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Biomedical subjects

F C Thien

Publications and source records attributed to F C Thien.

18 recordsLinked to original sources
PubMed2004

Induction of T 'regulatory' cells by standardized house dust mite immunotherapy: an increase in CD4+ CD25+ interleukin-10+ T cells expressing peripheral tissue trafficking markers.

BACKGROUND: Clinically effective subcutaneous allergen-specific immunotherapy (SIT) is associated with altered circulating T cell cytokine production and altered local cytokine responses with increased IL-10 following allergen challenge in target organs. OBJECTIVE: This study aimed to elucidate mechanisms for these T cell changes, by examining surface expression of markers for peripheral tissue trafficking on circulating cytokine-positive T cells following standardized house dust mite- (HDM-) SIT. METHODS: A randomized conventional HDM immunotherapy study was performed on a panel of 12 HDM-allergic subjects. Nine subjects received treatment with conventional HDM immunotherapy using a standardized extract and three subjects were treated by standard pharmacotherapy alone. Symptom and medication scores and allergen-induced cutaneous late-phase responses were assessed before and 9 months after institution of therapy. Before and at 3 and 9 months of SIT, peripheral blood mononuclear cells were cultured for 14 days with HDM extract and CD4+ and CD8+ T cell expression of CD62L, CD49d and CCR5 and production of IL-10, IFN-gamma and IL-4 were analysed by flow cytometry. Allergen-specific T cell proliferation was assessed by 3H-thymidine incorporation. RESULTS: At 9 months, all SIT-treated patients showed reduced symptom scores and late-phase cutaneous responses to HDM compared with baseline levels. The proportions of CD4+ T cells which were IL-10+ were increased (P < 0.01), and the proportions of CD4+ and CD8+ T cells which were IL-4+ decreased (P < 0.05) compared with baseline. CD4+ and CD8+ T cell IFN-gamma production, expression of surface markers for peripheral tissue trafficking and allergen-specific proliferation remained unchanged during SIT treatment. However, increased proportions of CD4+CD62L(-), CD4+CD49d(hi), CD4+CCR5+ T cells expressing IL-10 were detected at 9 months of SIT compared with baseline (P < 0.05). IL-10 staining co-localized with CD4+CD25+ T cells. CONCLUSION: Clinically effective subcutaneous immunotherapy with a standardized HDM Dermatophagoides pteronyssinus preparation results in decreased numbers of IL-4+ T cells and expansion of CD4+IL-10+ T cells expressing a peripheral tissue trafficking phenotype. The co-localization of IL-10+ staining to CD4+CD25+ T cells is consistent with the induction of a T regulatory cell population by SIT.

Adult↗
PubMed2001

Adverse events associated with rush hymenoptera venom immunotherapy.

OBJECTIVES: To determine the incidence and nature of adverse events associated with the induction of rush Hymenoptera venom immunotherapy. DESIGN: Retrospective descriptive case study. SETTING: The asthma and allergy unit at a major metropolitan teaching hospital, between 1 January 1989 and 30 June 1999. PATIENTS: All patients with anaphylaxis to stings of Hymenoptera insects who received rush venom immunotherapy as inpatients. OUTCOME MEASURES: Hypersensitivity reactions to venom administration, including angioedema, skin rashes, hypotension and asthma, as well as any other adverse events related to the inpatient stay. RESULTS: 68 venom-allergic patients received 73 courses of rush immunotherapy; 89% were desensitised to honey bee venom, 10% to yellow jacket wasp venom, and one to paper wasp venom. Hypersensitivity reactions occurred after 36 subcutaneous injections (3.8% of all injections given) in 26 patients (38%). CONCLUSION: In our cohort, immunotherapy was accompanied by a high incidence of adverse systemic events during the induction phase. Immunotherapy should only be given by experienced staff in centres where there are facilities for resuscitation.

Adult↗
PubMed2000

Dietary marine fatty acids (fish oil) for asthma.

BACKGROUND: Epidemiological studies suggest that a diet high in marine fatty acids (fish oil) may have beneficial effects on inflammatory conditions such as rheumatoid arthritis and possibly asthma. OBJECTIVES: 1. To determine the effect of marine n-3 fatty acid (fish oil) supplementation in asthma. 2. To determine the effect of a diet high in fish oil in asthma. SEARCH STRATEGY: The Cochrane Airways Review Group register was search using the terms: marine fatty acids OR diet OR nutrition OR fish oil OR eicosapentaenoic acid OR EPA. Bibliographies of retrieved trials were searched and fish oil manufacturers contacted. SELECTION CRITERIA: Randomised controlled trials in patients with asthma more than two years of age were included. The study duration had to be in excess of 4 weeks. Double blind trials were preferred, but single-blind and open trials were also reviewed for possible inclusion. Three reviewers read each paper, blind to its identity. Decisions concerning inclusion were made by simple majority. Quality assessment was performed by all three reviewers independently. DATA COLLECTION AND ANALYSIS: The only comparison possible was between marine n-3 fatty acid supplementation and placebo. There were insufficient trials to examine dietary manipulation alone. MAIN RESULTS: Eight randomised controlled trials conducted between 1986 and 1998 satisfied the inclusion criteria. Six were of parallel design and two were cross-over studies. Seven compared fish oil with placebo whilst one compared high dose vs low dose marine n-3 fatty acid supplementation. None of the included studies reported asthma exacerbations, health status or hospital admissions. There was no consistent effect on any of the analyzable outcomes: FEV1, peak flow rate, asthma symptoms, asthma medication use or bronchial hyper reactivity. The single study performed in children also combined dietary manipulation with fish oil supplementation and showed improved peak flow and reduced asthma medication use. There were no adverse events associated with fish oil supplements. REVIEWER'S CONCLUSIONS: There is little evidence to recommend that people with asthma supplement or modify their dietary intake of marine n-3 fatty acids (fish oil) in order to improve their asthma control. Equally, there is no evidence that they are at risk if they do so.

Adult↗
PubMed1999

Comparison of patients with asthma managed in general practice and in a hospital clinic.

OBJECTIVES: To compare knowledge and attitudes about asthma, self-management skills and impact of asthma on quality of life between patients managed in general practice (GP) and in a hospital clinic. DESIGN: Cross-sectional survey with six months' follow-up. PATIENTS AND SETTING: 105 adults with asthma: 61 from the Alfred Hospital Asthma and Allergy Clinic, Melbourne, and 44 from nearby general practices, in 1994-1995. MAIN OUTCOME MEASURES: Patient sociodemographic and clinical characteristics; patient knowledge, attitudes and beliefs about asthma; self-management skills; and impact of asthma on quality of life. RESULTS: GP patients were more educated (P = 0.04) and more likely to smoke (P = 0.04) and to have mild asthma (P = 0.04) than hospital patients; they were less likely to use theophylline (P = 0.006) and to have exercise limitation (P = 0.03), and had fewer previous hospital admissions (P = 0.01). Impact of asthma on quality of life was greater in the hospital group than in the GP group. At baseline, the GP group were less likely to have written asthma action plans (P = 0.018), and were less able to manage rapid onset attacks than the hospital group (P = 0.02). More subjects in the hospital group than the GP group felt their asthma was severe (P = 0.02) and were optimistic about their asthma improving (P = 0.03). GP patients increased their knowledge about asthma significantly (P = 0.002) over six months. CONCLUSIONS: Patients with asthma managed in general practice and in hospital differ in clinical parameters, quality of life and attitudes to asthma. Future educational initiatives should take such differences into account.

Adult↗
PubMed1998

Why do only some of the young adults with bronchial hyperreactivity wheeze?

The significance of nonspecific bronchial hyperreactivity (BHR) is a controversial issue in asthma. The natural history of BHR has not been investigated adequately although its importance as a cross-sectional risk factor for asthma is widely accepted. This paper investigates the risk factors for wheeze among people with BHR. Subjects were young adults who had participated in the second phase of the European Community Respiratory Health Survey in Melbourne, Australia. We compared the participants with wheeze and BHR (n=186) to those with asymptomatic BHR (n=66). Information was collected on sociodemographic factors, family history of asthma, and relevant environmental factors using an interviewer-administered questionnaire. Atopy to a range of aeroallergens was examined by skin prick tests. Risk factors were examined by adjusting the odds ratios (OR) by a logistic regression to control for confounding effects. Parental asthma (OR=4.2), keeping pets during childhood (OR=3.3), allergy to house dust mite (OR=2.7), allergic rhinitis (OR=2.6), and having ever smoked (OR=2.4) were associated with an increased risk of wheeze, independent of the other factors examined. When allergic rhinitis was not included as an explanatory variable, being atopic to any of the allergens assessed was found to increase the risk of current wheeze (OR=4.8). Allergic rhinitis may represent an intermediate stage in the natural history of BHR. Avoidance of pets during childhood, not smoking, and taking steps to minimize dust exposure are likely to prevent the progression from asymptomatic BHR to asthma.

Adult↗
PubMed1996

Asthma and anaphylaxis induced by royal jelly.

BACKGROUND: Asthma, together with, in some cases, anaphylaxis, was observed in seven subjects following ingestion of royal jelly, a secretion of honey bees which is used as a health tonic. OBJECTIVE: To determine if reactions were IgE-mediated and to identify allergenic components of royal jelly. METHODS: Skin-prick tests, immunoassays for specific IgE antibodies and protein blotting studies using patients' sera and anti-IgE second antibodies were employed. RESULTS: Immunoassays detected IgE antibodies to royal jelly proteins in sera of subjects who reacted to the substance. A total of 18 different IgE-binding components were detected on blots following electrophoretic separation of royal jelly under dissociating conditions. Examination of 63 sera from subjects allergic to bee venom showed that there is no direct relationship between IgE antibody reactivity to bee venom allergens and to royal jelly proteins although 38% of the sera reacted with a royal jelly solid phase. IgE antibody reactivity to royal jelly proteins was also detected in 52% of 75 subjects with allergies to inhalant and/or food allergens. Antibody binding of blotted royal jelly proteins was most marked in the molecular weight region 25-55 kDa and one component of MW approximately 55 kDa was detected by all of the reactive sera from royal jelly-allergic and control allergic subjects. CONCLUSIONS: Symptoms of asthma and anaphylaxis seen in subjects following ingestion of royal jelly were true IgE-mediated hypersensitivity reactions. The clinical significance of the antibodies found in the sera of control subjects is not known but they may arise in response to common inhalant allergens that show allergenic cross-reactivity with royal jelly.

Adult↗
PubMed1995

Eicosanoids and asthma: an update.

There have been significant advances in our understanding of the role of eicosanoids as mediators in inflammation since their discovery over 50 years ago. Our more recent understanding of asthma as an inflammatory disease has led to the appreciation of eicosanoids potentially being pivotal mediators in promoting some of the changes in asthma. Of particular importance are the cysteinyl LTs in producing bronchospasm and bronchial hyperresponsivenss, and PGE2 in modulating the bronchospastic and inflammatory response. Evidence from clinical studies suggests that other eicosanoids may also contribute, but their importance is secondary and their relative contributions vary between individuals. The development of new drugs based on our partial understanding of the role that eicosanoid mediators may play in asthma promises new approaches to the treatment of this common chronic inflammatory condition.

Asthma↗
PubMed1993

Effects of exogenous eicosapentaenoic acid on generation of leukotriene C4 and leukotriene C5 by calcium ionophore-activated human eosinophils in vitro.

Exogenous eicosapentaenoic acid (EPA) has been compared with exogenous arachidonic acid (AA) for its ability to modulate the oxidative metabolism of membrane-derived arachidonic acid by the 5-lipoxygenase pathway in ionophore-activated human eosinophils, and for its suitability as a parallel substrate in this pathway. Products were quantitated by specific RIA and tetraene and pentaene leukotrienes (LT) were separated by reverse-phase HPLC. Eosinophils were preincubated with control buffer, exogenous EPA or AA and stimulated optimally with 10 microM calcium ionophore (A23187) for 15 min. Mean generation of LTC4 in the absence of fatty acid was 6.0 = 1.1 ng/10(6) eosinophils (mean = SEM, n = 5). In the presence of EPA, the amount of LTC4 generated rose to peak at 16.5 +/- 1.9 ng/10(6) eosinophils at 10 micrograms/ml EPA and then fell to 8.3 +/- 3.1 ng/10(6) cells at 40 micrograms/ml EPA. The EPA derivative, LTC5 was first detectable at 5 micrograms/ml EPA with 4.8 +/- 1.2 ng/10(6) cells and gradually rose with increasing dose of EPA to be maximal at 40 micrograms/ml with 12.7 +/- 2.2 ng/10(6) cells. Identity of the LTC5 was confirmed by an identical retention time to synthetic LTC5 standard, immunoreactivity to a specific antibody against LTC4 and LTC5 and a typical UV absorbance spectrum. When eosinophils were preincubated with AA and similarly stimulated, LTC4 generation gradually increased from a baseline of 6.7 +/- 0.7 ng/10(6) cells in the absence of fatty acid to reach a maximum of 12.9 +/- 0.8 ng/10(6) cells at 40 micrograms/ml of AA. Total LTC generation was nearly twofold more with cells incubated with EPA than with cells incubated with AA (p < 0.05). Thus, EPA does not suppress LTC generation from eosinophils but stimulates it at lower doses and is a substrate for LTC5 generation.

Arachidonic Acid↗
PubMed1993

Dietary fish oil effects on seasonal hay fever and asthma in pollen-sensitive subjects.

The effects of taking 18 capsules a day of Max-EPA (3.2 g/day eicosapentaenoic acid) on clinical symptoms and bronchial hyperresponsiveness were studied in pollen-sensitive subjects over a pollen season in a parallel, double-blind, placebo-controlled (olive oil) fashion. The study was conducted over the 1990 and 1991 pollen seasons in London, England. A total of 37 nonsmoking pollen-sensitive asthmatic subjects were entered into the trial, and 25 completed the 6-month study period over the 2 yr. The preseasonal geometric mean PD35 SGaw of histamine for the fish oil (n = 12) and placebo (n = 9) groups were 0.62 and 0.42 mumol, respectively. During the middle of the pollen season, histamine PD35 SGaw fell significantly for both the fish oil (0.11 mumol, p < 0.0001) and placebo groups (0.10 mumol, p < 0.007), indicating increased bronchial reactivity compared with preseasonal values, but there was no significant difference between the groups. Similarly, morning and evening peak expiratory flow (PEF), diurnal variability in PEF, nocturnal cough and wheeze, daytime wheeze, and activity, as well as nasal symptoms and increased usage of medication, were not significantly different between the groups. Compliance was confirmed by neutrophil and plasma phospholipid analysis, which showed significant rises in eicosapentaenoic acid content in the fish oil group but not in the placebo group. We conclude that dietary fish oil supplementation does not prevent seasonal hay fever and asthma in pollen-sensitive subjects during the pollen season.

Adult↗
PubMed1992

Effect of dietary fish oil supplementation on the antigen-induced late-phase response in the skin.

We have studied the effect of dietary fish oil supplementation (3.2 gm/day of eicosapentaenoic acid and 2.2 gm/day of docosahexaenoic acid) for 10 weeks on the antigen-induced, cutaneous late-phase response (LPR) in 16 atopic individuals. All subjects developed an LPR to intradermal allergen injection. The mean +/- SEM area of induration at 6 hours was 1840 +/- 472 mm2. A biopsy was performed at the LPR site at 6 hours. Subjects were then randomized to receive fish oil or placebo olive oil in a double-blind, parallel fashion, for 10 weeks. After the diet, there were no significant differences between fish oil and placebo treatment in the size of the immediate wheal-and-flare response or the extent of induration at 4 and 6 hours, as compared with prediet values in each group. Histologically, at 6 hours, there was a significant infiltrate into the allergen site compared with that of the control diluent site of total inflammatory cells (p less than 0.002) as well as of eosinophils (p less than 0.001). However, there were no significant differences when pre- and postdiet values were compared. Hence, we conclude that dietary fish oil supplementation does not inhibit the cutaneous LPR clinically or histologically.

Adult↗
PubMed1992

Urinary leukotriene E4 in bronchial asthma.

Leukotriene E4 (LTE4) is excreted into the urine in a relatively constant proportion of 4-7% when either leukotriene C4 (LTC4) or LTE4 is intravenously infused, regardless of the magnitude of the infused dose. Measurement of LTE4 in urine is, therefore, a convenient and non-invasive method for assessing changes in the rate of total body sulphidopeptide leukotriene production. We assayed urinary LTE4 in 17 normal subjects, 31 subjects with asthma without aspirin sensitivity, and 10 aspirin-sensitive subjects. The relationship between urinary LTE4 and nonspecific bronchial hyperresponsiveness, as assessed by the provocative dose producing a 20% fall in forced expiratory volume in one second (PD20) to inhaled histamine, was examined in 19 non-aspirin-sensitive asthmatic subjects. The urinary LTE4 values were log-normally distributed. Urinary LTE4 was detected in 28 of the 31 non-aspirin-sensitive asthmatic subjects, and the geometric mean (95% confidence interval (CI) of 43 (32-57) pg.mg-1 creatinine was no different to that of 34 (25-48) pg.mg-1 creatinine measured in the normal subjects. The geometric mean of 101 (55-186) pg.mg-1 creatinine measured in the aspirin-sensitive asthmatics was significantly higher than that measured in the normal subjects (p less than 0.005) and in the asthmatic subjects who were non-aspirin-sensitive (p less than 0.002), but there was considerable overlap between the three groups. There was no relationship between urinary LTE4 and PD20, or between urinary LTE4 and baseline forced expiratory volume in one second (FEV1) (% predicted). Thus, measurement of LTE4 in a single sample of urine will not predict the extent of bronchial hyperresponsiveness or degree of airflow obstruction.

Adult↗
PubMedDate not supplied

Leukotrienes, fish-oil, and asthma.

Studies suggest that leukotrienes which have been metabolized from arachidonic acid released from membranes phospholipids during cell activation may play a significant role in a variety of inflammatory disorders including the pathophysiology of chronic allergic asthma. Two major types of polyunsaturated fatty acids prominent in marine fish oils are eicosapentaenoic acid (EPA) and docosahexaenoic acid (DCHA). These fish oils limit leukotriene synthesis and biological activities by substituting substrate fatty acids as alternatives to arachidonic acid. Both EPA and DCHA inhibit the conversion of arachidonic acid by the cyclooxygenase pathway to prostanoid metabolites and reduce the production of platelet-activating factor (PAF).

Animals↗