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D J Hill

Publications and source records attributed to D J Hill.

At least 19 recordsLinked to original sources
PubMed2006

Ontogeny of regeneration of beta-cells in the neonatal rat after treatment with streptozotocin.

We induced partial beta-cell loss within the pancreas of neonatal rats using streptozotocin (STZ) to better characterize the mechanisms leading to beta-cell regeneration postnatally. Rats were administered either STZ (70 mg/kg) or buffer alone on postnatal d 4, and the endocrine pancreas was examined between 4 and 40 d later. STZ-treated rats showed an approximately 60% loss of existing beta-cells and a moderate hyperglycemia (<15 mm glucose), with levels returning to near-control values after 20 d. Within preexisting islets, there was increased cell proliferation in both insulin- and glucagon-positive cells at 8 d as well as alpha-cell hyperplasia. These were associated with increased pancreatic content and circulating levels of glucagon. Pancreatic levels of glucagon-like polypeptide-1 (GLP-1) were increased 8 d after STZ compared with control values, and the GLP-1/glucagon ratio changed in favor of GLP-1. Administration of a GLP-1 receptor antagonist, GLP-1-(9-39), resulted in decreased recovery of beta-cells after STZ and worse glucose tolerance. Atypical glucagon-positive cells were found within islets that colocalized pancreatic duodenal homeobox-1 or glucose transporter-2. Pancreatic levels of insulin mRNA did not return to control values until 40 d after STZ. Insulin-positive cells were found after 8 d that colocalized glucagon and GLP-1. The model shows that the pancreas of the young rat can rapidly regenerate a loss of beta-cells, and this is associated with hyperplasia of alpha-cells with an altered phenotype of increased GLP-1 synthesis. The target cells of GLP-1 probably include immature beta-cells that coexpress proglucagon.

Animals↗
PubMed2004

Taurine supplement in early life altered islet morphology, decreased insulitis and delayed the onset of diabetes in non-obese diabetic mice.

AIMS/HYPOTHESIS: We hypothesised that nutritional taurine, which is important for the development of the endocrine pancreas and reduces cytokine-induced apoptosis in pancreatic beta cells, would prevent or delay the onset of autoimmune diabetes, if given early in life to the non-obese diabetic (NOD) mouse. METHODS: Pregnant NOD mice received a diet supplemented with taurine throughout gestation or until weaning, and the pancreas of the offspring was examined using immunohistochemistry. This was done at postnatal day 14 and after 8 weeks (assessment of insulitis). The animals were also monitored until they became diabetic. RESULTS: At 14 days, pancreatic islet mass was significantly greater in animals treated with taurine than in controls. This finding was associated with a greater incidence of islet cell proliferation and a lower incidence of apoptosis. At age 8 weeks the number of islets manifesting insulitis was reduced by more than half, and the area of insulitis was reduced by 90%. Taurine treatment delayed the mean onset time of diabetes from 18 to 30 weeks in females, and from 30 to 38 weeks in males, while 20% of treated females remained free of diabetes after one year. CONCLUSIONS/INTERPRETATION: Taurine supplementation in early life altered islet development, reduced insulitis and delayed the onset of diabetes in NOD mice.

Animals↗
PubMed2004

Low-protein diet during early life causes a reduction in the frequency of cells immunopositive for nestin and CD34 in both pancreatic ducts and islets in the rat.

Feeding a low-protein (LP) diet to pregnant and lactating rats impairs pancreatic islet mass and insulin release in the offspring, leading to glucose intolerance as adults. We hypothesized that an LP diet changes the number of pancreatic endocrine precursor cells or cells supporting endocrine cell neogenesis. Pregnant rats were given LP (8% protein) or a control (20% protein) diet from conception until postnatal d 21. Cells containing nestin, CD34, or c-Kit were quantified in pancreata of the offspring. Stellate cells immunoreactive for nestin were seen to be adjacent to ductal epithelium and were resident within the islets. These were proliferative and immunonegative for cytokeratin 20, fibronectin, tyrosine hydroxylase, pancreatic duodenal homeobox 1, Nk homeodomain transcription factor 6.1, or insulin, but expressed vimentin. Approximately 20% of islet nestin-positive cells also expressed the endothelial cell marker platelet endothelial cell adhesion molecule-1. Both ducts and islets also contained CD34- and c-Kit-positive cells with similar morphology to those expressing nestin. Offspring from rats fed the LP diet had significantly less nestin/CD34-positive cells and reduced expression of nestin mRNA. Within islets, there was an associated decrease in cell proliferation and in cells immunopositive for pancreatic duodenal homeobox 1. Nestin-positive cell number within islets correlated positively with the percent area of beta-cells. Supplementation of pregnant and lactating rats with taurine reversed the deficits in mean islet area and nestin-positive cells caused by the LP diet within the islets of the offspring. Nutritional programming of postnatal beta-cell mass may involve an altered abundance of cells expressing nestin and/or CD34, which may limit endocrine cell development.

Animals↗
PubMed2004

T cell recognition pattern of bovine milk alphaS1-casein and its peptides.

T cell recognition patterns of CAS1_Bovin, its limited hydrolysis, oxidized, reduced/alkylated, cyanogen bromide cleavage fractions and synthetic peptides were examined. Thirteen overlapping peptides covering the intact molecule, with chain lengths varied between 17 and 20 AA, were prepared by f-moc SPPS. In addition, six CNBr-cleavage fragments were obtained and extensively purified using RP/HPLC. Likewise, chemically modified derivatives and limited pepsin hydrolysate, were performed and the specificities were confirmed. Stimulation of PBMC and TCL cultures by the intact CAS1_Bovin molecule, synthetic peptides and modified derivatives were screened by [methyl-3H] thymidine incorporations. PBMC phenotype was performed by flow cytometry and the mean CD4+/CD8+ ratio of freshly prepared PBMC was compared with the ratio following specific CAS1_Bovin stimulation. CD4+ phenotypes (TH1/, TH2 and TH0) were assigned by assay of four marker cytokines IL-4, IL-6, IL-10 and IFN-gamma. Five CNBr fragments and seven of the thirteen tested peptides were recognized by specific TCL. The most reactive epitopes of CAS1_Bovin comprised seven motifs namely: peptides Cas 1-18, Cas 16-35, Cas 67-85, Cas 91-110, Cas 136-155, Cas 152-169 and Cas 166-183. The stimulation range for the seven peptides was 1058-2383 cpm. Stimulation for the CNBr fragments were, respectively, 8670, 5808, 3324, 5465, 2255 and 321 cpm. Cytokine assay showed that CD4+ TH2 phenotype was dominant for half the number of patients, while TH1 solely or combined TH0 were represented in the other four cell culture filtrates. The T cell reactive epitopes described and their antibodies will be useful tools for methods in progress for the detection of masked casein epitopes encompassed in processed food. In conclusion, T cell recognition pattern of CAS1_Bovin was examined using extensively purified synthetic peptides and CNBr fragments. Five large and seven small peptides were clearly recognized. Peptides of chain length less than six AA were left unrecognised. CD4+ TH2 phenotype was the most dominant TCL subpopulations found in atopic patients while CD4+ TH1 was representative in the non-IgE mediated type IV hypersensitivity.

Adolescent↗
PubMed2004

Evaluation of the allergenicity and antigenicity of bovine-milk alphas1-casein using extensively purified synthetic peptides.

Alphas1-Casein (CAS1_BOVIN), the major allergen of cow's milk (CM), is widely used as hydrolysates in infant diet formulae and additive to other processed food items. To date, most of the reported B-cell epitope mapping were performed on polyethylene pins or cellulose-derivative membrane. We sought to locate the motifs critical for human-specific IgE and rabbit polyclonal IgG binding using extensively purified CAS1_BOVIN, synthetic peptides and derivatives. Thirteen overlapping peptides covering the whole CAS1_BOVIN encompassing 17 : 20 amino acid (AA) were synthesized by f-moc AA solid-phase polyamide peptide synthesis. In addition, six cyanogen bromide (CNBr) cleavage fragments were prepared. Limited hydrolysis, oxidized and reduced/alkylated derivatives were also produced. The preparations were purified by ion exchange, gel filtration chromatography, reversed phase and high-performance liquid chromatography. The homogeneity was visualized by sodium dodecyl sulfate (SDS) and poly acryl amide gel electrophoresis (PAGE) followed by IgE and IgG immunoblotting. IgE binding was measured by Biotin Streptavidin (Bio/strep) fluoro enzyme immuno assay (FEIA) or ELISA-inhibition. Eighteen CM allergy (CMA) sera from 45 clinically examined children (Melbourne) and five adults (Bergen) were selected. Individual sera and pools were used for mapping IgE-binding epitopes. Rabbit IgG sera and pools were used for locating the antigenic sites of the molecule. Results indicated that all the individual CMA sera and pools recognized the intact molecule and three of the CNBr fragments as major antibody-binding allergens. The N- and C-terminal peptides (CAS 16-35; CAS 136-155) showed high IgE-binding affinity. CAS 1-18 and CAS 181-199 showed high IgG bindings. Considering the diversity of the antibody specificities, a reasonable agreement between IgE and IgG epitopes were found at the N- and C-terminals of CAS1_BOVIN. Mapping IgE B-cell epitopes by direct Bio/strep FEIA allowed the development of a sensitive modified technique for detecting unlabelled, casein immune dominant peptides in food products.

Allergens↗
PubMed2004

Maternal breast milk long-chain n-3 fatty acids are associated with increased risk of atopy in breastfed infants.

BACKGROUND: Australia has one of the highest prevalence rates internationally of allergic conditions, such as asthma and eczema. Atopy is one hallmark for the development of allergic disease and predisposes to allergic inflammation in the target organs. omega-3 (n-3) fatty acids (FAs) are thought to act as precursors to the formation of less active inflammatory mediators, with the potential to reduce inflammation. OBJECTIVE: To investigate whether increased n-3 FA levels in maternal breast milk are associated with a lower risk of developing atopy in infancy. METHODS: Subjects were part of the prospective Melbourne atopy cohort study, which involved 620 children born into families where at least one first-degree relative had an atopic disease. Some 224 women (mean age 31.4+/-4.2 (SD) years, with 73.2% (n=164) having self-reported atopy) provided either a colostrum (n=194) or 3-month expressed breast milk (EBM) sample (n=118). Maternal colostrum and 3-month EBM samples were analysed for FA content by gas chromatography. Skin prick tests (SPTs) to six common allergens were performed on infants at 6, 12 and 24 months of age and on mothers who agreed at study entry. RESULTS: For infants sensitized to foods at 6 months (n=29), the total n-3 FA level in the colostrum was significantly higher (P=0.004) as were levels of individual long-chain n-3 FAs, docosoapentaenoic acid (DPA, C22:5, P=0.001) and docosahexaenoic acid (DHA, C22:6, P=0.002) than in non-sensitized infants. Infants with aero-allergen sensitization at 24 months (n=30) had higher levels of the n-3 FA, DPA (P=0.002) and DHA (P=0.007), and similarly higher total n-3 FA (P=0.009) in maternal colostrum than those infants who were not sensitized. CONCLUSION: Higher n-3 FA levels in the colostrum do not appear to confer protection against, but may be a risk factor for, the eventual development of atopy in high-risk breastfed infants.

Adult↗
PubMed2004

A consensus protocol for the determination of the threshold doses for allergenic foods: how much is too much?

BACKGROUND: While the ingestion of small amounts of an offending food can elicit adverse reactions in individuals with IgE-mediated food allergies, little information is known regarding these threshold doses for specific allergenic foods. While low-dose challenge trials have been conducted on an appreciable number of allergic individuals, a variety of different clinical protocols were used making the estimation of the threshold dose very difficult. OBJECTIVE: A roundtable conference was convened to develop a consensus clinical protocol for low-dose challenge trials for the estimation of threshold doses for specific allergenic foods. METHODS: In May 2002, 20 clinical allergists and other interested parties were invited to participate in a roundtable conference to develop consensus of the key elements of a clinical protocol for low-dose challenge trials. RESULTS: A consensus protocol was developed. Patients with convincing histories of food allergies and supporting diagnostic evidence including past challenge trials or high CAP-RAST scores can be enrolled in low-dose challenge trials. Care must be taken with younger patients to assure that they have not outgrown their food allergy. An approach was developed for the medication status of patients entering such trials. Challenge materials must be standardized, for example, partially defatted peanut flour composed of equal amounts of the three major varieties of peanuts (Florunner, Virginia, Spanish). Challenge materials must be appropriately blinded with sensory evaluation used to confirm the adequacy of blinding. A double-blind, placebo-controlled design should be used for low-dose challenge trials. Low-dose challenge trials would begin at doses of 10 microg of the allergenic food and would continue with doses of 100 microg and 1 mg followed by specific higher doses up to 100 mg depending upon the expert judgement of the physician; even higher doses might be applied to assure that the patient is indeed reactive to the particular food. A 30-min time interval would be used between doses, and reactive doses would be expressed as both discrete and cumulative doses. The goal of each challenge would be to develop objective symptoms; trials should not be discontinued on the basis of subjective symptoms only. Statistically, a minimum of 29 patients would be enrolled in low-dose challenge trials for each allergenic food because 0 reactors out of 29 patients at a particular dose allow the conclusion that there is 95% certainty that 90% of allergic individuals will not react to that dose. CONCLUSION: A consensus protocol was developed. Using this protocol, it will be possible to estimate threshold doses for allergenic foods, the lowest amount that elicits mild, objective symptoms in highly sensitive individuals.

Allergens↗
PubMed2004

Food allergy and atopic dermatitis in infancy: an epidemiologic study.

Atopic dermatitis is common in infancy. The role of food allergy in atopic dermatitis of infancy is unclear. We examined the relationship between atopic dermatitis and immunoglobulin E (IgE)-mediated food allergy in infancy. A birth cohort of 620 infants with a family history of eczema, asthma, hayfever or immediate food allergy in a parent or sibling: 487 children had complete data including skin prick tests (SPTs) to evaluate IgE-mediated food allergy to cow milk, egg and peanut. Participants were grouped as no atopic dermatitis (Gp 0) or in quartiles of increasing severity of atopic dermatitis (Gps 1-4) quantified by days of topical steroid use as reported monthly. Adverse reactions to foods were recorded. The cumulative prevalence of atopic dermatitis was 28.9% to 12 months (10.3% of the cohort of moderate severity). As atopic dermatitis severity increased so did the prevalence of IgE-mediated food allergy (Gp 0, 40/346 vs. Gp 1, 6/36 vs. Gp 2, 8/35 vs. Gp 3, 12/35 vs. Gp 4, 24/35; chi(2) = 76; p < 10(-6)), and the frequency of reported adverse food allergy reactions (Gp 0, 43/346 vs. Gp 1, 4/36 vs. Gp 2, 8/35, vs. Gp 3, 5/35, vs. Gp 4, 13/35; chi(2) = 17; p = 0.002). The relative risk of an infant with atopic dermatitis having IgE-mediated food allergy is 5.9 for the most severely affected group. Atopic dermatitis is common in infancy. There is a strong association between IgE-mediated food allergy and atopic dermatitis in this age group.

Dermatitis, Atopic↗
PubMed2004

Is epidural anaesthesia acceptable at total hip arthroplasty? A study of the rates of urinary catheterisation.

Epidural anaesthesia, with and without opiate, is widely used in total hip arthroplasty (THA). It may cause urinary retention, leading to catheterisation, and a subsequent increase in the likelihood of deep infection. We investigated prospectively the rate of urinary catheterisation in patients after THA performed under general anaesthesia, with or without peri-operative fentanyl and bupivacaine opiate epidural anaesthesia. Of 173 patients, 75 received general anaesthesia alone and 98 both general and epidural management. The post-operative rate of catheterisation was 14.7% in those who received general anaesthesia alone and 13.3% in those who received both. Our findings suggest that the rate of post-operative urinary catheterisation does not increase when general anaesthesia is supplemented by epidural anaesthesia using fentanyl and bupivicaine.

Adjuvants, Anesthesia↗
PubMed2002

Survival of Escherichia coli O157:H7 in traditional African yoghurt fermentation.

Growth and survival of a nontoxigenic strain of Escherichia coli O157:H7 (ATCC 43888) was determined in traditionally fermented pasteurized milk. Preheated milk was inoculated with 1% (v/v) of a mixed culture of Lactobacillus delbrueckii ssp. bulgaricus (NCIMB 11778) and Streptococcus salivarius ssp. thermophilus (NCIMB 110368) and incubated at 25, 30, 37 or 43 degrees C for 24 h. E. coli O157:H7 (10(5) CFU/ml) were introduced into the milk pre- and post-fermentation. Fermented milk samples were subsequently stored at either 4 degrees C (refrigerator temperature) or 25 degrees C (to mimic African ambient temperature) for 5 days. After 24 h of fermentation, the pH of the samples fermented at the higher temperatures of 37-43 degrees C decreased from 6.8 to 4.4-4.0 ( +/- 0.2) whereas at the lower temperature of 25 degrees C, the pH decreased to pH 5.0 +/- 0.1. During this period, viable counts for E. coli O157:H7 increased from 10(5) to 10(8) - 10(9) CFU/ml except in milk fermented at 43 degrees C wherein viability declined to 10(4) CFU/ml. In fermented (25-30 degrees C) milk stored at 4 degrees C for 5 days, E. coli O157:H7 viability decreased from 10(8-9) to 10(6-7) CFU/ml whereas milk fermented at 43 degrees C resulted in loss of detectable cells. In contrast, storage of fermented milk samples at 25 degrees C for 5 days eventually resulted in complete loss of viability irrespective of fermentation temperature. Stationary phase E. coli O157:H7 inoculated post-fermentation (25 and 43 degrees C) survived during 4 degrees C storage, but not 25 degrees C storage. Fermentation temperature and subsequent storage temperature are critical to the growth and survival of E. coli O157:H7 in traditional fermented products involving yoghurt starter cultures.

Colony Count, Microbial↗
PubMed2002

Glucocorticoid receptor expression is altered in pancreatic beta cells of the non-obese diabetic mouse during postnatal development.

Glucocorticoids play a crucial role in the regulation of carbohydrate metabolism and in the immune response, and can influence the development of diabetes in certain animal models including autoimmune type 1 diabetes in the non-obese diabetic (NOD) mouse. In these animals, the onset of destructive autoimmune pancreatic changes (insulitis) occurs at around 3 weeks of age. Moreover, the incidence of diabetes is significantly higher in females compared to males. However, the underlying mechanisms for this sex-specificity are unknown. Therefore, the present study was undertaken to examine the expression of the glucocorticoid receptor (GR) in pancreatic islets of Langerhans of the NOD mouse during the first 3 weeks of postnatal development. Immunohistochemistry was used to determine pancreatic GR expression and to identify insulin-secreting beta cells in postnatal (1-, 2-, and 3-week-old) NOD mice. Age-matched NOD.SCID mice (immunodeficient animals with the same NOD genetic background) were used as control animals. In both strains, regardless of sex or age, GR staining was found predominantly in the cytoplasm of beta cells but was also present in other cell types within the islets. At all ages, the percentage of islet cells containing GR was similar between male and female animals of the same strain. In control mice, the percentage of islet cells containing GR increased progressively from 80% at 1 week of age to 100% at 3 weeks of age. In marked contrast, in the NOD mice, the proportion of islets containing GR decreased from 95% at week 1 to only 60% at 3 weeks of age. We conclude that sex-specific differences in the incidence of diabetes are not associated with altered pancreatic GR expression in NOD mice during early postnatal development. However, the distinct and remarkable decrease in islet GR levels at 3 weeks of age may contribute to the onset of insulitis, and potentially to the ontology of diabetes in NOD mice, as a result of the loss of protective immunosuppressive effects of glucocorticoids.

Aging↗
PubMed2002

Increased islet cell proliferation, decreased apoptosis, and greater vascularization leading to beta-cell hyperplasia in mutant mice lacking insulin.

The targeted disruption of the two nonallelic insulin genes in mouse was reported previously to result in intrauterine growth retardation, severe diabetes immediately after suckling, and death within 48 h of birth. We have further used these animals to investigate the morphology and cell biology of the endocrine pancreas in late gestation and at birth when insulin is absent throughout development. Pancreatic beta-cells were identified by detecting the activity of the LacZ gene inserted at the Ins2 locus. A significant increase in the mean area of the islets was found at embryonic d 18.5 (E18.5) and in the newborn in Ins1-/-, Ins2-/- animals compared with Ins1-/-, Ins2+/- and wild-type controls, whereas the blood glucose levels were unaltered. The individual size of the beta-cells in the insulin-deficient fetuses was similar to controls, suggesting that the relative increase in islet size was due to an increase in cell number. Immunohistochemistry for proliferating cell nuclear antigen within the pancreatic ductal epithelium showed no differences in labeling index between insulin-deficient and control mice, and no change in the number of beta-cells associated with ducts, but the relative size distribution of the islets was altered so that fewer islets under 5,000 microm(2) and more islets greater than 10,000 microm(2) were present in Ins1-/-, Ins2-/- animals. This suggests that the greater mean islet size seen in insulin-deficient animals represented an enlargement of formed islets and was not associated with an increase in islet neogenesis. The proportional contribution of alpha- and beta-cells to the islets was not altered. This was supported by an increase in the number of cells containing immunoreactive proliferating cell nuclear antigen in both islet alpha- and beta-cells at E18.5 in insulin-deficient mice, and a significantly lower incidence of apoptotic cells, as determined by molecular histochemistry using the terminal deoxynucleotidyl transferase-mediated deoxy-UTP nick end labeling reaction. The density of blood vessels within sections of whole pancreas, or within islets, was determined by immunohistochemistry for the endothelial cell marker CD31 and was found to be increased 2-fold in insulin-deficient mice compared with controls at E18.5. However, no changes were found in the steady-state expression of mRNAs encoding vascular endothelial growth factor, its receptor Flk-1, IGF-I or -II, the IGF-I and insulin receptors, or insulin receptor substrates-1 or -2 in pancreata from Ins1-/-, Ins2-/- mice compared with Ins1-/-, Ins2+/- controls. Thus, we conclude that the relative hyperplasia of the islets in late gestation in the insulin-deficient mice was due to an increased islet cell proliferation coupled with a reduced apoptosis, which may be related to an increased vascularization of the pancreas.

Animals↗
PubMed2001

NMR imaging of water sorption into poly(hydroxyethyl methacrylate-co-tetrahydrofurfuryl methacrylate).

The diffusion of water into a series of hydroxyethyl methacrylate, HEMA, copolymers with tetrahydrofurfuryl methacrylate, THFMA, has been studied over a range of copolymer compositions using NMR imaging analyses. For polyHEMA the diffusion was found to be consistent with a Fickian model. The mass diffusion coefficient of water in polyHEMA at 37 degrees C was determined from the profiles of the diffusion front to be 1.5 x 10(-11) m(2) s(-1), which is less than the value based upon mass uptake, 2.0 x 10(-11) m(2) s(-1). The profiles of the water diffusion front obtained from the NMR images showed that stress was induced at the interface between the rubbery and glassy regions which led to formation of small cracks in this region of the glassy matrix of polyHEMA and its copolymers with mole fractions of HEMA greater than 0.6. Water was shown to be able to enter these cracks forming water "pools". For copolymers of HEMA and THFMA with mole fractions of HEMA less than 0.6 the absence of cracks was attributed to the ability of the THFMA sequences to undergo stress relaxation by creep.

Absorption↗
PubMed2001

Reducing the need for food allergen challenges in young children: a comparison of in vitro with in vivo tests.

BACKGROUND: Double-blind placebo-controlled food challenges (DBPCFC), the gold standard for the diagnosis of food hypersensitivity, are time-consuming and not without risk. We have recently reported skin prick test (SPT) weal diameters to cow's milk, egg and peanut above which infants and young children referred for investigation of suspected food allergy showed an adverse reaction on food challenge. We have termed these the "100% diagnostic SPT levels". In this study, we compare in vivo with in vitro measurement of IgE antibody levels to three common food allergens--cow's milk, egg and peanut--in infants and young children with suspected food allergy, in order to reduce the need for food challenges. METHODS: SPT and Enzyme Allergo-sorbent Test (EAST) (from 1992 to 1998) and CAP values (from 1999 to 2000) were performed in 820 children < 2 years of age with suspected allergy to cow's milk and/or egg and/or peanut. SPT levels previously shown to be diagnostic of challenge-proven allergy to cow's milk, egg and peanut were used as the "100% diagnostic SPT levels" and compared with EAST and CAP values associated with IgE food allergy according to the manufacturer's definition. RESULTS: McNemar's test showed a significant difference between the "100% diagnostic SPT levels" and positive EAST in identifying patients who did not require food challenge for cow's milk (P = 0.01), egg (P < 10-6) and peanut (P < 10-6), and a significant difference between the "100% diagnostic SPT levels" and positive CAP (P < 10-6) for egg and peanut but not cow's milk. Twenty-three per cent of food challenges which, based on the results of EAST and CAP, would have been necessary to confirm the diagnosis of food allergy were avoided by the use of the "100% diagnostic SPT levels" . CONCLUSION: The use of the "100% diagnostic SPT levels" compared with in vitro measurement of IgE antibody to cow's milk, egg and peanut reduces the need for food challenge in young children with suspected food allergy.

Allergens↗
PubMed2001

The variable P5 proteins of typeable and non-typeable Haemophilus influenzae target human CEACAM1.

Haemophilus influenzae, a commensal of the human respiratory mucosa, is an important cause of localized and systemic infections. We have recently shown that numerous strains of capsulate (typeable) and acapsulate (non-typeable) H. influenzae target the carcinoembryonic antigen (CEA) family of cell adhesion molecules (CEACAMs). Moreover, the ligands appeared to be antigenically variable and, when using viable typeable bacteria, their adhesive functions were inhibited by the presence of capsule. In this report, we show that the antigenically variable outer membrane protein, P5, expressed by typeable and non-typeable H. influenzae targets human CEACAM1. Variants and mutants lacking the expression of P5 of all strains tested were unable to target purified soluble receptors. A non-typeable strain that did not interact with CEACAM1 was made adherent to both the soluble receptors and CEACAM1-transfected Chinese hamster ovary cells by transformation with the P5 gene derived from the adherent typeable strain Rd. However, several H. influenzae mutants lacking P5 expression continued to bind the cell-bound CEACAM1 receptors. These observations suggest that (i) CEACAM1 alone can support P5 interactions and (ii) some strains contain additional ligands with the property to target CEACAM1 but require the receptor in the cellular context. The identification of a common ligand in diverse strains of H. influenzae and the presence of multiple ligands for the same receptor suggests that targeting of members of the CEACAM family of receptors may be of primary significance in colonization and pathogenesis of H. influenzae strains.

Animals↗