Relevant bibliographies by topics / ST2 expression in asthma

Academic literature on the topic 'ST2 expression in asthma'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "ST2 expression in asthma"

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Ramirez-Carrozzi, Vladimir, Amy Dressen, Patrick Lupardus, Brian Yaspan, and Rajita Pappu. "Functional analysis of protective IL1RL1 variants associated with asthma risk (CCR6P.215)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 187.2. http://dx.doi.org/10.4049/jimmunol.194.supp.187.2.

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Abstract GWAS studies have identified polymorphisms in both IL33 and IL1RL1, the gene encoding ST2, the high affinity chain of the IL-33 receptor, that associate with asthma susceptibility. We identified amino acid changing variants in IL1RL1 associating with asthma incidence and found these SNPs to be protective from asthma risk in our study population. These variants result in coding changes to the intracellular region of ST2, which contains the TIR domain of the receptor that is critical for signaling downstream of IL-1 cytokine family and TLRs. Mutations or deletions to this region can inhibit ligand-induced responses. IL-33-mediated dimerization of ST2 and IL-1RAcP promotes TIR-TIR domain interaction and recruitment of the adaptor molecule MyD88 leading to AP-1 and NF-kB activation. IL-33 responses were diminished in cell lines expressing all 4 IL1RL1 missense variants. To further elucidate how this haplotype could affect IL-33 activity, we compared IL-33 activity and ST2 expression between donors carrying either haplotype. We observed reduced IL-33 mediated IL-8 secretion from purified blood eosinophils derived from individuals carrying the protective haplotype. We also observed greater soluble ST2 expression in these individuals. Our results provide a link between the genetic predisposition to asthma and IL-33 mediated responses. Given IL-33 promotes Th2 immunity, perturbations that diminish this response may provide protection from asthma risk.
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Kaur, Davinder, Latifa Chachi, Edith Gomez, Nicolas Sylvius, Shailendra R. Singh, Mohammadali Y. Ramsheh, Ruth Saunders, and Christopher E. Brightling. "ST2 expression and release by the bronchial epithelium is downregulated in asthma." Allergy 75, no. 12 (July 27, 2020): 3184–94. http://dx.doi.org/10.1111/all.14436.

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Taruselli, Marcela T., Amina Abdul Qayum, and John J. Ryan. "MicroRNA-146a is a negative regulator of IL-33 stimulated mouse mast cells." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 105.16. http://dx.doi.org/10.4049/jimmunol.200.supp.105.16.

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Abstract Interleukin 33 (IL-33) is an inflammatory cytokine that promotes allergic disease by activating ILC2, Th2 cells, and mast cells. IL-33 is increased in asthmatics, and its blockade suppresses asthma-like inflammation in mouse models. The IL-33 receptor, ST2, shares signaling cascades with the TLR family, but homeostatic control of ST2 function is poorly understood. MicroRNA-146a (miR-146a) is induced by LPS and suppresses TLR4 signaling in macrophages. Therefore, we explored whether miR-146a has a role in IL-33 signaling. IL-33 induced cellular and exosomal miR-146a expression in mouse bone marrow derived mast cells (BMMC). Induction required MyD88, Akt, and NFκB, since antagonizing these pathways decreased miR-146 expression. BMMC transfected with a miR-146a antagomir or derived from miR-146a KO mice showed enhanced cytokine expression in response to IL-33, suggesting that mir46a is a negative regulator of IL-33-ST2 signaling. Our data further suggest that miR-146a may act by targeting IRAK proteins, because mir146a KO BMMC have increased IRAK1 and IRAK4 expression. These results support the hypothesis that miR-146a is a feedback regulator of IL-33-mediated mast cell functions associated with allergic disease.
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Kee, Sydney Ann, Marcela T. Taruselli, John J. Ryan, and Amina Abdul Qayum. "MiR-146a is a negative regulator of IL-33-stimulated mouse mast cells." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 185.5. http://dx.doi.org/10.4049/jimmunol.202.supp.185.5.

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Abstract Interleukin-33 (IL-33) is an inflammatory cytokine that promotes allergic disease by activating ILC2, Th2, and mast cells. IL-33 is increased in asthmatics, and its blockade suppresses asthma-like inflammation in mouse models. The IL-33 receptor, ST2, shares signaling cascades with the TLR family, but homeostatic control of ST2 function is poorly understood. MicroRNA-146a (miR-146a) is induced by LPS and suppresses TLR4 signaling in macrophages. Therefore, we explored whether miR-146a has a role in IL-33 signaling. IL-33 induced cellular and exosomal miR-146a expression in mouse bone marrow derived mast cells (BMMC). Induction required MyD88, Akt, and NFkB, since antagonizing these pathways decreased miR-146 expression. BMMC transfected with a miR-146a antagomir or derived from miR-146a KO mice showed enhanced cytokine expression in response to IL-33, suggesting that miR-146a is a negative regulator of IL-33-ST2 signaling. Our data further suggest that miR-146a may act by targeting IRAK proteins, because mir-146a KO BMMC have increased TRAF6, IRAK1, and IRAK4 expression. In vivo, miR-146a expression in plasma exosomes was elevated after intraperitoneal injection of IL-33. Also mast cell deficient c-Kitw-sh mice acutely reconstituted with miR-146a KO BMMC intraperitoneally had elevated plasma IL-6 levels in comparison to their WT counterparts after IL-33 challenge. These results support the hypothesis that miR-146a is a feedback regulator of IL-33-mediated mast cell functions associated with allergic disease.
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Johnston, Laura K., Chia-Lin Hsu, Rebecca A. Krier-Burris, Krishan D. Chhiba, Karen B. Chien, Andrew McKenzie, Sergejs Berdnikovs, and Paul J. Bryce. "Eosinophil lineage commitment and IL-5-dependent expansion is regulated by IL-33 in mice." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 191.7. http://dx.doi.org/10.4049/jimmunol.196.supp.191.7.

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Abstract Eosinophils are important in the pathogenesis of many diseases, including asthma, eosinophilic esophagitis and eczema. While IL-5 is necessary for the maturation of eosinophil progenitors (EoP) into mature eosinophils (EoM), the signals that promote commitment to the eosinophil lineage are unknown. The IL-33 receptor, ST2, is expressed on several inflammatory cells, including eosinophils, and is best characterized for its role during the initiation of allergic responses in the peripheral tissues. Recently, ST2 expression was described on hematopoietic stem cells, where its function remains unclear. Here, we sought to determine whether IL-33 and ST2 contribute to hematopoietic lineage decisions. We found that both IL-33- and ST2-deficient mice exhibited diminished peripheral blood eosinophils at baseline. Correspondingly, IL-33 administration increased EoM as well as IL-5 in the blood and bone marrow in WT and IL-33-deficient but not ST2-deficient mice. Blocking IL-5 with a neutralizing antibody prevented IL-33-expanded EoP from maturing into EoM, while transgenic overexpression of IL-5 in ST2-deficient mice resulted in significantly lower hypereosinophilia than transgenic IL-5 mice. Finally, we observed that IL-33, but not IL-5, specifically expanded EoP and upregulated IL-5Rα on EoP as well as increased IL-5 after bone marrow was cultured for three days. Our findings identify a basal defect in eosinophilopoiesis in IL-33- and ST2-deficient mice. Furthermore, we establish unappreciated roles for IL-33 and ST2 in eosinophil development via progenitor regulation and define a mechanism whereby IL-33 licenses commitment into the eosinophil lineage by driving both responsiveness to IL-5 and IL-5 production.
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Paplinska-Goryca, Magdalena, Paulina Misiukiewicz-Stepien, Malgorzata Proboszcz, Patrycja Nejman-Gryz, Katarzyna Gorska, and Rafal Krenke. "The Expressions of TSLP, IL-33, and IL-17A in Monocyte Derived Dendritic Cells from Asthma and COPD Patients are Related to Epithelial–Macrophage Interactions." Cells 9, no. 9 (August 22, 2020): 1944. http://dx.doi.org/10.3390/cells9091944.

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Background. The cross-talk between the external and internal environment in the respiratory tract involves macrophage/dendritic cell (DC) transepithelial network. Epithelium triggers dendritic cell-mediated inflammation by producing thymic stromal lymphopoietin (TSLP), IL-33, and IL-17A. The study aimed to evaluate the expression of TSLP, IL-33, and IL-17A in human monocyte derived dendritic cells (moDCs) co-cultured with respiratory epithelium and monocyte derived macrophages (moMφs) in asthma, chronic obstructive pulmonary disease (COPD) and healthy controls. Methods. The study used a triple-cell co-culture model, utilizing nasal epithelial cells, along with moMφs and moDCs. Cells were cultured in mono-, di-, and triple-co-cultures for 24 h. Results. Co-culture with epithelium and moMφs significantly increased TSLP in asthma and did not change IL-33 and IL-17A mRNA expression in moDCs. moDCs from asthmatics were characterized by the highest TSLP mRNA expression and the richest population of TSLPR, ST2, and IL17RA expressed cells. A high number of positive correlations between the assessed cytokines and CHI3L1, IL-12p40, IL-1β, IL-6, IL-8, TNF in moDCs was observed in asthma and COPD. Conclusion. TSLP, IL-33, and IL-17A expression in moDCs are differently regulated by epithelium in asthma, COPD, and healthy subjects. These complex cell–cell interactions may impact airway inflammation and be an important factor in the pathobiology of asthma and COPD.
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Boberg, Emma, Kristina Johansson, Carina Malmhäll, Julie Weidner, and Madeleine Rådinger. "House Dust Mite Induces Bone Marrow IL-33-Responsive ILC2s and TH Cells." International Journal of Molecular Sciences 21, no. 11 (May 26, 2020): 3751. http://dx.doi.org/10.3390/ijms21113751.

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Type 2 innate lymphoid cells (ILC2s) and their adaptive counterpart type 2 T helper (TH2) cells respond to interleukin-33 (IL-33) by producing IL-5, which is a crucial cytokine for eosinophil development in the bone marrow. The aim of this study was to determine if bone marrow ILC2s, TH cells, and eosinophils are locally regulated by IL-33 in terms of number and activation upon exposure to the common aeroallergen house dust mite (HDM). Mice that were sensitized and challenged with HDM by intranasal exposures induced eosinophil development in the bone marrow with an initial increase of IL5Rα+ eosinophil progenitors, following elevated numbers of mature eosinophils and the induction of airway eosinophilia. Bone marrow ILC2s, TH2, and eosinophils all responded to HDM challenge by increased IL-33 receptor (ST2) expression. However, only ILC2s, but not TH cells, revealed increased ST2 expression at the onset of eosinophil development, which significantly correlated with the number of eosinophil progenitors. In summary, our findings suggest that airway allergen challenges with HDM activates IL-33-responsive ILC2s, TH cells, and eosinophils locally in the bone marrow. Targeting the IL-33/ST2 axis in allergic diseases including asthma may be beneficial by decreasing eosinophil production in the bone marrow.
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Ota, Kyoko, Mio Kawaguchi, Satoshi Matsukura, Masatsugu Kurokawa, Fumio Kokubu, Junichi Fujita, Yuko Morishima, et al. "Potential Involvement of IL-17F in Asthma." Journal of Immunology Research 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/602846.

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The expression of IL-17F is seen in the airway of asthmatics and its level is correlated with disease severity. Several studies have demonstrated that IL-17F plays a pivotal role in allergic airway inflammation and induces several asthma-related molecules such as CCL20. IL-17F-induced CCL20 may attract Th17 cells into the airway resulting in the recruitment of additional Th17 cells to enhance allergic airway inflammation. We have recently identified, for the first time, that bronchial epithelial cells are its novel cell source in response to IL-33 via ST2-ERK1/2-MSK1 signaling pathway. The receptor for IL-17F is the heterodimeric complex of IL-17RA and IL-17RC, and IL-17F activates many signaling pathways. In a case-control study of 867 unrelated Japanese subjects, a His161 to Arg161 (H161R) substitution in the third exon of the IL-17F gene was associated with asthma. In atopic patients with asthma, prebronchodilator baseline FEV1/FVC values showed a significant association with the H161R variant. Moreover, this variant is a natural antagonist for the wild-type IL-17F. Moreover, IL-17F is involved in airway remodeling and steroid resistance. Hence, IL-17F may play an orchestrating role in the pathogenesis of asthma and may provide a valuable therapeutic target for development of novel strategies.
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Ferrini, Maria M., Zeina Jaffar, and Kevan Roberts. "Critical role for IL-33 in orchestrating group 2 innate lymphoid cell and natural killer cell function in the lungs." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 119.28. http://dx.doi.org/10.4049/jimmunol.202.supp.119.28.

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Abstract The alarmin, IL-33, acting via ST2 receptors initiates innate immunity to inhaled allergens and environmental particulates. IL-33 belongs to the IL-1 family and is largely derived from epithelial cells, endothelial cells and fibroblasts. The cytokine plays a critical role in underpinning type 2 immunity at mucosal sites and the IL-33/ST2 axis has been implicated in bronchial asthma and virus-induced exacerbations of allergic airway disease. In this study, we found that IL-33 instillations into the airways of C57BL/6 mice, for 3 days over a 7 day period, induced a marked increase in the number of group 2 innate lymphoid cells (ILC2s) and their production of type 2 cytokines IL-13 and IL-5 and this was associated with a pronounced pulmonary eosinophilic inflammation and airway mucus production. Interestingly, IL-33 administration also resulted in an increase in the number of CD11b+CD11C+MHCII+ dendritic cells and evoked a marked expansion of Th2 cells in the lung mucosa. Concomitant with this response, there was a significant reduction in IFN-γ production by pulmonary CD3−CD19−DX5+NK1.1+ NK cells. Flow cytometry revealed that ST2 expression was predominantly expressed by pulmonary ILC2s rather than NK cells, raising the possibility that ILC2s, either directly or indirectly, regulate the NK cell response. These findings reveal that IL-33 plays critical roles in both initiating pulmonary innate and adaptive immune responses, thus providing an essential axis for rapid immune responses and tissue homeostasis in the lung as well as influencing the development of chronic airway inflammation and remodeling.
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Bachert, Claus, Marc Humbert, Nicola A. Hanania, Nan Zhang, Stephen Holgate, Roland Buhl, and Barbara M. Bröker. "Staphylococcus aureus and its IgE-inducing enterotoxins in asthma: current knowledge." European Respiratory Journal 55, no. 4 (January 24, 2020): 1901592. http://dx.doi.org/10.1183/13993003.01592-2019.

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While immunoglobulin (Ig) E is a prominent biomarker for early-onset, its levels are often elevated in non-allergic late-onset asthma. However, the pattern of IgE expression in the latter is mostly polyclonal, with specific IgEs low or below detection level albeit with an increased total IgE. In late-onset severe asthma patients, specific IgE to Staphylococcal enterotoxins (se-IgE) can frequently be detected in serum, and has been associated with asthma, with severe asthma defined by hospitalisations, oral steroid use and decrease in lung function. Recently, se-IgE was demonstrated to even predict the development into severe asthma with exacerbations over the next decade. Staphylococcus aureus manipulates the airway mucosal immunology at various levels via its proteins, including superantigens, serine-protease-like proteins (Spls), or protein A (SpA) and possibly others. Release of IL-33 from respiratory epithelium and activation of innate lymphoid cells (ILCs) via its receptor ST2, type 2 cytokine release from those ILCs and T helper (Th) 2 cells, mast cell degranulation, massive local B-cell activation and IgE formation, and finally eosinophil attraction with consequent release of extracellular traps, adding to the epithelial damage and contributing to disease persistence via formation of Charcot–Leyden crystals are the most prominent hallmarks of the manipulation of the mucosal immunity by S. aureus. In summary, S. aureus claims a prominent role in the orchestration of severe airway inflammation and in current and future disease severity. In this review, we discuss current knowledge in this field and outline the needs for future research to fully understand the impact of S. aureus and its proteins on asthma.
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Dissertations / Theses on the topic "ST2 expression in asthma"

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Bradding, Peter. "Cytokine expression in allergic mucosal inflammation." Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295929.

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Osman, Mustafa. "The expression of asthma in relation to sex and sex steroids from birth to adulthood." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2008. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25474.

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Stinson, Sally Elizabeth. "Exploring the expression and function of CRTh2 in asthma." Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/31996.

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CRTh2 (DP2) is implicated in the pathogenesis of asthma; however, currently there is a lack of data describing the protein expression of CRTh2 in bronchial biopsies in asthma. This has limited the cell types that CRTh2 function has been explored within. A thorough understanding of CRTh2 expression within the airways and whether changes in receptor expression correlates with disease severity, may aid in the design of future CRTh2 antagonist clinical studies. This study aimed to investigate the expression of CRTh2 expression in bronchial biopsies of subjects with asthma and healthy controls. The novel finding that CRTh2 was expressed on bronchial epithelial cells in asthma prompted further investigation into the expression and activation of CRTh2 on bronchial epithelial cells in vitro, using the selective CRTh2 agonist 13, 14-dihydro-15-keto prostaglandin D2 (DK-PGD2) and the CRTh2 selective antagonist AZD6430. This study is the first to describe differential CRTh2 expression within bronchial tissue in asthma compared to healthy controls. The number of sub-mucosal CRTh2+ cells was found to be increased in asthma compared to healthy controls. CRTh2 was found to be expressed on the bronchial epithelium and its expression was decreased in asthma compared to healthy controls with similar differences observed in vitro by primary epithelial cells. Squamous metaplasia of the bronchial epithelium was increased in asthma and related to decreased CRTh2 expression. DK-PGD2 promoted epithelial cell migration, and in air-liquid interface cultures increased the number of MUC5AC+ and involucrin+ cells, which were blocked with the CRTh2 antagonist, AZD6430. This study describes the novel findings that CRTh2 is expressed by the bronchial epithelium in both health and asthma, and its activation drives epithelial differentiation. These data suggests that CRTh2 could contribute to airway remodelling in asthma and this information may contribute to the understanding of the effects of CRTh2 antagonists in asthmatic patients.
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Seymour, Michelle L. "Expression of eicosanoid pathway enzymes in inflammatory cells." Thesis, University of Southampton, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310699.

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Kuitert, Lieske Meta Elizabeth. "Eicosanoid synthetic enzymes : aspects of regulation and expression in asthma." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248441.

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Konstantinidis, Athanasios. "Genetics and airway expression of interleukin-13 receptors in asthma." Thesis, University of Southampton, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418599.

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Cowburn, Andrew Stephen. "Regulation of eicosanoid enzyme expression in inflammatory leukocytes in asthma." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266655.

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Lacson, Ronilda, Michael Mbagwu, Hisham Yousif, and Lucila Ohno-Machado. "Assessing the quality of annotations in asthma gene expression experiments." BioMed Central, 2010. http://hdl.handle.net/10150/610165.

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BACKGROUND:The amount of data deposited in the Gene Expression Omnibus (GEO) has expanded significantly. It is important to ensure that these data are properly annotated with clinical data and descriptions of experimental conditions so that they can be useful for future analysis. This study assesses the adequacy of documented asthma markers in GEO. Three objective measures (coverage, consistency and association) were used for evaluation of annotations contained in 17 asthma studies.RESULTS:There were 918 asthma samples with 20,640 annotated markers. Of these markers, only 10,419 had documented values (50% coverage). In one study carefully examined for consistency, there were discrepancies in drug name usage, with brand name and generic name used in different sections to refer to the same drug. Annotated markers showed adequate association with other relevant variables (i.e. the use of medication only when its corresponding disease state was present).CONCLUSIONS:There is inadequate variable coverage within GEO and usage of terms lacks consistency. Association between relevant variables, however, was adequate.
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Tuttle, Camilla Susannah Laura. "The expression of HAT and HDAC enzymes in asthma airways." Thesis, Queensland University of Technology, 2013. https://eprints.qut.edu.au/62873/1/Camilla_Tuttle_Thesis.pdf.

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Asthma is chronic inflammatory disease of the lower airways that is both, genetically inherited and environmentally influenced. This project investigated how molecular mechanisms known to be influenced both genetically and environmentally, contribute to the onset of asthma.
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Hillaby, Caroline Wendy. "Expression of phosphodiesterase isoenzymes in inflammatory cells in allergic airway disease." Thesis, University of Southampton, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370062.

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Books on the topic "ST2 expression in asthma"

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(Editor), Duncan F. Rogers, and Louise E. Donnelly (Editor), eds. Human Airway Inflammation: Sampling Techniques and Analytical Protocols (Methods in Molecular Medicine). Humana Press, 2001.

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Book chapters on the topic "ST2 expression in asthma"

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Corrigan, C. J. "Cytokine Expression in Asthma." In Molecular Biology of the Lung, 85–99. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8784-7_5.

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Sordillo, Joanne, and Benjamin A. Raby. "Gene Expression Profiling in Asthma." In Heterogeneity in Asthma, 157–81. Boston, MA: Springer US, 2013. http://dx.doi.org/10.1007/978-1-4614-8603-9_10.

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Izuhara, Kenji, Sachiko Kanaji, Shoichiro Ohta, Hiroshi Shiraishi, Kazuhiko Arima, and Noriko Yuyama. "Gene expression patterns in asthma." In Microarrays in Inflammation, 107–14. Basel: Birkhäuser Basel, 2008. http://dx.doi.org/10.1007/978-3-7643-8334-3_10.

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Schmidt-Weber, Carsten B. "Gene Expression Profiling in Allergy and Asthma." In Allergy and Asthma in Modern Society: A Scientific Approach, 188–94. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000090281.

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Ying, S. "C-C Chemokine Expression in Atopic and Nonatopic Asthma." In Immunological Mechanisms in Asthma and Allergic Diseases, 178–88. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000058826.

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San Segundo-Val, Ignacio, Virginia García-Solaesa, and Asunción García-Sánchez. "Real-Time PCR for Gene Expression Quantification in Asthma." In Methods in Molecular Biology, 45–55. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3652-6_4.

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Mori, Akio, Matsunobu Suko, Osamu Kaminuma, Yoko Nishizaki, Toshifumi Nagahori, Tadashi Mikami, Takeo Ohmura, Akihiko Hosino, Yumiko Asakura, and Hirokazu Okudaira. "Enhanced Production and Gene Expression of IL-5 in Bronchial Asthma." In Advances in Experimental Medicine and Biology, 439–50. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5855-2_64.

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García-Sánchez, Asunción, and Fernando Marqués-García. "Review of Methods to Study Gene Expression Regulation Applied to Asthma." In Methods in Molecular Biology, 71–89. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3652-6_6.

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Paplińska-Goryca, Magdalena, Patrycja Nejman-Gryz, Katarzyna Górska, Katarzyna Białek-Gosk, Joanna Hermanowicz-Salamon, and Rafał Krenke. "Expression of Inflammatory Mediators in Induced Sputum: Comparative Study in Asthma and COPD." In Advances in Experimental Medicine and Biology, 101–12. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/5584_2016_165.

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San Segundo-Val, Ignacio, and Catalina S. Sanz-Lozano. "Validation of Reference Genes in mRNA Expression Analysis Applied to the Study of Asthma." In Methods in Molecular Biology, 57–69. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3652-6_5.

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Conference papers on the topic "ST2 expression in asthma"

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Gordon, Erin D., Margaret Solon, Prescott Woodruff, and John V. Fahy. "Dysregulation Of IL-33 And ST2 In Stable Asthma And Acute Asthma Exacerbations." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4269.

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Ravanetti, Lara, Annemiek Dijkhuis, Yanaika S. Sabogal Pineros, and Renè Lutter. "Targeting IL33-ST2 pathway in virus-induced exacerbation of experimental asthma." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa3632.

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Li, Hong, Qingyuan Chen, Ernst W. Spannhake, Viswanathan Natarajan, and Yutong Zhao. "Lysophosphatidic Acid Increases Soluble ST2 Expression And Secretion In Human Bronchial Epithelial Cells." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1403.

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Balitzer, Dana, Lan Tang, Rongrong Wu, Tyson Torres, Edwin Yoo, Adriano Chan, and Timothy D. Bigby. "T1/ST2 Expression Is Increased In Airway Epithelial Cells In A Mouse Ovalbumin Model." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5598.

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Pitman, NI, GE Murphy, P. Kewin, D. Xu, C. McSharry, NC Thomson, and MC Shepherd. "ST2 Gene-Deletion Attenuates Airways Inflammation and IgE Production in an Adjuvant-Free Model of Asthma." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2248.

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Riffo-Vasquez, Yanira, Varsha Kanabar-Raivadera, Valerie Corrigall, and Clive Page. "TNFAIP3/A20 expression in allergic asthma." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2372.

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Sanden, C., P. Siddhuraj, J. Jönsson, C. Lindö, J. Nys, D. Schofield, I. Scott, et al. "Altered Site-Specific Expression Patterns of Interleukin-33 and its Receptor ST2 in COPD Lungs." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.2119.

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Saferali, A., J. H. Yun, S. Lee, R. Chase, P. Castaldi, and C. P. Hersh. "Gene Expression Signature of Asthma COPD Overlap." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4555.

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Lau, JY, BG Oliver, M. Baraket, SD Wilton, C. Williams, JL Black, and JK Burgess. "Fibulin-1: Expression and Function in Asthma." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5144.

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Li, J., J. M. Magat, J. L. Thomas, and J. P. Dumouchel. "Endogenous IL-33 and Its Auto-Amplification of IL-33/ST2 Pathway Play an Important Role in Asthma." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2945.

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Reports on the topic "ST2 expression in asthma"

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Roman, Jesse. Prenatal Exposure to Nicotine and Childhood Asthma: Role of Nicotine Acetylcholine Receptors, Neuropeptides, and Fibronectin Expression in Lung. Fort Belvoir, VA: Defense Technical Information Center, December 2005. http://dx.doi.org/10.21236/ada452269.

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Roman, Jesse. Prenatal Exposure to Nicotine and Childhood Asthma: Role of Nicotine Acetylcholine Receptors, Neuropeptides and Fibronectin Expression in Lung. Fort Belvoir, VA: Defense Technical Information Center, December 2008. http://dx.doi.org/10.21236/ada508588.

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