluoride-free placebo and a clinically proven USP dentifrice reference standard for SMFP/silica were included as controls. Three groups of 45 SDV-free Sprague Dawley weanlings were infected by a cariogenic strain of Streptococcus sobrinus and fed cariogenic diet NIH 2000 ad libitum. Animals were treated twice daily (once on weekends) with the assigned dentifrice using a cotton-tipped applicator, for 5 wks, after which they were terminated and caries scored using Larson's modification of the Keyes method. RESULTS: Analyses of variance were used to compare inter-group means, the total E lesion score was the primary efficacy variable. Compared with the fluoride-free vehicle control, the experimental dentifrice and USP reference standard dentifrice produced a statistically significant reductions of 18.3% and 12.2% respectively for total caries score (P<0.001). Compared with the clinically tested USP positive control dentifrice, the experimental dentifrice produced a statistically significant reduction in the total caries score of 6.9% (P=0.028). The results of this study show that 1) both the new dentifrice containing essential oils and USP dentifrice are statistically significantly effective in reducing caries in the rat model, 2) the anticaries activity of the SMFP dentifrice is not adversely affected with the addition of essential oils.

A model for clinical evaluation of anti-microbial effects of agents on plaque colonization.

PURPOSE: To evaluate a new improved method of microbial analysis in a cross-over clinical study by investigating the efficacy of a single application of an essential oil-containing (EOC) dentifrice as compared to its vehicle control (VC) over a 6-hr period. MATERIALS AND METHODS: Acrylic stents with retention areas for 7, 3 mm x 3 mm hydroxyapatite (HA) squares were fabricated for 12 subjects. 30 min following stent placement, one HA square was removed and sampled for viable microflora. After stent replacement, subjects were assigned either the EOC dentifrice or its VC and brushed under supervision for 1 min. Stents remained in place for the next 6 hrs. A HA square was removed at hourly intervals for 6 hrs following brushing. The microflora was analyzed for total anaerobes on Schaedler's media, for total gram-negative anaerobes on Schaedler-NV selective media, and for total Fusobacterium species on CVE selective media. Plates were incubated anaerobically at 37 degrees C for 2-5 days. Colony forming units were calculated. For each time point, pairwise t-tests were performed using the adjusted means and the pooled error term from the analysis of variance (ANOVA). RESULTS: Treatment with the EOC dentifrice resulted in a statistically reduced plaque growth. Differences were seen as reductions in: (1) total gram-negative anaerobes seen from 1-6 hrs (P < or = 0.011), (2) total anaerobic bacteria which achieved significance at 3 hrs and continued through 6 hrs (P < or = 0.005), and (3) Fusobacterium species as seen from 4-6 hrs (P < or = 0.002).

A rapid method for evaluating microbicidal activity of dentifrice formulations against salivary bacteria ex vivo.

A new rapid ex vivo method was developed for evaluating the short-term bactericidal activity of dentifrices against salivary microorganisms. Dentifrice aliquots of 0.25 or 1.0 g were rapidly dispersed into 3.5 mL of freshly pooled human saliva, and 1.0 mL aliquots of the dentifrice-saliva suspension were collected after 30 or 60 seconds of exposure, diluted in neutralizing broth and plated on non-selective agar media for enumeration of surviving total cultivable microflora. Eight experimental dentifrices containing increasing amounts (0 to 2.6%) of a fixed ratio of essential oils (thymol, menthol, methyl salicylate and eucalyptol) were dispersed in saliva at a 0.25:3.5 (w/v) dentifrice:saliva ratio. Recoverable CFUs/mL at 30 sec. were reduced in a dose-responsive manner from > 10(6) to < 10(4). Additional tests using both 0.25 and 1.0 g amounts of dentifrice prototypes containing 2.1% of the essential oil mixture showed that the experimental dentifrices exhibited highly significant (approximately 2.5 log) reductions in viable recoverable microorganisms relative to essential oil-free placebos after both 30- and 60-second exposures. When compared to in vitro models previously used to evaluate the antimicrobial activity of dentifrices, this method provides a rapid, reproducible, more biologically representative means of screening dentifrice formulations for microbicidal activity using dilutions and exposure times approximating those achieved during toothbrushing. However, since other factors may influence microbicidal activity of dentifrice formulations in vivo, conclusions drawn using this model require clinical confirmation.

A professional curriculum vitae will open career doors.

In today's challenging healthcare environment, it is essential for nurse practitioners to be able to describe themselves professionally on paper to compete for practice and academic opportunities. Nurse practitioners are competing with physician assistants as well as physicians for primary and acute care positions. A carefully compiled curriculum vitae will present the individual in the best light possible to help open career doors and enhance chances of success. Preparing a curriculum vitae will serve to highlight relevant professional accomplishments, whatever the setting, toward the fulfillment of professional goals. This article reviews the current professional print and electronic literature on preparing a curriculum vitae to assist the nurse practitioner in developing this vital document.

Effect of an antiseptic mouthrinse on salivary microbiota.

PURPOSE: To evaluate the effect of rinsing with original formulation Listerine Antiseptic (LA) on the level of viable salivary bacteria for periods up to 1 hour. MATERIALS AND METHODS: In this double-blind, controlled, cross-over study, unstimulated saliva was collected from 25 subjects, serially diluted, and cultured on selective and non-selective media under aerobic and anaerobic conditions. Streptococci, Veillonella sp., and total aerobic and anaerobic flora were enumerated just prior to and 2, 15, 30, and 60 minutes after rinsing for 30 seconds with either 20 ml of LA or a 5% hydroalcohol control rinse. RESULTS: After the control rinse, total flora cultivated on MM10 agar exhibited a non-significant (P > 0.05) 10%-20% decrease relative to baseline. In contrast, rinsing with LA resulted in a significant (P < 0.05) 60%-65% decrease from baseline in all four microbial groups at 2 minutes; except in the case of Veillonella, the significant decreases were sustained up to 60 minutes. Total Listerine group aerobic, anaerobic and streptococcal counts were significantly lower than placebo (P < 0.05). The significant reduction in salivary bacterial levels seen in the Listerine group for up to 60 minutes suggests that this antiseptic mouthrinse may have use clinically as a pre-procedural rinse to decrease the level of viable microorganisms in aerosols generated during dental procedures.

Collagen-induced arthritis in mice: synergistic effect of E. coli lipopolysaccharide bypasses epitope specificity in the induction of arthritis with monoclonal antibodies to type II collagen.

DBA/1 mice develop a chronic peripheral arthritis after immunization with type II collagen termed collagen-induced arthritis. We have localized the main arthritogenic determinants of CB11, a CNBr-generated arthritogenic fragment of chick type II collagen (CII), using 3 smaller peptide fragments of CB11 generated by endoproteinase LysC, LysC1 (CII 124-290), LysC2 (CII 291-374) and LysC3 (CII 375-402) and a panel of monoclonal antibodies (mAb) specific to CB11. MAb specific to the arthritogenic region of CB11 were also used to study the synergistic effect of E. coli lipopolysaccharide (LPS) on antibody-mediated arthritis in naive DBA/1 mice. LysC2 contained a minimum essential arthritogenic fragment of type II collagen: LysC2 induced arthritis by active immunization, also, a combination of four mAb specific to LysC2 passively transferred arthritis to naive mice. A single i.p. injection of LPS (50 micrograms/mouse) reduced the threshold values of the arthritogenic dose of mAb from 1 mg to 50 micrograms/clone per mouse, and decreased the number of mAb required for inducing arthritis from 4 to 2 clones. These observations suggest that LysC2, an 84 amino acid residue fragment, contains the main arthritogenic determinants within chick CB11. Importantly, LPS, a strong inducer of pro-inflammatory cytokines, negates the required multiple epitope specificity of autoantibodies in the passive transfer model and acts synergistically in the induction of arthritis by autoantibody.

Identification of a cyanogen bromide fragment of porcine type II collagen capable of modulating collagen arthritis in B10.RIII (H-2r) mice.

Previous studies directed towards identifying epitopes on type II collagen (CII) important in collagen induced arthritis (CIA) in mice have focused primarily on responses mounted in susceptible H-2q strains. However, the nature of T and B cell responses against CII in susceptible H-2r strains remains ill-defined. In an effort to identify regions on CII important in CIA in H-2r mice, we examined the cellular and humoral response of susceptible B10.RIII (H-2r) mice against cyanogen bromide (CB)-cleaved fragments of porcine CII. Following immunization with native porcine CII, LNC from B10.RIII mice mounted proliferative responses predominantly to peptide CB10, while negligible proliferation was detected against fragment CB9, 7, CB8, CB11 or CB12. In contrast, sera from arthritic B10.RIII mice displayed a heterogeneous pattern of reactivity against porcine CII, with strong antibody binding measured against the major fragments CB11, CB8 and CB10. To determine the in vivo significance of the dominant cellular response to CB10, B10.RIII mice received an i.v. injection of soluble CB10 seven days before immunization with native porcine CII. Mice pretreated with CB10 were highly resistant to CIA compared to control animals. Interestingly, B10.RIII mice pretreated with fragment CB11, a region of CII implicated in H-2q restricted CIA, remained susceptible to arthritis induction. Collectively, our findings indicate that the CB10 region of porcine C11 bears determinants which may be important in the induction and/or regulation of CIA in the H-2r haplotype.

Collagen-induced arthritis and TCRs in SWR and B10.Q mice expressing an Ek alpha transgene.

B10.Ek alpha transgenic mice were mated with H2-E B10.Q and SWR mice. F1 and F1 x parental strain backcross progeny were tested for arthritis and autoimmune reactivity to mouse type II collagen (MII) after immunization with bovine, chick, deer, or human type II collagen. The results were correlated with the H-2 haplotype (b/q vs q/q) and the TCR V beta profile of peripheral blood T cells in each mouse. Hybrid progeny expressed TCR profiles different from either parent because of the TCR V beta genomic deletions of SWR mice (V beta a), the wild-type TCR allele of C57Bl/10 (B10) mice (V beta b), and the intrathymic negative selection processes resulting from cell surface expression of Ek alpha-A q beta or Eb beta-Ek alpha, together with the integrated retroviral genes Mtv-9 originating in B10 mice and Mtv-7 (Mls-1a) from SWR mice. (B10.Ek alpha x SWR)F1 mice developed higher IgG anti-MII Ab titers, but much milder arthritis than (B10.E x B10.Q)F1 mice. Expression of Ek alpha did not change the level of IgG anti-MII Ab nor the degree of susceptibility to collagen-induced arthritis (CIA) in the H-2q/q and H-2b/q progeny of (B10.Ek alpha x B10.Q)F1 x B10.Q matings, indicating that the Mtv-9-reactive, TCR V beta 5+, and V beta 11+ T cells are not critical to CIA. Among bovine type II collagen-immunized (B10.Ek alpha x SWR)F1 x SWR backcross mice: 1) arthritis severity is associated with the presence of V beta b (p < or = 0.01) and expression of Ek alpha (p < or = 0.05), but not with the MHC haplotype (b/q vs q/q); 2) regression analysis showed a significant association (R = 0.99) between IgG anti-MII Ab titers and the level of Mtv-7-reactive V beta 6+ T cells that was detectable in the IgG1, but not the IgG2a subclass. The data prompt the speculation that Mtv-7-reactive V beta 6+ (or V beta 7+) T cells in (B10.EK alpha x SWR)F1 x SWR mice express Th2-type properties, and thus contribute to the combination of mild arthritis but high anti-MII Ab titers that characterize mice of SWR heritage.

Exacerbation of collagen-induced arthritis in rats by rat cytomegalovirus is antigen-specific.

Collagen-Induced Arthritis (CIA) is an experimentally induced and genetically controlled animal model of chronic joint inflammation. In rats, there are informative strain differences in susceptibility to CIA. DA rats (RT1avl) develop severe CIA after immunization with bovine (BII), chick (CII), or homologous rat (RII) type II collagens. In contrast, the MHC-congenic DA. 1N(BN) and WF.1N(BN) rats (RT1n) are relatively resistant to CIA and develop moderate CIA in response to immunization with CII but not BII or RII. We previously found that simultaneous infection with rat cytomegalovirus (RCMV) greatly exacerbates the severity of arthritis that develops in BII-immunized DA rats. To examine the mechanism of RCMV amplification of CIA, the effect of simultaneous infection with RCMV on arthritis and autoimmunity to type II collagen was determined in WF.1N and DA.1N rats after immunization with BII, CII and RII. RCMV increased the incidence of CIA and the level of autoimmunity to type II collagen (skin-testing and IgG antibody titer) selectively in DA.1N and WF.1N rats immunized with CII, but not in littermates immunized with BII, although the transient reversal of CD4+/CD8+ mononuclear cell ratios in peripheral blood that is associated with RCMV infection occurred equally in both BII- and CII- immunized DA.1N rats. Likewise, RCMV infection moderately increased the levels of anti-RII autoimmunity and arthritis in DA rats sub-optimally immunized with RII but had no consistent effect on either anti-RII immunity or arthritis in RII-immunized DA.1N and WF.1n rats. The data show that RCMV augments arthritis only in rats that are genetically susceptible to CIA and that are appropriately immunized with a species of type II collagen that is arthritogenic for the MHC-haplotype being tested. Two possible mechanisms are suggested by these data: RCMV-associated increases in anti-RII autoimmunity in rats with CIA may result from amino acid sequence homologies between RCMV and type II collagen; alternatively, virus-induced pro-inflammatory cytokines may activate RII-reactive lymphocytes thereby potentiating autoimmunity and arthritis.

Short-term microbiological and clinical effects of subgingival irrigation with an antimicrobial mouthrinse.

Fifty chronic adult periodontitis patients completed a 6-week controlled, double-blind, split mouth clinical study to determine the effects of subgingival irrigation with an antimicrobial mouthrinse on periodontal microflora, supragingival plaque, and gingivitis when used as an adjunct to normal oral hygiene. Qualifying subjects had at least four sites, two on each side of the mouth, with probing depths between 4 and 6 mm, which bled on gentle probing. Following baseline examinations, subjects received a half mouth scaling and prophylaxis and full mouth subgingival irrigation with either the antimicrobial mouthrinse or sterile colored water control professionally delivered. Subjects continued irrigation at home once daily for 42 days with their assigned rinse delivered via a subgingival delivery system. All sites in the mouth were scored at baseline and at day 42 for supragingival plaque, bleeding on probing, and redness. For the four selected periodontitis sites, probing depth and attachment level were measured at baseline and on day 42; additionally, supragingival plaque and gingival redness were scored on days 7 and 21. Subgingival plaque samples for microbiological analysis were harvested from the selected periodontal sites at baseline and on days 7, 21, and 42. Microbiologically, irrigation with the antimicrobial mouthrinse resulted in statistically significant reductions compared to control in putative periodontopathogens, including black pigmenting species, which persisted at 42 days. Clinically, subgingival irrigation with the antimicrobial mouthrinse produced a significant reduction in supragingival plaque (P < 0.001), bleeding on probing (P = 0.019), and redness (P = 0.017) compared to the control, whether or not the area irrigated received a prophylaxis.(ABSTRACT TRUNCATED AT 250 WORDS)

T-cell receptors and collagen induced arthritis in H-2r mice.

Mouse strains B10, B10.RIII, RIIIS/J and the F1 and backcross progeny arising from them were tested for susceptibility to porcine type II collagen-induced arthritis (PII-CIA). The clinically severe arthritis of rapid onset that is characteristic of PII-immunized B10.RIII mice developed predominantly in hybrid offspring that had inherited at least one copy of wild type T cell receptor (TCR) genes (V beta b genotype) from the B10 or B10.RIII parent. The results indicate that, in the development of PII-CIA, mice expressing the H-2r/r haplotype preferentially utilize TCR V beta genes that are normally encoded within the TCR V beta genomic deletion region of RIIIS mice (V beta c). After aggressive immunization with PII, the use of alternative TCR V beta genes, encoded outside of the RIIIS deletion region, produced a high IgG antibody response that was cross-reactive with mouse type II collagen (MII) and equivalent to that of B10.RIII mice, but only a very mild, late onset arthritis of 56% (27/48) incidence in RIIIS male mice and 28% (10/35) incidence in RIIIS female mice. In comparison, B10.RIII mice routinely developed early onset of PII-CIA of significantly higher incidence (100%; p < 0.005) and four-fold greater severity, even after milder immunization protocols. The data are compatible with the proposal that the clinically weak CIA response of RIIIs mice may be primarily antibody driven while the severe CIA of B10.RIII mice reflects the added inflammatory effects of collagen-reactive effector-T cells in the joint.(ABSTRACT TRUNCATED AT 250 WORDS)

Passive transfer of adjuvant-induced arthritis into irradiated DA recipient rats.

Adjuvant-induced arthritis (AIA) can be passively transferred in Dark Agouti (DA) rats by spleen and lymph node cells after culture with Concanavalin A (Con A). A model not requiring in vitro Con A expansion and activation would be important in investigations of anti-rheumatic drugs in AIA. A new model using irradiated recipients fills this need. Donor DA rats treated with 0.1 ml complete Freund's adjuvant (CFA) containing 7.5 mg M. butyricum/ml were sacrificed 11 days after CFA injection, donor spleen cells harvested, and donor spleen cells injected intravenously into recipient DA rats previously irradiated with 5 Gy. Recipient rats developed arthritis 4-14 days after spleen cell transfer. This model can now be used to further define the effects of anti-rheumatic drugs in the passive transfer of AIA by eliminating the need for the in vitro Con A-induced expansion and/or activation of donor cells.

Transamidase and collagenase activity in healthy and diseased human gingival tissues.

Transamidases are a class of calcium-dependent mammalian enzymes which cross-link proteins by catalyzing the formation of (gamma-glutamyl)-epsilon-lysine bonds. It is possible that these enzymes play an important anabolic role in tissue healing. This study was to quantitate transamidase activity in human gingival tissue and examine the relation between transmidase activity and degree of inflammation. Forty-four out of a total 120 collected human gingival specimens from healthy and diseased patients were selected based on histometric and microbiologic criteria. Specimens were minced and homogenized in 10 mM CaCl2 and then extracted for 30 min, in 50 mM tris-HCl buffer (pH 7.5) containing 100 mM CaCl2. Following low speed centrifugation at 4 degrees C, the supernatant solution was assayed for both transamidase and collagenase activities by radioactive amine incorporation, and digestion of tritiated collagen, respectively. Appreciable levels of transamidase and collagenase activities in healthy gingivae were found. These enzyme activities were significantly elevated in the diseased and healing tissues. Unlike other transamidases, calcium was required in the enzyme extraction process.

RNA binding specificity of a Drosophila snRNP protein that shares sequence homology with mammalian U1-A and U2-B" proteins.

We have characterized a recombinant Drosophila melanogaster RNA binding protein, D25, by virtue of its antigenic relationship to mammalian U1 and U2 small nuclear ribonucleoprotein (U snRNP) proteins. Sequence analysis revealed that D25 bears strong similarity to both the human U1 snRNP-A (U1-A) and U2 snRNP-B" (U2-B") proteins. However, at residues known to be critical for the RNA binding specificities of U1-A and U2-B" D25 sequence is more similar to U2-B". Using direct RNA binding assays D25 selected U1 RNA from either HeLa or Drosophila Kc cell total RNA. Furthermore, D25 bound U1 RNA when transfected into mammalian cells. Thus, D25 appears to be a Drosophila homolog of the mammalian U1-A protein, despite its sequence similarity to U2-B".

Immunogenetics of collagen-induced arthritis in rats. Both MHC and non-MHC gene products determine the epitope specificity of immune response to bovine and chick type II collagens.

Seven inbred, RT1-congenic rat strains were immunized with native bovine (BII), porcine (PII), or chick (CII) type II collagen and observed for onset, incidence, and severity of arthritis. Clinical results were compared with IgG reactive with native rat type II collagen (RII) and the purified, renatured cyanogen-bromide peptides of BII, CII, or RII. Immunodominant responses to CB11, CB9,7, and CB12 of RII were identified. Secondary responses to CB8 and CB10 also occurred. Reproducible patterns of peptide reactivity were defined in each strain and reflected both RT1 and non-RT1 genotypes plus the species of immunizing collagen. BN non-RT1 gene products moderated clinical arthritis but increased the levels of reactivity to CB11 in three strains carrying RT1l,n,av1 haplotypes. WF (RT1u) rats were susceptible to collagen-induced arthritis (CIA) and developed very high levels of autoantibodies with dominant responses to rat CB11 after CII injections and to rat CB11 and CB9,7 after BII injections. DA (RT1av1) rats developed the most severe arthritis but had only moderate (total) levels of anti-RII IgG: a broad response to CB11, CB10, and CB9,7 after CII injections but predominantly to CB12 and CB9,7 after BII injections. Three RT1n strains--DA.1N(BN), WF.1N(MAXX), and BN--were resistant to BII-induced CIA but developed mild arthritis after immunization with CII. After BII: BN IgG reacted with CB9-7, CB11, and CB12; DA.1N and WF.1N IgG reacted with CB9,7 and CB12. After CII: BN IgG reacted broadly with CB11, CB9-7, CB12, and CB8; WF.1N IgG reacted to CB9-7, CB11, CB8, and CB12; DA.1N IgG reacted with CB8, CB11, and CB9-7. Thus, selective induction of CIA in BN, WF.1N, and DA.1N rats by CII correlated with serum IgG reactivity to rat CB11, but overall strain results identified no single cyanogen-bromide peptide as expressing the sole "arthritogenic" epitope in CIA.

The effects of flurbiprofen on the passive transfer of adjuvant-induced arthritis.

The effect of flurbiprofen on the passive transfer of adjuvant-induced arthritis was studied to determine if flurbiprofen acted in the donor and/or recipient arms of this model. Groups of donor and recipient rats were treated with either placebo or flurbiprofen 4 mg/kg. Joint scores were markedly decreased in recipient rats treated with flurbiprofen irrespective of the whether donor animals were treated with placebo or flurbiprofen (p less than 0.01). There was also a moderate decrease in the ability of donor cells from rats treated with flurbiprofen to suppress the severity of arthritis (p less than 0.01); however, this effect was less marked than that seen in recipient animals. These data imply that flurbiprofen may act at multiple sites in adjuvant-induced arthritis, but the major site of action of flurbiprofen in this model is in the recipient animals.