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Search Results: 1 - 10 of 974 matches for " interleukin-4 "
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Uric Acid; a Possible Mediator of the Adjuvant Effect of Alum in Mice Immunized with Ovalbumin  [PDF]
Nayla S. Al-Akl, Marita Chakhtoura, Natalie F. Kazzi, Julnar Usta, Camille A. Chamoun, Alexander M. Abdelnoor
World Journal of Vaccines (WJV) , 2011, DOI: 10.4236/wjv.2011.14015
Abstract: One proposed mechanism by which alum enhances an immune response is by its ability to induce an inflammatory response that results in the release of uric acid from necrotic cells. Uric acid is thought to be a mediator in enhancing the immune response. The aim of this study was to investigate the immunopotentiating effect of uric acid. Groups of BALB/c mice were injected intraperitoneally with ovalbumin, ovalbumin + alum, ovalbumin + uric acid, uric acid, alum, or allopurinol. Two other groups were pretreated with allopurinol and were given ovalbumin + alum, or ovalbumin + uric acid 24 hours later. An additional two groups served as controls. On days 4, 7 and 10 post-injection, the numbers of Interleukin 4(IL-4) and Interferon-γ (IFN-γ) secreting spleen cells were determined by the ELISPOT assay. Serum uric acid levels were determined using an autoanalyser and nitric oxide using the Greiss reagent. The groups that received alum + ovalbumin or uric acid + ovalbumin had the highest numbers of IL-4 and INF-γ secreting cells as compared to all the groups. Allopurinol administration one day prior to alum + ovalbumin or uric acid + ovalbumin resulted in a decrease in the number of IL-4 and INF-γ secreting cells when compared to alum+ ovalbumin or uric acid + ovalbumin allopurinol - untreated groups. Groups that received alum, alum + ovalbumin, uric acid, and uric acid + ovalbumin had high serum uric acid levels as compared to all the groups. All groups that received alum had the highest levels of nitric oxide when compared to the groups that were not given alum. In conclusion, it appears that uric acid might be a mediator in the adjuvant effect of alum.
Interleukin-4 production in BALB/c mice immunized with Anisakis simplex
Perteguer, María Jesús;Cuéllar, Carmen;
Memórias do Instituto Oswaldo Cruz , 2001, DOI: 10.1590/S0074-02762001000700016
Abstract: we investigated the interleukin (il-4) levels in balb/c mice immunized with anisakis extract in single or multiple doses and in mice orally infected with a larva. from animals immunized maximum responses were obtained with the multiple doses with an only il-4 peak. conversely, in the mice inoculated with a larva per os, the il-4 levels showed two peaks of different rates.
Interleukin-4 production in BALB/c mice immunized with Anisakis simplex
Perteguer María Jesús,Cuéllar Carmen
Memórias do Instituto Oswaldo Cruz , 2001,
Abstract: We investigated the interleukin (IL-4) levels in BALB/c mice immunized with Anisakis extract in single or multiple doses and in mice orally infected with a larva. From animals immunized maximum responses were obtained with the multiple doses with an only IL-4 peak. Conversely, in the mice inoculated with a larva per os, the IL-4 levels showed two peaks of different rates.
Clinical Investigation of the Role of Interleukin-4 and Interleukin-13 in the Evolution of Prostate Cancer
Robert Goldstein,Charles Hanley,Jonathan Morris,Declan Cahill,Ashish Chandra,Peter Harper,Simon Chowdhury,John Maher,Sophie Burbridge
Cancers , 2011, DOI: 10.3390/cancers3044281
Abstract: Prostate cancer is the most common cancer in men, both in the USA and Europe. Although incurable, metastatic disease can often be controlled for years with anti-androgen therapy. Once the disease becomes castrate resistant, the median survival is 18 months. There is growing evidence that the immune system, and in particular cytokines, play an important role in prostate cancer immunosurveillance and progression. Here, we have undertaken a clinical investigation of the role of two closely related cytokines, IL-4 and IL-13 in prostate cancer. In the largest series studied to date, we show that serum IL-4, but not IL-13 is significantly elevated in castrate resistant, compared to androgen sensitive disease. Notably however, serum IL-4 levels are also raised in patients with benign prostatic disease. Analysis of benign and malignant prostate tissue demonstrates that the source of IL-4 is epithelial cells rather than infiltrating leukocytes. Together, our data are consistent with a dual role for IL-4 in prostate cancer development. In benign disease, our data add to the evidence that IL-4 serves a protective role. By contrast, the data support a direct role for IL-4 in the progression of prostate cancer from androgen responsive, to advanced castrate-resistant disease.
Interleukin-4 receptor alpha gene variants and allergic disease
Ian P Hall
Respiratory Research , 2000, DOI: 10.1186/rr3
Abstract: Several genome-wide screens have now been performed in different populations, looking for susceptibility genes for asthma and allergic disease. In general, the results of these genome screens have been somewhat disappointing in that, although chromosomal regions showing linkage have been identified, the strength of linkage at any given site has been inconsistent. These data suggest that a number of genes of moderate effect rather than a small number of genes with marked effects contribute to the genetic basis of allergic disease.To try to dissect out the important candidate genes that contribute to the risk of developing asthma or its important sub-phenotypes, several groups have concentrated on strong candidate genes that map to known susceptibility loci for asthma and atopy. Several such candidates have been identified (Table 1), including the gene for interleukin-4 receptor α (IL-4Rα), which is situated on chromosome 16p and is known to contain a number of polymorphisms. The recent paper from Carole Ober and colleagues [1] provides important information on the potential relevance of IL-4Rα gene variants in determining the risk of developing atopic disease.The IL-4Rα subunit forms part of the signalling complex for IL-4 itself but also serves as the α chain of the IL-13 receptor. Both IL-4 and IL-13 themselves have been implicated as potential candidate genes in the development of asthma, both being present in the TH2 cytokine locus on chromosome 5q23-31 [2]. Both IL-4 and IL-13 have overlapping functions, including mediating isotype switching to IgE synthesis.Several previous studies have suggested association and/or linkage between IL-4Rα gene variants and allergic disease, although not all studies have been positive. Mitsuyasu et al [3] reported the Ile50 allele of the IL-4Rα to be associated with atopic asthma, whereas Kruse et al [4] reported an association between the Pro478 and Arg551 alleles and low IgE levels. Hershey et al [5] reported an association bet
The gene encoding interleukin-13: a susceptibility locus for asthma and related traits
Marsha Wills-Karp
Respiratory Research , 2000, DOI: 10.1186/rr7
Abstract: Asthma is a complex inflammatory lung disease controlled by both environmental and genetic factors. Although the exact genes controlling susceptibility to asthma have not been identified, several genome-wide searches have provided evidence for the linkage of asthma or asthma-related traits (serum IgE levels, skin test reactivity, bronchial hyper-responsiveness, blood eosinophils) to loci on multiple autosomal chromosomes [1,2,3,4,5,6]. Of particular interest is the 5q31-33 region, which contains the T helper type 2 (Th2) cytokine gene cluster [interleukin (IL)-4, IL-13, IL-5 and IL-9] and has been linked to asthma or related phenotypes in many studies [2,3,4,5,6,7,8]. In addition to the linkage data, many human and animal studies have implicated these cytokines, either individually or in concert, in the pathophysiology of asthma. Of the Th2 cytokines in this chromosomal region, IL-4 has been extensively studied because it is known to be important in the differentiation of T cells into Th2 cytokine-producing cells. A polymorphism has been identified in the promoter of this gene (-590C/T) [9] which was initially associated with elevated serum IgE levels. This polymorphism has been associated with asthma in some studies [10,11] but not in others [12,13,14]. Thus attention has turned to other genes in this region. Recent studies in animal models that support the dominance of the gene encoding IL-13, which resembles IL-4, in the allergic response have spurred an extensive study of this molecule in susceptibility to asthma [15,16,17].The gene encoding IL-13 is located only 25 kilobases upstream of the gene for IL-4 and in the same orientation, leading to the speculation that these genes arose as a duplication event during evolution. In addition to their structural similarities they share considerable functional similarities. They are both known to have a number of actions relevant to the asthmatic diathesis such as the regulation of isotype class switching in B cells to I
Interleukin-4 and interleukin-5 as targets for the inhibition of eosinophilic inflammation and allergic airways hyperreactivity
Foster, Paul S;Hogan, Simon P;Matthaei, Klaus I;Young, Ian G;
Memórias do Instituto Oswaldo Cruz , 1997, DOI: 10.1590/S0074-02761997000800009
Abstract: clinical and experimental investigations suggest that allergen-specific cd4+ t-cells, ige and the cytokines il-4 and il-5 play central roles in initiating and sustaining an asthmatic response by regulating the recruitment and/or activation of airways mast cells and eosinophils. il-5 plays a unique role in eosinophil development and activation and has been strongly implicated in the aetiology of asthma. the present paper summarizes our recent investigations on the role of these cytokines using cytokine knockout mice and a mouse aeroallergen model. investigations in il-5-/- mice indicate that this cytokine is critical for regulating aeroallergen-induced eosinophilia, the onset of lung damage and airways hyperreactivity during allergic airways inflammation. while il-4 and allergen-specific ige play important roles in the regulation of allergic disease, recent investigations in il4-/- mice suggest that allergic airways inflammation can occur via pathways which operate independently of these molecules. activation of these il-4 independent pathways are also intimately associated with cd4+ t-cells, il-5 signal transduction and eosinophilic inflammation. such il-5 regulated pathways may also play a substantive role in the aetiology of asthma. thus, evidence is now emerging that allergic airways disease is regulated by humoral and cell mediated processes. the central role of il-5 in both components of allergic disease highlights the requirements for highly specific therapeutic agents which inhibit the production or action of this cytokine.
Expresión de IL-10, IL-4 e IFN- γ en lesiones activas de piel en ni?os con urticaria papular por picadura de pulga
García,Elizabeth; Duarte,Silvia; Calderón,Camila; González,John Mario; Cuéllar,Adriana; Gómez,Alberto; Halpert,Evelyne; Rodríguez,Adriana;
Biomédica , 2011,
Abstract: introduction: papular urticaria caused by the bites of fleas traditionally has been defined as a chronic allergic disease. however, currently no clear relationship has been described between this pathology and common allergic diseases. objective: the expression of il-10, il-4 and ifn-γ as markers of effector t cell responses was examined in skin lesions of patients with papular urticaria by flea bite. materials and methods: fourteen skin lesion biopsies were sampled from children with a clinical diagnosis of papular urticaria by flea bite and were compared with 5 healthy skin biopsies of children with no history of the disease. all children were under 12 years old. rna was extracted with trizol and the expression levels of cytokines were analyzed by real time pcr technique. results: a wide range in the expression levels of ifn-γ and il-10 was noted as well as constant low values of il-4. three distinct profiles were observed, but which did not correspond to a recognizable pattern among the patients. the samples obtained from healthy tissues showed no expression of any of the cytokines. conclusions: this is the first characterization of cytokines that mediate the immune response at the site of the skin lesion in children with papular urticaria by flea bite. the data indicated that the local response was mixed and that a single phenotype is not predominant among the patients.
Interleukin-4 and interleukin-5 as targets for the inhibition of eosinophilic inflammation and allergic airways hyperreactivity
Foster Paul S,Hogan Simon P,Matthaei Klaus I,Young Ian G
Memórias do Instituto Oswaldo Cruz , 1997,
Abstract: Clinical and experimental investigations suggest that allergen-specific CD4+ T-cells, IgE and the cytokines IL-4 and IL-5 play central roles in initiating and sustaining an asthmatic response by regulating the recruitment and/or activation of airways mast cells and eosinophils. IL-5 plays a unique role in eosinophil development and activation and has been strongly implicated in the aetiology of asthma. The present paper summarizes our recent investigations on the role of these cytokines using cytokine knockout mice and a mouse aeroallergen model. Investigations in IL-5-/- mice indicate that this cytokine is critical for regulating aeroallergen-induced eosinophilia, the onset of lung damage and airways hyperreactivity during allergic airways inflammation. While IL-4 and allergen-specific IgE play important roles in the regulation of allergic disease, recent investigations in IL4-/- mice suggest that allergic airways inflammation can occur via pathways which operate independently of these molecules. Activation of these IL-4 independent pathways are also intimately associated with CD4+ T-cells, IL-5 signal transduction and eosinophilic inflammation. Such IL-5 regulated pathways may also play a substantive role in the aetiology of asthma. Thus, evidence is now emerging that allergic airways disease is regulated by humoral and cell mediated processes. The central role of IL-5 in both components of allergic disease highlights the requirements for highly specific therapeutic agents which inhibit the production or action of this cytokine.
Th-1 and Th-2 cytokine production in infants with virus-associated wheezing
Pitrez, P.M.C.;Machado, D.C.;Jones, M.H.;Andrade, F.;Camozzato, C.;Stein, R.T.;
Brazilian Journal of Medical and Biological Research , 2005, DOI: 10.1590/S0100-879X2005000100008
Abstract: wheezing associated with respiratory viral infections in infancy is very common and results in high morbidity worldwide. the th1/th2 pattern of immune response in these patients remains unclear and previous studies have shown controversial results. the aim of the present study was to compare the type of th1/th2 cytokine response between infants with acute bronchiolitis, recurrent wheezing and upper respiratory infections from a developing country. infants younger than 2 years of age admitted to hospital s?o lucas, porto alegre, rs, brazil, between may and november 2001, with an acute episode of wheezing associated with viral respiratory infection were selected. subjects with upper respiratory infections from the emergency department were selected for the control group. interferon-g (ifn-g) and interleukin-4 (il-4) levels from nasal aspirates were determined by elisa from peripheral mononuclear cell cultures. twenty-nine subjects with acute bronchiolitis, 18 with recurrent wheezing and 15 with upper respiratory infections were enrolled. there were no differences in family history of atopy or parental smoking between groups. oxygen requirement was similar for the acute bronchiolitis and recurrent wheezing groups. the percentage of positive tests for the cytokines studied and the ifn-g/il-4 ratio was similar for all groups. comparison of the polarized th1/th2 cytokine results for the various groups showed no specific pattern of cytokine production. infants with wheezing from a developing country do not show any specific predominant pattern of th1/th2 cytokine production, suggesting that multiple factors may be involved in the pathogenesis of this illness.
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