Determination of salivary and serum immunoglobulin concentrations in the cat

The concentrations of immunoglobulin(Ig)G, IgM, and IgA were determined in unstimulated saliva (n=14), stimulated saliva (n=6), and serum (n=14) from healthy adult cats. Analysis by single radial immunodiffusion (SRID) was compared with class-specific enzyme linked immunoassays (ELISA), and good correlation was demonstrated between the two techniques. Mean (s.d.) serum concentrations of 19.08 (5.38) mg/ml IgG, 2.04 (0.83) mg/ml IgM and 2.6 (2.16) mg/ml IgA were obtained by SRID. The immunoglobulin concentrations of the saliva samples frequently fell below the quantification limits for SRID, however, all samples could be quantified by ELISA making this the method of choice for the determination of salivary immunoglobulin concentrations. IgA was the predominant class of immunoglobulin secreted by the major feline salivary glands, and the concentration of each immunoglobulin class was greater in unstimulated versus stimulated saliva. Analysis of sequential unstimulated saliva samples collected each morning and evening over a 4-day period from four cats revealed the salivary immunoglobulin concentrations to be relatively constant.     

Gonadotropic and luteotropic cells in chickens treated with estrogen after hatching

IgA concentrations were determined in saliva from epileptic patients taking phenytoin and in saliva from healthy controls, by single radial immunodiffusion technique. Mean salivary IgA in epileptic children was 7.23 mg/ml; in healthy children, 16.44 mg/ml. Corresponding values for adults were 13.53 and 19.48 mg/ml, respectively. In 14 out of 84 samples, salivary IgA levels were too low for quantitative analysis. Salivary IgA levels were normal in untreated patients and fell during treatment with phenytoin. Gingival inflammation was commonly accompanied by an increase of salivary IgG and serum-derived IgA, whereas compensatory increase of IgM was infrequent. Phenytoin-induced deficiency of salivary IgA can result in increased susceptibility to gingival inflammation, which is considered one of the predisposing factors for subsequent development of gingival hyperplasia.     

cDNA cloning and characterization of rat C5a anaphylatoxin receptor

lnterleukin-2 (IL-2) is known to cause xerostomia and skin manifestations similar to graft-versus-host disease (GVHD). We therefore evaluated major salivary gland function in patients with hematological malignancies treated with IL-2 and interferon-alpha (IFN-alpha) after ABSCT. Eleven patients (seven male, four female) of median age 40 (24-47) were evaluated, seven with non-Hodgkin lymphoma (NHL); one with Hodgkin's disease (HD) and three with acute myelogenous leukemia (AML). Parotid and submandibular salivary gland function was assessed before, during and after IL-2/IFN-alpha administration by evaluation of the salivary flow rate and the composition of secreted saliva. Significant reductions in both the resting and stimulated parotid and submandibular salivary flow rates were observed during IL-2/IFN-alpha immunotherapy compared with the pre- and post-therapy values (P < 0.01), while no hyposalivation was observed in the control patients who underwent ABSCT and did not received IL-2. Sialochemical evaluation revealed a significant increase in potassium concentration (24.4+/-0.6 mEq/l to 28.9+/-1.4 mEq/l) and a significant decrease in sodium concentration (6.7+/-2.1 mEq/l to 3.3+/-1.0 mEq/l) (P < 0.05) in the stimulated parotid gland saliva secreted during IL-2/IFN-alpha administration. Salivary protein concentrations were not altered by the IL-2/IFN-alpha immunotherapy. Similar changes were previously observed in mice and humans with chronic GVHD. We conclude that IL-2 immunotherapy induces major salivary gland dysfunction in humans, similar to our previous observations in patients with chronic GVHD, which may indicate similar pathophysiologic mechanisms.     

Salivary immunoglobulin G assay to diagnose Helicobacter pylori infection in children

An in-house enzyme-linked immunosorbent assay (ELISA) for measurement of Helicobacter pylori-specific immunoglobulin G (IgG) and IgA in saliva was evaluated by comparison with histopathologic (Giemsa staining) and biochemical (urease quick test) examination of gastric biopsy specimens obtained from 112 children referred for diagnostic gastroscopy. Serum H. pylori IgG was also measured in a subgroup of 50 children by the same ELISA. Salivary H. pylori IgG levels were significantly higher in H. pylori-positive (n = 57) than in H. pylori-negative (n = 55) children (P < 0.001). The sensitivity and specificity of the salivary IgG test were 93 and 82%, respectively; the positive and negative predictive values were 84 and 92%, respectively; and the accuracy was 87.5%. Salivary H. pylori IgA did not distinguish H. pylori-positive from H. pylori-negative children. The performance of serum H. pylori IgG was slightly (3 to 6%) better than that of salivary H. pylori IgG. The salivary IgG test can be considered a useful tool for the screening of H. pylori infection in children.     

Axonal transection in the lesions of multiple sclerosis

We explored the relationship between mutans streptococcal infection and the development of salivary IgA antibody during initial colonization. Repetitive swabbing (n = 292) of the teeth of 33 children revealed that 45% became infected with mutans streptococci between 13 and 36 months of age. In contrast, mutans streptococci could not be detected in 18 children whose last sample was taken at 39-81 months of age (median age = 62 months). During the period of mutans streptococcal infectivity, immunoglobulin A (IgA) antibody to several mutans streptococcal antigens appeared in most children, whether or not infection had been demonstrated. Robust responses to mutans streptococcal components occurred during or shortly after, but not before the period of mutans streptococcal infectivity. No consistent differences were observed among the summarized patterns of response of infected and uninfected groups of children, although the IgA Western blot patterns of individual subjects were often quite distinct. For example, sets of siblings, who would be presumed to be challenged with similar maternal mutans streptococcal clonotypes, were shown to develop qualitatively different salivary IgA responses to mutans streptococcal components. These results support a discrete period for mutans streptococcal infection and may suggest that the level of maternal infection is a factor in the success of infection of the child during this period. The data also suggest that exposure to mutans streptococci is a sufficient condition for robust mucosal IgA responses to mutans streptococcal antigens during the period of infectivity and that these responses may be different, even among siblings.     

Longitudinal evaluation of salivary cortisol levels in full-term and preterm neonates

The aim of the present study was to test the practicability of sequential cortisol determinations in saliva of low birth weight neonates and to evaluate the impact of systemic and inhaled glucocorticoid therapy on saliva concentrations of cortisol in preterm neonates with bronchopulmonary dysplasia (BPD). Salivary cortisol levels were measured by RIA in saliva samples from 10 full-term and 10 preterm healthy neonates and from 20 preterm neonates with BPD during systemic [dexamethasone (DEX); n = 10] or topical steroid therapy [budesonide (BUD); n = 10]. Saliva samples of each individual were collected on 3 consecutive days at 06.00, 12. 00, 18.00 and 24.00 h. Cortisol levels in saliva ranged from 0.8 to 60.6 nmol/l (median 6.5 nmol/l) in full-term neonates, from 0.6 to 52.1 nmol/l (median 5.5 nmol/l) in preterm neonates, from 0.4 to 14. 0 nmol/l (median 1.0 nmol/l) in preterm neonates treated with DEX and from 0.4 to 15.2 nmol/l (median 2.5 nmol/l) in preterm neonates treated with BUD. Autocorrelation analysis revealed a distinct endogenous cortisol rhythm in 2 of the 10 healthy full-term neonates and in 3 of the 10 healthy preterm neonates with a wavelength of 12-30 h. Salivary cortisol levels in preterm neonates treated with DEX or BUD were significantly lower than those measured in healthy preterm neonates. These results demonstrate that the measurement of salivary cortisol levels is a reliable and practicable way of assessing adrenal function in full-term and preterm neonates. This study also shows for the first time that some neonates display an endogenous cortisol rhythm which is not coupled to the exogenous day/night cycle. Furthermore, systemic and nebulized glucocorticoids suppress adrenal function in low-birth-weight neonates. After treatment these children should be closely monitored for potential adrenal insufficiency.     

Salivary factors in children with recurrent parotitis. Part 2: Protein, albumin, amylase, IgA, lactoferrin lysozyme and kallikrein concentrations

The concentrations of total protein, albumin, amylase, IgA, lactoferrin, lysozyme and kallikrein in parotid saliva from 17 children with juvenile recurrent parotitis (JRP) in a non-active phase of disease and in healthy controls of the same number, sex and age were analysed after gustatory stimulation with 1%, 2% and 6% citric acid. There was a great individual variation in all analysed variables, especially in saliva from the diseased glands. Significantly raised levels of albumin, IgA, lactoferrin and kallikrein were found in the saliva from the JRP-children compared with the controls (p < 0.01-0.001), while total protein and alpha-amylase did not differ significantly. The sialo-chemical findings are discussed in the light of histological and bacteriological findings and support the hypothesis that the etiology of juvenile recurrent parotitis is a combination of congenital malformation of portions of the salivary ducts and a set-in infection.     

Induction of mucosal immunity by intranasal application of a streptococcal surface protein antigen with the cholera toxin B subunit

The level and distribution of isotype-specific antibodies in various secretions and of antibody-secreting cells in corresponding lymphoid organs and tissues were compared in mice immunized with Streptococcus mutans surface protein antigen I/II (AgI/II) conjugated to the cholera toxin B subunit (CTB), given intranasally (i.n.) or intragastrically (i.g.), with or without free cholera toxin (CT) as an adjuvant. Immunization i.n. induced stronger initial antibody responses to AgI/II in both serum and saliva than immunization i.g., but salivary immunoglobulin A (IgA)-specific antibody responses to immunization about 3 months later were not increased relative to total salivary IgA concentrations. Specific antibodies induced by i.n. immunization were as widely distributed in serum, saliva, tracheal wash, gut wash, and vaginal wash as those induced by i.g. immunization. Likewise, specific antibody-secreting cells were generated in the spleen, salivary glands, intestinal lamina propria, and mesenteric and cervical lymph nodes by either route of immunization. The strongest salivary IgA antibody response was induced by AgI/II-CTB conjugate given i.n., but the addition of CT did not further enhance it. However, free CTB could effectively replace CT as an adjuvant in i.n. immunization with unconjugated AgI/II. Booster i.n. immunization with AgI/II plus either free CT or CTB induced stronger recall serum antibody responses than conjugated AgI/II-CTB with or without CT as an adjuvant. Therefore, i.n. immunization with a protein antigen and free or coupled CTB is an effective means of generating IgA antibody responses expressed at several mucosal sites where protective immunity may be beneficial.     

Hepatitis C virus infection of salivary gland epithelial cells. Lack of evidence

BACKGROUND: Hepatitis C virus genome (HCV-RNA) has been detected in whole salivary gland tissue of chronically infected patients. However, contamination of the tissue by plasma or blood cells was not excluded by the previous reports. AIMS: To assess whether HCV infects the salivary gland epithelial cells in patients with chronic HCV liver disease. METHODS: Twenty unselected patients with chronic active hepatitis (11 cases) or active cirrhosis (nine cases) were examined. Serum and saliva samples were obtained from all patients, 12 of whom (seven, chronic active hepatitis; five, active cirrhosis) underwent salivary gland biopsy. PCR for HCV-RNA was performed on RNA extracted from serum, saliva and salivary gland epithelial cells collected by isokinetic gradient separation after trypsin digestion of whole salivary gland tissue. Saliva samples were also examined for the presence of secretory IgA anti-HCV by gel chromatography and ELISA testing. RESULTS: HCV-RNA was detected in all sera with titers ranging from 5.42 x 10(5) genome equivalents/ml to 123.2 x 10(5) genome equivalents/ml. Thirteen patients were infected with genotype 1b, four patients had genotype 1a, two patients had genotype 2a and one patient was unclassifiable. Low titer HCV-RNA (<2 x 10(5) genome equivalents/ml) was detected in 3/20 saliva samples (15%) from highly viremic patients infected with 1b genotype. RNA extracted from salivary gland epithelial cells consistently tested negative for HCV-RNA. In addition, all saliva specimens tested negative for secretory-IgA (S-IgA) anti-HCV, even after a 10-fold concentration of the samples. CONCLUSIONS: There was no evidence that HCV infects the salivary gland epithelial cells in our viremic patients with HCV chronic liver disease. Low level HCV-RNA in saliva is most probably due to virus spillover from blood.     

MR arthrography of the shoulder: rethinking traditional imaging procedures to meet the technical requirements of MR imaging guidance

Increased serum levels of mucin-associated antigen have been previously demonstrated in patients with cystic fibrosis (CF) and interstitial pneumonia, and in lung-transplant recipients. The present study assessed the serum airway mucin levels in patients with acute respiratory distress syndrome (ARDS). An enzyme-linked immunosorbent assay (ELISA) method with a human-airway-mucin-specific monoclonal antibody (17Q2) was used to measure serum mucin levels in normal subjects, chronic smokers, patients with chronic bronchitis and other pulmonary diseases, patients with acute cardiogenic lung edema, and patients with ARDS. The serum mucin levels measured 9.9 +/- 0.8 ng/ml (mean +/- SEM, n = 59) in normal subjects, 12.7 +/- 1.6 ng/ml (n = 29) in chronic smokers, 21.8 +/- 1.9 ng/ml (n = 28) in patients with chronic bronchitis and other pulmonary diseases, 9.0 +/- 3.1 ng/ml (n = 5) in patients with acute cardiogenic lung edema. The serum mucin level was 53.8 +/- 6.6 ng/ml (n = 13) in patients with ARDS (p < 0.05, as compared with the four other groups). Serial measurements of serum mucin levels were obtained in patients with ARDS. Statistical analysis showed an inverse correlation of serial measurements of serum mucin with static respiratory-system compliance (p = 0.021), an inverse correlation of sequential serum mucin levels and log(Pa(O2)/Fl(O2)) (p = 0.016), and a positive correlation of sequential serum mucin levels and lung injury score (LIS) (p = 0.019). Gel-filtration analysis showed that mucin-associated antigens in ARDS sera were polydispersed and smaller than the antigens in normal sera. This study indicates that an increasing amount of degraded mucin occurs in patients with ARDS.     

Impact of Streptococcus pneumoniae bacteremia and human immunodeficiency virus type 1 on oral mucosal immunity

To determine whether defects in mucosal immunity were associated with invasive disease caused by a mucosal pathogen, Streptococcus pneumoniae, levels of salivary immunoglobulins and nonspecific immune factors were compared in subjects with human immunodeficiency virus type 1 (HIV-1) infection and in HIV-1-seronegative subjects with and without pneumococcal bacteremia. The IgA2 subclass may be of particular importance because S. pneumoniae produces IgA1 protease, which cleaves IgA1 but not IgA2. Levels (37-56 micrograms/mL) and proportions (11%-17%) of IgA2 were similar among groups. Serotype-specific capsular salivary IgA was present in a minority of patients with acute bacteremia. Levels of lactoferrin were increased with bacteremia. Neither selective mucosal IgA2 deficiency nor impaired nonspecific upper respiratory mucosal responses were associated with invasive pneumococcal disease during HIV-1 infection; thus, other defects in mucosal cellular responses and systemic immunity may predispose HIV-1-infected patients to invasive pneumococcal disease.     

Chest illness in infancy and chronic respiratory disease in later life: an analysis by month of birth

BACKGROUND: Cohorts born at different times of year differ in their risk of exposure to seasonal respiratory infections in early life, but are likely to have similar socioeconomic status and lifestyle thereafter. METHODS: We investigated the long-term consequences of acute chest illness in infancy for later development of chronic respiratory disease by analysing variations by month of birth in hospital admissions for respiratory illness (total n = 49,866), chronic respiratory symptoms and ventilatory function among British school children (n = 11,482) and middle-aged adults (total n = 55,829). RESULTS: Admission for bronchiolitis in the first year of life was three times more common for infants born September to November (autumn) than those born March to May, yet people born in the autumn experienced fewer respiratory symptoms and had better ventilatory function. In two surveys of middle-aged men, forced expiratory volume in one second/forced ventilatory capacity (FEV1/FVC) was significantly (P = 0.025) higher among autumn births. Hospital admissions for chronic bronchitis/emphysema and pneumonia varied little with season of birth. Admissions for asthma were significantly (P < 0.05) more common among children and young adults born in the autumn. CONCLUSIONS: These findings do not support the hypothesis of a causal link between chest illness in infancy and the later development of chronic bronchitis and emphysema. The variation in asthma admissions with month of birth deserves further investigation.     

IgA levels and carrier rate of pathogenic bacteria in 27 children previously tonsillectomized

The object of the present paper is to present laboratory and clinical data on 27 children of ages between 6 and 11 years, who in connection with tonsillectomy 2 1/2 years earlier had been found to have low serum and saliva IgA levels, low serum IgE levels, and a considerable lack of IgA and IgE plasma cells in the excised tonsils; correlation between deficiency in IgA and culture of pathogenic bacteria from the tonsils was significant. From a clinical point of view, 22 of the children had benefit of the tonsillectomy and had no longer a tendency towards a development of recurrent infections. The remaining 5 patients continued to complain of recurring respiratory infections; in addition, levels of serum and saliva IgA were low. Furthermore, 4 or these 5 children harboured pathogenic bacteria in their throats. Many of the 27 patients still had low serum IgA and IgE levels as compared with levels in healthy, age-related controls; in 3 patients, however, the IgE levels in serum had risen considerably parallel with the development of atopic diseases. Saliva IgA was rather constant after tonsillectomy as compared with the preoperative levels, though it had risen in some of the children. As regards serum IgG and IgM, these immunoglobulins had decreased significantly, and the question is raised, whether it might had been due to the tonsillectomy, either by the removal of chronically infected organs or by the removal of important immunological tissue.     

The relationship between long-term job strain and morning and evening saliva cortisol secretion among white-collar workers.

The objective of this study was to assess long-term job strain impact on morning and evening salivary cortisol secretion. In all 77 white-collar workers (31% women; sample mean age, 42 years at baseline) volunteered to sample morning (immediately after waking up) and evening (10 p.m.) salivary cortisol for 7 consecutive days. By median split on aggregated self-reported isostrain from three consecutive questionnaires distributed in a period of approximately 3.5 years the participants were classified into a high or low long-term isostrain condition. Regardless of strain condition, there was a significant reduction in morning salivary cortisol secretion from the working week to the weekend, whereas evening salivary cortisol secretion showed no significant variation during the week. Although chronic isostrain did not affect the morning saliva cortisol measures, evening cortisol secretion was significantly elevated in the chronic high isostrain group throughout the whole week. The elevated evening cortisol measures associated with chronic high strain are concordant with the findings in other studies on long-term strain. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cell-mediated cytotoxicity: a predictor of chronic rejection in pediatric HLA haploidentical renal transplants

BACKGROUND: Recipient antidonor cytotoxic T-cell activity has been associated with graft loss and acute rejection in renal allograft recipients. The role of immunologic mechanisms in the development of chronic graft rejection is controversial. We analyzed all living related renal transplants performed at Children's Hospital (Boston, MA) from 1983 to 1995 to assess whether cell-mediated cytotoxicity, determined in vitro and measured before transplantation, was predictive of chronic rejection. METHODS: Eighty-three patients were studied retrospectively. Fifty-seven patients with one haplotype-matched renal transplants from living related donors were studied to determine the association between cell-mediated lympholysis (CML) level, acute rejection, chronic rejection, and graft failure. Acute rejection was defined by the decision to treat. Chronic rejection was defined by histology and/or the absolute serum creatinine value using an increasing serum creatinine level >1.0 mg/dl for children less than 3, a creatinine level >1.5 mg/dl for children between 3 and 10 years of age, and a creatinine level >2.0 mg/dl for children above 10 years of age. Return to dialysis or retransplantation was considered graft failure. RESULTS: Of the 57 haploidentical patients, there were 33 males and 24 females. The mean age at transplant was 11.1 years (SD=6.7). Twelve patients developed chronic rejection, 24 patients developed acute rejection, and 7 patients had graft failure. Pretransplant cytotoxic T lymphocyte activity was associated with chronic rejection (P=0.001) and graft failure (P=0.013) but only marginally with acute rejection (P=0.058). Controlling for age and sex, Cox's proportional hazards model revealed that CML level was predictive of time to chronic rejection (P<0.01) but not acute rejection (P=0.11). It was estimated that every 1-unit increase in CML level raises the monthly risk of chronic rejection by 7%. Ten children received HLA-identical kidneys from their siblings. There were no episodes of chronic rejection after 5 years. Two patients with high CML levels had episodes of acute rejection; both patients responded to treatment. CONCLUSION: Our data demonstrate an association between pretransplant cell-mediated cytotoxicity and the occurrence of chronic rejection in living related one-haploidentical renal transplants in pediatric patients.     

Competitive time-resolved immunofluorometric assay for quantifying carbonic anhydrase VI in saliva

A competitive time-resolved immunofluorometric assay sensitive and robust enough for quantifying human salivary carbonic anhydrase isoenzyme VI (HCA VI) was developed. The solid-phase immunoassay is based on competition between Eu(3+)-labeled HCA VI and salivary HCA VI for polyclonal rabbit anti-HCA VI antibodies that are attached to microtiter plate wells precoated with sheep anti-rabbit IgG. The subsequent immunoassay including the separation of free and bound HCA VI requires only one incubation step, after which the Eu3+ of the bound labeled antigen is released into an enhancement solution. The highly fluorescent Eu chelates formed in this solution are then quantified by time-resolved fluorometry (Delfia). The time-resolution principle effectively obviates possible interferences from complex biological material such as saliva. The assay detection limit was 1.5 micrograms/L. Intra- and interassay imprecisions (CVs) were 5.1% and 5.3%, respectively. The mean analytical recovery was 93%. The mean +/- SD concentration of HCA VI in paraffin-stimulated saliva was 6.8 +/- 4.3 mg/L (n = 30) and the secretion rate was 10.2 +/- 7.9 micrograms/min. The method was useful for further investigations of the role of HCA VI in difficult matrices, e.g., saliva.     

Association between mother-infant salivary contacts and caries resistance in children: a cohort study

We selected 327 7-month-old infants and divided them into two groups based on the frequency of salivary close contacts between mother and infant. Five to seven years later, all first-born children (N = 55) whose dental development had been followed regularly, were examined for dental caries and prevalence of salivary mutans streptococci (MS) and lactobacilli. The children with frequent maternal close contacts (F group, N = 21) had significantly less MS in saliva than the children with rare close contacts (R group, N = 34, P = 0.02). Only 19% of the children in F group compared with 56% in R group had experienced caries in their primary molars and/or canines (P < 0.01). A significantly greater proportion of the children in F group (57%) than in R group (27%, P < 0.05) had a high intake of sugar-containing foods and drinks in a 2-day dietary history. The F and R groups did not differ significantly with respect to other children's caries risk factors, or in age, sex, stage of dental development, dental treatment, or the social aspects studied. There were no significant differences between F and R groups in maternal caries experience, salivary MS or lactobacillus counts, or in maternal background factors (age, breast feeding, or education). Frequent transfer of maternal saliva to the mouth of the baby before tooth eruption was negatively associated with oral infection by MS and to caries in the primary dentition, possibly due to protective immune mechanisms.     

Mobilisation of healthy donors with lenograstim and transplantation of HLA-genoidentical blood progenitors in 54 patients with hematological malignancies: a pilot study

Blood cell transplantation (BCT) is now common practice in the autologous setting. We performed a pilot study of allogeneic BCT, collected after the priming of an HLA-identical sibling with a glycosylated rhu-G-CSF (lenograstim) (10 microg/kg). Fifty-four patients were included (38 +/- 11; M/F = 33/21; CML (n = 17), AML (n = 14), ALL (n = 15); MDS (n = 8)). Transplant procedures were standard (TBI regimen = 47 (87%); MTX-CsA: n = 37; CsA-PDN: n = 17). No serious adverse events were reported in donors. A median of 11 (3.5-29.1) x 10(6)/kg CD34+ cells, 332 (33-820) x 10(6)/kg CD3+ cells were collected. Four patients did not engraft (early death: n = 2; graft failure: n = 2). Fifty-one patients initially recovered 0.5 x 10(9)/l ANC and 25 x 10(9)/l platelets at 15 (10-30) and 13 (9-188) days. 29/51 and 29/38 experienced grade > or =2 acute and chronic GVHD. With a median follow-up of 25 months (18-36), relapse rate is 16% +/- 8, survival and DFS probabilities are similar (50% +/- 13). A better outcome is documented for patients under 45 years and in the early phase of the disease (n = 28), with an identical survival and DFS of 71% +/- 13. In conclusion, lenograstim is a potent rhu-G-CSF for mobilisation of allogeneic hematopoietic progenitors. Two-year follow-up indicates good haematological recovery but some concerns about graft failure and chronic GVHD have arisen deserving prospective evaluation.     

Antigenicity of a synthetic peptide from glucosyltransferases of Streptococcus mutans in humans

Human salivary immunoglobulin A (IgA) and serum IgG antibodies to the Streptococcus mutans glucosyltransferases (Gtfs) and to a synthetic peptide of 19 amino acids from a conserved region in the Gtfs (residues 435 to 453) were determined in young adults by enzyme-linked immunosorbent assay. Varying levels of antibody to Gtfs were detected in saliva or serum, with significantly higher levels of antibody to GtfD than to GtfB/C or GtfC. Anti-Gtf IgA levels in saliva did not correlate with those of IgG in serum. Caries-free (CF) volunteers exhibited significantly higher salivary IgA antibody levels to the peptide and to GtfB/C or GtfC than did the caries-active (CA) subjects. Preincubation of CF saliva and serum with the peptide inhibited the antibodies to the Gtfs in a dose-dependent manner, whereas preincubation of the samples from the CA group resulted in only partial inhibition. Our results indicated that this 19-amino-acid peptide includes one of the major B-cell epitopes of Gtfs and that CF individuals have higher titers of antibodies than CA subjects.     

Impaired tumorigenicity of IL-4-producing murine neuroblastoma cells in immunodeficient nude mice

OBJECTIVE: Our purpose was to evaluate the clinical utility of serum uric acid measurements in the hypertensive diseases of pregnancy. STUDY DESIGN: We performed a nested case-control study to assess the clinical utility of serum uric acid measurements in women with hypertensive diseases of pregnancy. We identified 344 women who had serum uric acid measurements at term and categorized them into five diagnostic groups according to definitions of hypertensive diseases in pregnancy published by the National Working Group on Hypertension in Pregnancy: transient hypertension of pregnancy (n = 69), preeclampsia (n = 130), chronic hypertension (n = 23), chronic hypertension with superimposed preeclampsia (n = 29), and normal (n = 93). We compared the mean uric acid concentration for each group with use of a one-way analysis of variance and Scheffe's post hoc test and calculated the sensitivities and specificities in diagnosing preeclampsia as well as the likelihood ratios for serum uric acid values of 5.5, 6.0, and 6.5 mg/dl. We also examined the correlation between serum uric acid levels and several clinical outcome measures in women with hypertensive diseases of pregnancy. RESULTS: The mean serum uric acid values for women with preeclampsia (6.2 +/- 1.4 mg/dl) and transient hypertension (5.6 +/- 1.7 mg/dl) were significantly higher than those of controls (4.3 +/- 0.8 mg/dl, p < 0.05). The difference in mean serum uric acid values between women with chronic hypertension (4.9 +/- 1.0 mg/dl) and superimposed preeclampsia (5.8 +/- 1.4 mg/dl) were not statistically significant. The likelihood ratio of having preeclampsia with a serum uric acid value of 5.5 mg/dl was 1.41 in gestational hypertension of pregnancy and 2.5 in chronic hypertension. With use of a receiver-operator characteristic curve, we were unable to identify a serum uric acid value that could be used to differentiate various hypertensive diseases of pregnancy. There was a weak correlation between serum uric acid values and several clinical outcome measures of preeclampsia (r = 0.06 to 0.26). CONCLUSION: Although mean serum uric acid values are elevated in women with preeclampsia, the clinical utility of serum uric acid values in differentiating various hypertensive diseases of pregnancy appears to be limited. In the setting of chronic hypertension, however, a serum uric acid level of > or = 5.5 mg/dl could identify women with an increased likelihood of having superimposed preeclampsia.