Relevant bibliographies by topics / Atopy; Cytokines; Atopic

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Atopy; Cytokines; Atopic'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 February 2022

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Journal articles on the topic "Atopy; Cytokines; Atopic"

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Kazimirsky, A. N., J. M. Salmasi, G. V. Poryadin, O. A. Svitich, B. G. Bragvadze, A. A. Alekseeva, and L. V. Gankovskaya. "The role of epithelial cells in atopy pathogenesis." Bulletin of Siberian Medicine 18, no. 1 (May 16, 2019): 201–10. http://dx.doi.org/10.20538/1682-0363-2019-1-201-210.

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Aim. The study of the mechanisms of atopic disease formation and a model of immunopathogenesis of the atopic diseases.Methods. Determination of surface lymphocytes receptors in peripheral blood of atopic bronchial asthma and atopic dermatitis patients with the help of monoclonal antibodies using the indirect immunofluorescence method. Expression of genes encoding TLR2, TLR4 and TLR9 receptors of airborne epithelial cells by real-time polymerase chain reaction, as well as determination of cytokine TSLP, IL-33, IL-4 and TGFβ (eBioscience) in airway flushes in atopic asthma patients and healthy people.Results. During the exacerbation of atopic diseases in peripheral blood lymphocytes, an intensive activation process develops with impaired lymphocytes activating apoptosis aimed at the formation of plasma cells capable of developing intensive IgE synthesis. To search for signals that could explain the mechanism of rearrangement of the B-cell part of the immune system during atopy, the epithelium cells of the airways were examined in a group of patients with atopic asthma and found an increase in gene expression coding for TLR2, TLR4, TLR9 in 6, 3 and 2.5 times respectively. Along with increased expression of TLRs genes in patients with bronchial asthma, an increased content of TSLP and IL-33 cytokines secreted by epithelial cells of the airways was detected. These cytokines have an immunoregulatory action - their nearby antigen presenting functions format the Th2 type of immune response, promote the production of cytokines (IL-4, IL-9, IL-13) and cause the development of an allergic type of inflammation.Conclusion. We suppose that the main link in pathogenesis is a disruption of the interaction of TLRs with the corresponding ligands caused by spontaneous dimerization of TLRs under the malonic dialdehyde influence. The intake of slowly metabolized dimers of TLRs into epithelial cells is a signal for genome activation, which leads to the synthesis of allergic cytokines IL-33 and TSLP. Thus, the main immunopathogenesis pathway of atopic diseases is the pathological functional interaction between epithelial cells and peripheral blood B-lymphocytes.
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Brutsche, Martin H., Ingrid Carlen Brutsche, Peter Wood, Nesrin Mogulkoc, Adnan Custovic, Jim Egan, and Ashley Woodcock. "B-cell isotype control in atopy and asthma assessed with cDNA array technology." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 4 (April 1, 2001): L627—L637. http://dx.doi.org/10.1152/ajplung.2001.280.4.l627.

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B-cell isotype switching and the production of IgE is regulated by a variety of gene products through different mechanisms. A better understanding of these processes has the potential to identify markers of disease and new therapeutic targets. The aim of the study was to investigate human B-cell isotype control and IgE production in atopy and asthma with cDNA array technology. Eighteen atopic asthmatic, eight atopic nonasthmatic, and fourteen healthy control subjects were included. Peripheral blood mononuclear cells were separated by gradient centrifugation, mRNA was purified, and the reverse-transcribed probes were hybridized to cDNA membranes. Group differences were assessed with the Mann-Whitney U-test. Twenty-three of seventy-eight tested IgE-related genes had significantly altered expression in atopy and asthma compared with that in the healthy subjects. The differentially expressed genes include surface molecules involved in T- and B-cell interaction and activation, cytokines, intracellular signaling products, and transcription factors. In conclusion, both atopic nonasthmatic and atopic asthmatic individuals had activated proinflammatory pathways, a minimal requirement for B-cell isotype switching, and a clear net pro-IgE cytokine climate.
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Kruglova, L. S., and E. M. Gensler. "Atopic dermatitis: new horizons of therapy." Medical alphabet 1, no. 7 (March 5, 2019): 29–32. http://dx.doi.org/10.33667/2078-5631-2019-1-7(382)-29-32.

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Over the past decades, the first breakthrough milestone in the treatment of severe forms of atopic dermatitis (AD) has been targeted therapy aimed at inhibiting IL-4 and IL-13. This was made possible thanks to advances in the understanding of the pathogenesis of AD, the driver of which is the Th2-type immune response, which also underlies such manifestations of atopy as bronchial asthma, allergic rhinitis, and polynosis. In the case of the Th2-type immune response, cytokines IL-4 and IL-13 are secreted, which are the main promoters of the inflammatory response in AD. Inhibition of IL-4 and IL-13 leads to the prevention of inflammation and is an effective approach to therapy. The use of therapy aimed at inhibition of cytokines allows you to effectively cope with the manifestations of severe and moderately severe blood pressure.
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Ashwi, Shaima, Ahmad Alobaisy, Nawal Herzallah, Fatema Alwaheed, Ibtihal Hadi, Duaa Alabbas, Faisal Al-Rasheed, Nawaf Alshuraym, and Esra Alzein. "Atopic dermatitis in sickle cell children." International Journal Of Community Medicine And Public Health 5, no. 3 (February 24, 2018): 842. http://dx.doi.org/10.18203/2394-6040.ijcmph20180420.

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Sickle cell disease is an autosomal recessive disease characterized by recurrent vaso-occlusive events. Despite the genetic basis of its pathophysiology, recent researchers stated that it is an inflammatory immune-mediated disease where inflammation plays a crucial role in the initiation of adherence between sickle cells and vascular endothelial cells. Allergic, as well as infectious, inflammation is proposed to contribute to the initiation of vaso-occlusive events. Although several researchers reported an association between sickle cell disease and atopic conditions such as bronchial asthma and allergic rhino-conjunctivitis, few cases have reported an association between sickle cell disease and atopic dermatitis. Atopy was reported to be considerably linked to sickle cell disease for several reasons. Firstly, patients with sickle cell disease have higher IgE levels than the general population. Secondly, the mechanism of activation of molecular adhesion between endothelial and blood cells are similar between both sickle cell disease and atopic disease. Thirdly, the cytokines produced from platelet activation are the same cytokines that stimulate allergic inflammation in atopic diseases and promote adherence of sickle cells and endothelium in sickle cell disease. Lastly, sickle cell disease was reported to be associated with other atopic diseases.
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Smirnova, Galina I. "CURRENT CONCEPTS OF ATOPIC DERMATITIS IN CHILDREN: PROBLEMS AND PROSPECTS." Russian Pediatric Journal 20, no. 2 (April 30, 2019): 99–107. http://dx.doi.org/10.18821/1560-9561-2017-20-2-99-107.

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There are presented modern data describing the current understanding of the pathogenesis of atopic dermatitis (AD): a genetic predisposition to atopy, disruptions of epidermal barrier integrity and a cascade of immune responses, contributing allergic inflammation in the skin. There are both described several mechanisms of acute and chronic phases of AD, the main directions of pathogenetically substantiated treatment of AD in children and indicated the prospects of new preparations specific blockers of proinflammatory cytokines involved in the development of AD - crisaborole, apremilast, dupilumab, lebrikizumab, tralokinumab, tezepelumab. There is especially presented in details external therapy of atopic skin lesions in children with the use of means of modern dermatological cosmetics.
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Smirnova, G. I. "CURRENT CONCEPTS OF ATOPIC DERMATITIS IN CHILDREN: PROBLEMS AND PROSPECTS." Russian Journal of Allergy 14, no. 4-5 (December 15, 2017): 30–39. http://dx.doi.org/10.36691/rja292.

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Modern data describing the current understanding of the pathogenesis of atopic dermatitis (AD): a genetic predisposition to atopy, disturbances of the intestinal microbiome, disruptions of epidermal barrier integrity and a cascade of immune responses, contributing allergic inflammation in the skin are presented. There are both described several mechanisms of acute and chronic phases of AD, the main directions of pathogenetically substantiated treatment of AD in children and indicated the prospects of new preparations specific blockers of proinflammatory cytokines involved in the development of AD - crisaborole, dupilumab, apremilast et al. External therapy of atopic skin lesions in AD children with modern dermatological cosmetics is presented.
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Kay, A. B., S. Ying, V. Varney, M. Gaga, S. R. Durham, R. Moqbel, A. J. Wardlaw, and Q. Hamid. "Messenger RNA expression of the cytokine gene cluster, interleukin 3 (IL-3), IL-4, IL-5, and granulocyte/macrophage colony-stimulating factor, in allergen-induced late-phase cutaneous reactions in atopic subjects." Journal of Experimental Medicine 173, no. 3 (March 1, 1991): 775–78. http://dx.doi.org/10.1084/jem.173.3.775.

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Cryostat sections from skin biopsies from 24-h allergen-induced late-phase cutaneous reactions (LPR) in 14 human atopic subjects were hybridized with 35S-labeled RNA probes for a number of cytokines. mRNA was detected for interleukin 3 (IL-3) (8/14), IL-4 (10/14), IL-5 (11/14), and granulocyte/macrophage colony-stimulating factor (GM-CSF) (13/14). Only 5 of 14 gave hybridization signals for IL-2, and 0 of 14 for interferon gamma. Biopsies from diluent controls gave only occasional weak signals. These results suggest that cells infiltrating the site of the 24-h LPR transcribe mRNA for the IL-3, IL-4, IL-5, and GM-CSF gene cluster and support the hypothesis that atopy is associated with preferential activation of cells having a similar cytokine profile to the murine T helper type 2 subset.
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Teixeira, Renata, Gerson dos Santos Leite, Renata Gorjao, Patricia Palmeira, Cesar Santos, Raquel Zambonatto, Heloisa de Oliveira, Adriana Levada, Iara Fiks, and Celso Carvalho. "Immune and Inflammatory Response in Atopic Elite Endurance Athletes." International Journal of Sports Medicine 39, no. 09 (June 25, 2018): 720–25. http://dx.doi.org/10.1055/a-0633-9001.

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AbstractThe present study aimed to compare the immune and inflammatory responses between atopic (n=20) and non-atopic (n=39) elite endurance athletes. Fifty-nine elite runners and triathletes were assessed for the following measurements: Th1, Th2 and lymphocyte phenotyping and plasma levels of cortisol, chemokines, inflammatory cytokines and specific immunoglobulin E (IgE). Levels of salivary IgA, allergic symptoms and training data were also evaluated. No difference was observed in baseline lymphocyte levels. However, the Th1 lymphocytes of atopic athletes presented a lower response after activation. In contrast to this result, levels of salivary IgA and CXCL9 chemokine were higher in the atopic athletes. It was observed that the volume of training per week was linearly associated with Th1 levels, allergic symptoms and IgE levels. In addition, linear multiple regression analysis demonstrated that the volume of training was the only factor associated with allergic symptoms in atopic athletes (r=0.53; p=0.04). These results suggest that compared to non-atopic athletes, atopic athletes present a reduced Th1 response and higher levels of salivary IgA. Training volume is associated with the immune response and allergic symptoms, which suggests that they may play a role in the atopy in elite endurance athletes.
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Young, Sarah L., Mary A. Simon, Margaret A. Baird, Gerald W. Tannock, Rodrigo Bibiloni, Kate Spencely, Juliette M. Lane, et al. "Bifidobacterial Species Differentially Affect Expression of Cell Surface Markers and Cytokines of Dendritic Cells Harvested from Cord Blood." Clinical Diagnostic Laboratory Immunology 11, no. 4 (July 2004): 686–90. http://dx.doi.org/10.1128/cdli.11.4.686-690.2004.

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ABSTRACT The gut microbiota may be important in the postnatal development of the immune system and hence may influence the prevalence of atopic diseases. Bifidobacteria are the most numerous bacteria in the guts of infants, and the presence or absence of certain species could be important in determining the geographic incidence of atopic diseases. We compared the fecal populations of bifidobacteria from children aged 25 to 35 days in Ghana (which has a low prevalence of atopy), New Zealand, and the United Kingdom (high-prevalence countries). Natal origin influenced the detection of bifidobacterial species in that fecal samples from Ghana almost all contained Bifidobacterium infantis whereas those of the other children did not. Choosing species on the basis of our bacteriological results, we tested bifidobacterial preparations for their effects on cell surface markers and cytokine production by dendritic cells harvested from cord blood. Species-specific effects on the expression of the dendritic-cell activation marker CD83 and the production of interleukin-10 (IL-10) were observed. Whereas CD83 expression was increased and IL-10 production was induced by Bifidobacterium bifidum, Bifidobacterium longum, and Bifidobacterium pseudocatenulatum, B. infantis failed to produce these effects. We concluded that B. infantis does not trigger the activation of dendritic cells to the degree necessary to initiate an immune response but that B. bifidum, B. longum, and B. pseudocatenulatum induce a Th2-driven immune response. A hypothesis is presented to link our observations to the prevalence of atopic diseases in different countries.
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Elisyutina, O. G., M. N. Boldyreva, O. Yu Rebrova, and E. S. Fedenko. "AD endotypes evaluation with molecular-genetic analysis of local immune response." Russian Journal of Allergy 15, no. 6 (December 15, 2018): 33–44. http://dx.doi.org/10.36691/rja100.

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The basis for the development of atopic dermatitis (AD) is genetic predisposition, hypersensitivity to allergens, Th1/Th2 disbalance, increased degranulation of mast cells and antigen-presenting activity of Langerhans cells, as well as epidermal barrier dysfunction. Recently, genotypes, phenotypes and endotypes of AD, and biomarkers, which can be used to assess the effectiveness of therapy and to develop personalized approaches to the diagnosis, treatment and prognosis of the disease, have been actively studied. The aim of this study was to determine the endotypes of atopic dermatitis on the basis of molecular genetic study of cytokine gene expression in the skin of AD patients. Materials and methods. The study was performed as a «case-control», 90 AD patients and 30 healthy individuals without signs of atopy were included. The material for evaluation of cytokine gene expression was skin biopsy samples taken by punch biopsy. The level of gene expression was determined by real-time PCR with preliminary reverse transcription of mRNA of the corresponding genes («DNA-Technology», Moscow). The transcript levels of ILB, IL2, IL2r, IL4, IL5, IL6, IL7, IL8, IL10, IL12A, IL12B, IL15, IL17A, IL18, IL23, IL28, IL29, IFNy, TNF, TGFß, FOXP3 genes were studied. Results. Based on the molecular genetic study of the local immune response the following endotypes of AD were determined: endotype with predominance of Th1-type immune response (3% of patients); endotype with predominance of Th2-type immune response (3% of patients); mixed endotype with increased expression of IL2 (20% of patients); mixed endotype with reduced expression of IL10 (64% of patients); mixed endotype with increased expression of TGFß (9% of patients). Clinically significant biomarkers of inflammation in atopic dermatitis - decreased mRNA level of IL1ß gene expression and increased mRNA level of IL2R, IL4, IL5, IL6, IL8, IL10, IL12ß, IL23, IL29, IFNy and TGFß genes expression were determined in the skin of AD patients compared to healthy individuals. Conclusion. The use of molecular genetic method for evaluation of local immune response on the basis of cytokines gene expression measurement in the skin allows to identify the most significant biomarkers characterizing different endotypes of AD, and to determine the type of immune response in the individual patient.
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Dissertations / Theses on the topic "Atopy; Cytokines; Atopic"

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Zhang, Youming. "A genome-wide search for asthma-associated quantitative traits loci in a mouse model of allergic asthma." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312554.

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Böttcher, Malin, Jenny Bjurström, Xiaomei Mai, Lennart Nilsson, and Maria Jenmalm. "Allergen-induced cytokine secretion in atopic and non-atopic asthmatic children." Linköpings universitet, Pediatrik, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-26399.

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Atopic asthma is characterized by excessive T helper 2 (Th2)-like immunity to allergens in the bronchial mucosa. The Th2-cytokine interleukin (IL)-4 induces IgE production, while the Th2-cytokine IL-5 promotes eosinophilic inflammation in the airways of asthmatics. Most asthmatics are atopic, but a subgroup is non-atopic. We hypothesize that allergen-induced Th2, particularly IL-5, responses can be observed in peripheral blood in both atopic and non-atopic asthmatic children but not in healthy control children. The aim of the present study was to determine IL-4, IL-5, IL-9, IL-10, IL-13 and IFN-γ secretion induced from peripheral blood mononuclear cells (PBMC) by a broad panel of inhalant allergens (timothy, cat, birch, dog and house dust mite) in asthmatic children with and without sensitization. The study included 13 atopic asthmatic, 5 non-atopic asthmatic, and 12 non-atopic non-asthmatic children. PBMC were stimulated with allergens and cytokine production was measured with enzyme-linked immunosorbent assay (ELISA). Higher levels of cat and dog antigen-induced IL-5 release were more commonly observed in both atopic and non-atopic asthmatics than in controls. Children with atopic, but not non-atopic, asthma produced higher levels of allergen-induced IL-4 and IL-9 than controls. Non-atopic asthmatics produced more IL-10 than atopic asthmatics after cat stimulation. High levels of eosinophilia-associated IL-5 responses are induced by cat and dog allergen in both atopic and non-atopic asthmatic children. The Th2 cytokines IL-4 and IL-9 were associated only with atopic asthma, probably due to their IgE-inducing properties.
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Parry, Robin Geoffrey. "Cytokines in minimal change nephropathy." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341511.

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Larsson, Anna-Karin. "Early life cytokines, viral infections and IgE-mediated allergic disease." Doctoral thesis, Stockholm : Wenner-Gren Institute for Experimental Biology, Stockholm university, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-1224.

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Taylor, Rebecca Chantelle. "Effects of toll-like receptor 2 ligands on T-cell responses to mite allergen in humans." University of Western Australia. School of Paediatrics and Child Health, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0107.

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[Truncated abstract] The last few decades have witnessed an increase in the prevalence, morbidity and economic burden associated with asthma and allergic disease. This rising incidence cannot be completely explained by changes in genetic factors or by improvements in diagnostic procedures. Environmental factors, particularly those associated with a westernised lifestyle, are considered to be involved in this increase. In the late 1980’s Strachan was the first to link environmental factors with allergic disease, this theory became to be known as the ‘hygiene hypothesis’. This hypothesis links the “cleaner” more “healthy ” environment we now live in, with an increased risk of developing allergic disease. This effect is highlighted by studies linking farm and animal exposure (rich in microbial compounds) during early life with a decrease in allergic disease. Since then numerous studies have been undertaken to ascertain the factors present in the microbe rich environment, which elicit this protective effect. Many studies have revolved around endotoxin, however microbial components (mainly from Gram-positive bacteria) which signal through Toll-like receptor 2 (TLR2), have also shown that they can alter the allergic immune response. In mice models TLR2 has been shown to both exacerbate and inhibit allergic disease. The above research highlights the need for further studies into the effect of TLR2 ligands, and to define the mechanisms by which they exert their effects in human allergic disease. These mechanisms will be relevant to understanding the pathogenesis of allergy, but also might provide novel ways to treat allergy. The aims of the study outlined in this thesis were to determine whether in vitro exposure to TLR2 ligands could modify the established immune response to house dust mite allergen (HDM), and to examine the mechanisms by which this occurs. ... The addition of glucocorticoids to LTA enhanced the ability of this TLR2 ligand to inhibit IL-5 and IL-13 production by HDM-activated blood mononuclear cells. In conclusion, this study shows that TLR2 ligands have the ability to inhibit the Th2 response to mite allergen in previously sensitized individuals by an as yet unknown mechanism. However the findings described herein do provide an impetus for future studies designed to uncover novel mechanisms by which allergic responses can be ameliorated, and may open new treatment modalities.
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Faria, Camila Domingues de Oliveira. "Avaliação do uso de células-tronco mesenquimais nos lipídeos epidérmicos e na resposta inflamatória da dermatite atópica canina pela técnica de imunoistoquímica." Botucatu, 2019. http://hdl.handle.net/11449/191173.

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Orientador: Luiz Henrique de Araújo Machado
Resumo: A dermatite atópica canina é uma importante alergopatia de ordem genética, inflamatória, pruriginosa e crônica. Os tratamentos existentes atualmente são sintomáticos, algumas vezes insatisfatórios no controle da doença e passíveis de efeitos colaterais. As células-tronco mesenquimais (CTM), pelas suas propriedades imunomoduladores e anti-inflamatórias, podem ser uma alternativa no tratamento da dermatite atópica. Foi realizado um estudo longitudinal, duplo-cego, com período inicial de tratamento placebo com três aplicações quinzenais de soro fisiológico, com posterior aplicação de CTM heterólogas, derivadas de tecido adiposo, em seis cães com dermatite atópica, totalizando três aplicações quinzenais na dose de 5x106 células por animal. A escala visual de prurido esclarecido (EVPE), o escore de lesões cutâneas (CADESI-4), a resposta inflamatória cutânea pela análise das citocinas IL4, IL6, IL10, IL31 e TNF-alfa e da proteína filagrina pela técnica de imunoistoquímica e a avaliação dos lipídeos epidérmicos pela coloração de Sudam III foram comparadas entre o tratamento placebo e com as CTM. O tratamento com CTM foi benéfico para a melhora das manifestações clínicas nos animais com dermatite atópica, diminuindo de forma significativa o escore CADESI-4 e EVPE, com redução consistente de mais de 50% destes dois parâmetros ao final do tratamento com CTM. A melhora clínica evidente nos animais com DA tratados com terapia celular aliadas à baixa frequência de efeitos colaterais, sina... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: The atopic canine is an inflammatory allergic dermatitis frequent and important. The distinct treatment available is symptomatic, currently unsatisfactory in the control of the disease and susceptible to collateral effects. The mesenchymal Stem Cells (MSC) by their immunomodulators and anti-inflammatory characteristics can be an alternative in the treatment of the atopic dermatitis. A longitudinal study was performed, blind-double, with an initial period of placebo treatment within saline solution, after the application of 5x106 heterologous CTM, derived from adipose tissue, in six dogs with atopic dermatitis. Each treatment constituted of three applications in by-weekly intervals. The visual analog scale of pruritis, the score of skin lesions (CADESI-4), the skin inflammatory response and filaggrin through the immunohistochemistry technique and the evaluation of the skin lipids by the Sudam III coloration were compared between the placebo treatment and the CTM treatment. The treatment with CTM with the used protocol was beneficial to the improvement of the clinical responses of the animals with atopic dermatitis, decreasing significantly the CADESI-4 and EVDP score, with a significant reduction of more than 50% of these two parameters at the end of the treatment with CTM while compared to the placebo. The clinical improvement was evident in animals with DA treated with cellular therapy allied to the low frequency of the collateral effects, indicates that with CTM can be cons... (Complete abstract click electronic access below)
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Masekela, Refilwe. "Chronic inflammatory lung disease in human immunodeficiency virus (HIV)-infected children. Epidemiological considerations, aetiological determinants and the efficacy of low dose erythromycin in bronchiectasis." Thesis, University of Pretoria, 2012. http://hdl.handle.net/2263/24164.

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Human immunodeficiency virus (HIV) infection has reached epidemic proportions in South Africa. The availability of highly active anti-retroviral therapy (HAART) prolongs life in HIV-infected persons, who may subsequently present with chronic manifestations of HIV-infection. The respiratory morbidity attendant to HIV-infection, even in the presence of HAART is high, the aftermath of which is lung tissue destruction and bronchiectasis. As a consequence of the political decision not to offer HAART to HIV-infected children, a number of children in South Africa have been left with severe consequences of uncontrolled HIV-infection. Bronchiectasis is one of those and because children with this devastating condition were numerous in the Pretoria region, the author and her colleagues began a Chronic Lung Disease Clinic in that region. This prompted the idea of investigating both the epidemiological profiles of these children and an attempt to intervene with both standard bronchiectasis guideline care and the use of a form of therapy commonly employed in other forms of bronchiectasis. This thesis explores those ideas. Important new and novel findings that were consequent were; that bronchiectasis is diagnosed late in HIV-infected children at a mean age of 6.9 years. The predominant organisms cultured from the airways are Haemophilus influenzae and parainfluenzae in 49% of samples. Pseudomonas aeruginosa (PA), common in cystic fibrosis (CF)-bronchiectasis is an uncommon pathogen in HIV-related bronchiectasis; isolated in only 2% of specimens. Tuberculosis (TB), at least as reported, is a significant antecedent of bronchiectasis, reported in 48.5%of children. A further 21.2% of the patients had received more than two courses of anti-TB treatment. However, proof of TB infection has been lacking. Respiratory morbidity is significant with the mean forced expiratory flow in one second (FEV1) of 53%, in this cohort at the time of presentation. Thirty-six percent of all children were exposed to environmental tobacco smoke, although this was not correlated with disease severity or HIVdisease progression. There is elevation of immunoglobulins in HIV-related bronchiectasis, with a mean IgE of 79 kU/l. This was not, though, associated with HIV disease progression as previously described in adult studies, nor with the presence of allergic bronchopulmonary aspergillosis (ABPA). The elevation in IgE was also not associated with an elevation of T helper-2 mediated cytokines, confirming the lack of association with atopy. The predominant cytokine, identified is interleukin (IL)-8, both systemically and locally (in airway secretions). There was elevation of other T helper-1 driven cytokines, reflecting an ability to mediate adequate inflammatory responses, which was independent of the level of immunosuppression. With the presence of HAART, there was a decline in the pro-inflammatory cytokines over time, which may be attributed to the ongoing effect of HAART that ties in to, or goes beyond the restoration of T cell numbers. Soluble triggering receptor expressed on myeloid cells (sTREM), an innate immune marker, is elevated in children with HIV-related bronchiectasis when compared to a control group of children with cystic fibrosis-related bronchiectasis. sTREM is not associated with the presence of exacerbations and the level of immunosuppression. The use of an anti-inflammatory drug erythromycin also did not impact the sTREM values. There was also no relationship between sTREM and pro and antiinflammatory cytokines and chemokines. Fluorine-18-fluorodeoxyglucose positron emission tomography (18F-FDG PET) could not reliably predict the presence of pulmonary exacerbations. Its diagnostic value was limited to identifying disease activity in acute pneumonia. 18F-FDG PET also had no significant correlation with CRP, inflammatory cytokines or markers of HIV disease activity. In a randomised controlled trial of erythromycin, a cost-effective immunomodulatory drug, compared to placebo, erythromycin was ineffective in reducing the number of pulmonary exacerbations. Erythromycin also failed to demonstrate any effect on systemic and local pro- and anti-inflammatory cytokines/chemokines. With access to anti-retroviral therapy, airway clearance, nutritional rehabilitation and vigilant follow up there was an improvement in pulmonary function parameters and stability of the degree of bronchiectasis that we propose is probably in keeping with an organ system disease modifying effect that may be, an as yet, undefined and undescribed byproduct of HAART.
Thesis (PhD)--University of Pretoria, 2012.
Paediatrics and Child Health
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Book chapters on the topic "Atopy; Cytokines; Atopic"

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Akdis, C. A., M. Akdis, D. Simon, B. Dibbert, M. Weber, S. Gratzl, O. Kreyden, et al. "Role of T Cells and Cytokines in the Intrinsic Form of Atopic Dermatitis." In The Atopy Syndrome in the Third Millennium, 37–44. Basel: KARGER, 1999. http://dx.doi.org/10.1159/000060607.

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"Asthma and Atopy." In Cytokine Gene Polymorphisms in Multifactorial Conditions, 257–72. CRC Press, 2006. http://dx.doi.org/10.1201/9781420005325-24.

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Virta, Miia, Kati Adjers, Mikko Hurme, and Jussi Karjalainen. "Asthma and Atopy." In Cytokine Gene Polymorphisms in Multifactorial Conditions, 228–43. CRC Press, 2006. http://dx.doi.org/10.1201/9781420005325.ch16.

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Conference papers on the topic "Atopy; Cytokines; Atopic"

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Turner, Stephen, Danielle Spiteri, David Miller, Alison Scaife, Graham Devereux, and Garry Walsh. "Nasal airway epithelial cells cytokine responses in children stratified by asthma and atopy." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa4986.

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Manise, Maite, Gabi Holtappels, Florence Schleich, Claus Bachert, and Renaud Louis. "Sputum IgE And Cytokines In Asthma: Relationship With Disease Severity, Sputum Cellular Profile And Atopy." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4309.

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3

Chang, Daniel V., Edgar E. Sarria, Rita Mattiello, Christina J. Tiller, Jeffrey Kisling, Rebeka Tabbey, Zhangsheng Yu, Weiguo Yao, Mark H. Kaplan, and Robert S. Tepper. "Relationship Of Atopy, Airway Function, Exhaled Nitric Oxide And Cytokine Production Early In Life To Airway Function And Current Asthma At 5-Years Of Age." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2339.

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You might also be interested in the extended bibliographies on the topic 'Atopy; Cytokines; Atopic' for particular source types:
Journal articles
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