Bibliografie tematiche / Eotaxin

Letteratura scientifica selezionata sul tema "Eotaxin"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 28 gennaio 2023

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Articoli di riviste sul tema "Eotaxin"

1

Varlamov, E. E., T. V. Vinogradova, A. A. Chuslyaeva, T. S. Okuneva e A. N. Pampura. "BIOMARKERS ALLERGIC INFLAMATION AND SEVERITY OF ATOPIC DERMATITIS AT CHILDREN". Russian Journal of Allergy 9, n. 5 (15 dicembre 2012): 31–35. http://dx.doi.org/10.36691/rja694.

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Abstract (sommario):
Background.To establish the relationship between the serum concentrations of IL4, IL5, eotaxin, eotaxin2, ECP and the severity of atopic dermatitis in children. Methods. The study included 40 children with atopic dermatitis, patients were divided into two clusters with KMeans method, index SCORAD was taken as a criterion of clustering. All patients were conducted to determine the concentration of IL4, IL5, eotaxin, eotaxin2, ECP. Results. The SCORAD index was significantly higher in the second cluster in comparison to the first one. In second cluster the level of eotaxin2 was significantly higher, in terms of the ECP, IL4, IL5,eotaxin patient groups did not differ. The second cluster was characterized by patients with a concentration of IL5 of 1,5 p/ml. Conclusion. In assessing the severity of allergic inflammation in atopic dermatitis concentration of eotaxin2 was most informative.
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2

Badewa, A. P., C. E. Hudson e A. S. Heiman. "Regulatory Effects of Eotaxin, Eotaxin-2, and Eotaxin-3 on Eosinophil Degranulation and Superoxide Anion Generation1". Experimental Biology and Medicine 227, n. 8 (settembre 2002): 645–51. http://dx.doi.org/10.1177/153537020222700814.

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Abstract (sommario):
Eosinophilic leukocytes have been implicated as primary effector cells in inflammatory and allergic diseases. When activated by cytokines, human eosinophils secrete and produce a variety of proinflammatory or tissue damaging substances. Although well known for their chemoattractant effects, little is known about the precise contribution of the eosinophil-selective chemokines, eotaxin, eotaxin-2, and eotaxin-3 to the effector functions of eosinophils. This forms the central focus of these investigations for which clone 15-HL-60 human eosinophilic cells were used as the in vitro model. Investigation results suggest that all three subtypes of eotaxin directly stimulate eosinophil superoxide anion generation that is inhibited by neutralizing eotaxin antibody or pretreatment of cells with the receptor antibody anti-CCR3. Pretreatment or co-treatment with each of the eotaxins augmented phorbol myristate-induced superoxide generation. Concentration-dependent degranulation of eosinophil peroxidase was noted for all three chemokines, and potentiation of calcium lonophore-induced degranulation was observed with eotaxin pretreatments. Results of interleukin-5 pretreatment studies suggest that the eotaxin chemokines may act cooperatively to enhance effector functions of eosinophils. Collectively, the present studies have advanced knowledge of the eotaxin family of chemokines to include eosinophil priming and modulation of eosinophil activation and secretion effector functions.
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3

Haley, Kathleen J., Mary E. Sunday, Yolanda Porrata, Colleen Kelley, Anne Twomey, Aliakbar Shahsafaei, Benjamin Galper, Larry A. Sonna e Craig M. Lilly. "Ontogeny of the eotaxins in human lung". American Journal of Physiology-Lung Cellular and Molecular Physiology 294, n. 2 (febbraio 2008): L214—L224. http://dx.doi.org/10.1152/ajplung.00086.2007.

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Abstract (sommario):
The ontogeny of the C-C chemokines eotaxin-1, eotaxin-2, and eotaxin-3 has not been fully elucidated in human lung. We explored a possible role for eotaxin in developing lung by determining the ontogeny of eotaxin-1 (CCL11), eotaxin-2 (CCL24), eotaxin-3 (CCL26), and the eotaxin receptor, CCR3. We tested discarded surgical samples of developing human lung tissue using quantitative RT-PCR (QRT-PCR) and immunostaining for expression of CCL11, CCL24, CCL26, and CCR3. We assessed possible functionality of the eotaxin-CCR3 system by treating lung explant cultures with exogenous CCL11 and analyzing the cultures for evidence of changes in proliferation and activation of ERK1/2, a signaling pathway associated with CCR3. QRT-PCR analyses of 22 developing lung tissue samples with gestational ages 10–23 wk demonstrated that eotaxin-1 mRNA is most abundant in developing lung, whereas mRNAs for eotaxin-2 and eotaxin-3 are minimally detectable. CCL11 mRNA levels correlated with gestational age ( P < 0.05), and immunoreactivity was localized predominantly to airway epithelial cells. QRT-PCR analysis detected CCR3 expression in 16 of 19 developing lung samples. Supporting functional capacity in the immature lung, CCL11 treatment of lung explant cultures resulted in significantly increased ( P < 0.05) cell proliferation and activation of the ERK signaling pathway, which is downstream from CCR3, suggesting that proliferation was due to activation of CCR3 receptors by CCL11. We conclude that developing lung expresses the eotaxins and functional CCR3 receptor. CCL11 may promote airway epithelial proliferation in the developing lung.
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4

Varlamov, E. E., O. G. Elisyutina, T. V. Vinogradova, E. S. Fedenko e A. N. Pampura. "AGE-RELATED PATHOGENTIC SPECIFICITY OF CYTOKINE PROFILE IN ATOPIC DERMATITIS PATIENTS". Russian Journal of Allergy 13, n. 4-5 (15 dicembre 2016): 37–42. http://dx.doi.org/10.36691/rja358.

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Abstract (sommario):
Background. In this article the results of own research of the cytokine profile in atopic dermatitis (AD) adults and children depending on age are provided. Materials and methods. 88 patients with AD (54 children aged from 1 year to 16 years old and 24 adults aged from 21 years to 56 years old) were included in the study. Cytokine profile of a number of cytokines: IL-4, IL-5, IL-22, IL-31, IL-33, and transforming growth factor TGFβ1, eotaxin, eotaxin2 was examined. Results. Significant differences in IL-22, CC chemokines (eotaxin and eotaxin-2) and TGFβ levels depending on the age and severity of atopic dermatitis were found.
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5

Diny, Nicola, Xuezhou Hou, Jobert G. Barin, Monica V. Talor, Noel R. Rose e Daniela Cihakova. "The eotaxin-CCR3 pathway is required for eosinophil trafficking to the heart in eosinophilic myocarditis". Journal of Immunology 196, n. 1_Supplement (1 maggio 2016): 117.10. http://dx.doi.org/10.4049/jimmunol.196.supp.117.10.

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Abstract (sommario):
Abstract Cardiac manifestations are a major cause of morbidity and mortality in patients with eosinophil-associated diseases. Eosinophils have been proposed to play a pathologic role in the heart. Nevertheless, the pathways that recruit eosinophils to the heart have not been described. In IFNγ−/− IL-17A−/− mice, induction of experimental autoimmune myocarditis results in a Th-2-driven, eosinophilic inflammation. IFNγ−/− IL-17A−/− mice had much higher expression of the eosinophil-attracting chemokines eotaxin-1 (Ccl11) and eotaxin-2 (Ccl24) in the heart than wildtype mice. Genetic ablation of the eotaxin receptor CCR3 resulted in a dramatic decrease in heart infiltrating eosinophils. Adoptive transfer experiments with CCR3+/+ or CCR3−/− eosinophils into eosinophil-deficient ΔdblGATA1 or IFNγ−/− IL-17A−/− ΔdblGATA1 recipients showed that two conditions have to be met for efficient eosinophil trafficking to the inflamed heart: high eotaxin expression in the heart and expression of CCR3 by eosinophils. We identified the source of cardiac eotaxins by RT-PCR of FACS sorted heart cells and by immunohistochemistry. Eotaxin-1 was mainly produced by cardiac fibroblasts with interstitial localization in the heart. In vitro culture of cardiac fibroblasts with IL-4 and IL-13 induced eotaxin-1 expression. In contrast, eotaxin-2 was expressed by multiple inflammatory cell types, located at inflammatory foci, and substantial expression was only found in mice lacking IFNγ and IL-17A during myocarditis. In conclusion, eosinophil trafficking to the heart is dependent on the eotaxin-CCR3 pathway in mice with eosinophilic myocarditis. Blockade of this pathway may be a useful therapeutic approach to prevent eosinophil-mediated heart damage.
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Rothenberg, Marc E. "Eotaxin". American Journal of Respiratory Cell and Molecular Biology 21, n. 3 (settembre 1999): 291–95. http://dx.doi.org/10.1165/ajrcmb.21.3.f160.

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7

Jo, Jung Hyun, Yong-Tae Kim, Ho Soon Choi, Ho Gak Kim, Hong Sik Lee, Young Woo Choi, Dong Uk Kim et al. "KG 4/2015: A randomized, controlled, multicenter, open-label phase III clinical trial of GV1001 with gemcitabine/capecitabine in previous untreated, eotaxin-high patients with advanced pancreatic ductal adenocarcinoma." Journal of Clinical Oncology 39, n. 15_suppl (20 maggio 2021): 4020. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.4020.

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Abstract (sommario):
4020 Background: In the TeloVac study, GV1001 with Gemcitabine/capecitabine (G/C) did not show increased overall survival (OS) than G/C in patients (pts) with advanced pancreatic ductal adenocarcinoma (PDA). But cytokine examination suggested high serum eotaxin level may predict improved survivals in pts received GV1001 with G/C. This phase III trial was designed to assess the efficacy of GV1001 with G/C for previous untreated eotaxin-high Korean pts with advanced PDA. Methods: Eligible pts with histologically proven locally advanced and metastatic PDA (except peritoneal carcinomatosis), age > 18 years, and ECOG PS 0–2 were recruited. Pts were randomly assigned (1:1) to receive either G/C or G/C with GV1001 (G/C/GV). All pts receiving G/C/GV were with high serum eotaxin level (≥81.02 ng/mL), and the pts receiving G/C were randomly assigned again (1:1) to eotaxin-high and eotaxin-low pts. Study was designed according to Korean MFDS guidance for approval of clinical trial. G/C treatment included G (1000 mg/m2, 30 min IVF, D 1, 8, & 15) and C (830 mg/m2 BID for 21 days per month (m). G/C/GV treatment included an intradermal injection of GM-CSF (75 μg) and GV1001 (0.56 mg; D 1, 3, & 5, once on week 2–4, & 6, then monthly thereafter) from the start of G/C. The primary endpoint was OS. The secondary endpoints included time to progression (TTP), objective response rate, and safety. Survival data was analyzed using the copula graphic estimate method under dependent censoring. The response was independently assessed per RECIST v1.1. Under the one-sided significance level of 2.5% and to achieve the power of 80% of the statistical significance with the median OS difference from 7.9 to 14.9 m (HR = 0.53), 85 events and 118 registrations needed. Considering 20% drop-outs, 148 registrations were required. Results: Between Nov 2015 and Apr 2020, of 511 pts screened in 16 centers, eotaxin-high pts were identified as 34.7% (174 / 502 pts). 148 pts randomly assigned to G/C/GV (n = 75; all eotaxine-high) and G/C (n = 73; 37 eotaxine-high, 36 eotaxine-low). Median OS was significantly improved in the G/C/GV group with 11.3m [95% CI 8.6-14.0] than G/C group with 7.5 m [95% CI 5.1-10.0] (p = 0.021). Also, median TTP was significantly improved in the G/C/GV group (7.3 m [95% CI 5.0-9.7]) than in the G/C group (4.5 m [95% CI 3.2-5.8], p = 0.021). In other secondary endpoints, no statistical significance was confirmed between the two groups. Grade 3-4 treatment-emergent adverse events were reported in 49 pts (73.13%) vs. 58 pts (77.33%) in the G/C and G/C/GV group, without significant differences (p = 0.562). Conclusions: G/C/GV treatments significantly extend OS and TTP in advanced PDA than G/C, and specific safety-related issues had not been found. GV1001 should be considered as one of the options in PDA pts with high serum eotaxin levels. Clinical trial information: NCT02854072.
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Beal, Dominic R., David M. Stepien, Sudha Natarajan, Jiyoun Kim e Daniel G. Remick. "Reduction of eotaxin production and eosinophil recruitment by pulmonary autologous macrophage transfer in a cockroach allergen-induced asthma model". American Journal of Physiology-Lung Cellular and Molecular Physiology 305, n. 11 (1 dicembre 2013): L866—L877. http://dx.doi.org/10.1152/ajplung.00120.2013.

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Abstract (sommario):
We sought to investigate the effects of cockroach allergen (CRA) exposure on the lung macrophage population to determine how different macrophage phenotypes influence exacerbation of disease. CRA exposure caused significantly reduced expression of CD86 on lung macrophages. These effects were not systemic, as peritoneal macrophage CD86 expression was not altered. To investigate whether naïve macrophages could reduce asthma-like pulmonary inflammation, autologous peritoneal macrophages were instilled into the airways 24 h before the final CRA challenge. Pulmonary inflammation was assessed by measurement of airway hyperresponsiveness, mucin production, inflammatory cell recruitment, and cytokine production. Cell transfer did not have significant effects in control mice, nor did it affect pulmonary mucin production or airway hyperresponsiveness in control or CRA-exposed mice. However, there was significant reduction in the number of eosinophils recovered in the bronchoalveolar lavage (BAL) (5.8 × 105vs. 0.88 × 105), and total cell recruitment to the airways of CRA-exposed mice was markedly reduced (1.1 × 106vs. 0.57 × 106). The reduced eosinophil recruitment was reflected by substantially lower levels of eosinophil peroxidase in the lung and significantly lower concentrations of eotaxins in BAL (eotaxin 1: 3 pg/ml vs. undetectable; eotaxin 2: 2,383 vs. 131 pg/ml) and lung homogenate (eotaxin 1: 1,043 vs. 218 pg/ml; eotaxin 2: 10 vs. 1.5 ng/ml). We conclude that CRA decreases lung macrophage CD86 expression. Furthermore, supplementation of the lung cell population with peritoneal macrophages inhibits eosinophil recruitment, achieved through reduction of eotaxin production. These data demonstrate that transfer of naïve macrophages will reduce some aspects of asthma-like pulmonary inflammation in response to CRA.
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9

Forssmann, Ulf, Mariagrazia Uguccioni, Pius Loetscher, Clemens A. Dahinden, Hanno Langen, Marcus Thelen e Marco Baggiolini. "Eotaxin-2, a Novel CC Chemokine that Is Selective for the Chemokine Receptor CCR3, and Acts Like Eotaxin on Human Eosinophil and Basophil Leukocytes". Journal of Experimental Medicine 185, n. 12 (16 giugno 1997): 2171–76. http://dx.doi.org/10.1084/jem.185.12.2171.

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Abstract (sommario):
A novel human CC chemokine consisting of 78 amino acids and having a molecular mass of 8,778.3 daltons (VVIPSPCCMF FVSKRIPENR VVSYQLSSRS TCLKAGVIFT TKKGQQ SCGD PKQEWVQRYM KNLDAKQKKA SPRARAVA) was isolated together with three minor COOH-terminally truncated variants with 73, 75, and 76 residues. The new chemokine was termed eotaxin-2 because it is functionally very similar to eotaxin. In terms of structure, however, eotaxin and eotaxin-2 are rather distant, they share only 39% identical amino acids and differ almost completely in the NH2-terminal region. Eotaxin-2 induced chemotaxis of eosinophils as well as basophils, with a typically bimodal concentration dependence, and the release of histamine and leukotriene C4 from basophils that had been primed with IL-3. In all assays, eotaxin-2 had the same efficacy as eotaxin, but was somewhat less potent. The migration and the release responses were abrogated in the presence of a monoclonal antibody that selectively blocks the eotaxin receptor, CCR3, indicating that eotaxin-2, like eotaxin, acts exclusively via CCR3. Receptor usage was also studied in desensitization experiments by measuring [Ca2+]i changes in eosinophils. Complete cross-desensitization was observed between eotaxin-2, eotaxin and MCP-4 confirming activation via CCR3. No Ca2+ mobilization was obtained in neutrophils, monocytes and lymphocytes, in agreement with the lack of chemotactic responsiveness. Intradermal injection of eotaxin-2 in a rhesus monkey (100 or 1,000 pmol per site) induced a marked local infiltration of eosinophils, which was most pronounced in the vicinity of postcapillary venules and was comparable to the effect of eotaxin.
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Struyf, Sofie, Paul Proost, Dominique Schols, Erik De Clercq, Ghislain Opdenakker, Jean-Pierre Lenaerts, Michel Detheux et al. "CD26/Dipeptidyl-Peptidase IV Down-Regulates the Eosinophil Chemotactic Potency, But Not the Anti-HIV Activity of Human Eotaxin by Affecting Its Interaction with CC Chemokine Receptor 3". Journal of Immunology 162, n. 8 (15 aprile 1999): 4903–9. http://dx.doi.org/10.4049/jimmunol.162.8.4903.

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Abstract (sommario):
Abstract Chemokines attract and activate distinct sets of leukocytes. The CC chemokine eotaxin has been characterized as an important mediator in allergic reactions because it selectively attracts eosinophils, Th2 lymphocytes, and basophils. Human eotaxin has a penultimate proline, indicating that it might be a substrate for dipeptidyl-peptidase IV (CD26/DPP IV). In this study we demonstrate that eotaxin is efficiently cleaved by CD26/DPP IV and that the NH2-terminal truncation affects its biological activity. CD26/DPP IV-truncated eotaxin(3–74) showed reduced chemotactic activity for eosinophils and impaired binding and signaling properties through the CC chemokine receptor 3. Moreover, eotaxin(3–74) desensitized calcium signaling and inhibited chemotaxis toward intact eotaxin. In addition, HIV-2 infection of CC chemokine receptor 3-transfected cells was inhibited to a similar extent by eotaxin and eotaxin(3–74). Thus, CD26/DPP IV differently regulates the chemotactic and antiviral potencies of eotaxin by the removal of two NH2-terminal residues. This physiological processing may be an important down-regulatory mechanism, limiting eotaxin-mediated inflammatory responses.
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Più fonti

Tesi sul tema "Eotaxin"

1

Pope, Samuel M. "Specific Role of Eotaxin-1 and Eotaxin-2 in Allergic Pulmonary Eosinophilia". Cincinnati, Ohio : University of Cincinnati, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=ucin1098472372.

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Benarafa, Charaf. "Equine eotaxin : cloning, expression and biological activity". Thesis, Royal Veterinary College (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394942.

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3

Watanabe, Kimiko. "Eotaxin -1, -2 and -3 generation by different cell types". Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404880.

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4

Mariano, Nadia Sabrina. "Estudo da resposta inflamatoria pulmonar alergica em ratos expostos a enterotoxina estafilococica do tipo A (SEA)". [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308954.

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Abstract (sommario):
Orientadores: Edson Antunes, Ivani Aparecida de Souza
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-14T02:35:58Z (GMT). No. of bitstreams: 1 Mariano_NadiaSabrina_M.pdf: 621386 bytes, checksum: b01cd4d186fa15a5e8ea3c7657df604a (MD5) Previous issue date: 2009
Resumo: O Staphylococcus aureus é um tipo de bactéria gram-positiva que produz e secreta uma série de enterotoxinas com propriedade imunomoduladoras. Entretanto, pouco é conhecido sobre os mecanismos envolvidos na exacerbação do influxo celular observado em indivíduos asmáticos expostos a enterotoxinas estafilocócicas. O objetivo desse trabalho é investigar os efeitos da exposição das vias aéreas à enterotoxina estafilocócica do tipo A (SEA) sobre o recrutamento de leucócitos para o pulmão de ratos sensibilizados e desafiados com ovalbumina (OVA). Em nossos protocolos experimentais, ratos foram expostos à SEA 4 h antes ou 4 h após o desafio antigênico com OVA. O lavado broncoalveolar (LBA), a medula óssea e o tecido pulmonar foram obtidos 24 h após o desafio com OVA. A pré-exposição à SEA aumentou significativamente o número de eosinófilos no LBA e no tecido pulmonar de ratos desafiados com OVA, enquanto que o número de neutrófilos e células mononucleares não foi significativamente alterado. Na medula óssea, a pré-exposição à SEA isoladamente aumentou significativamente o número de eosinófilos, sendo esse aumento potencializado em ratos desafiados com OVA. Por outro lado, a pós-exposição à SEA não afetou o número de eosinófilos, neutrófilos ou células mononucleares observadas no LBA. A pré-exposição ao LPS em animais desafiados com OVA aumentou somente o número de neutrófilos no LBA. No LBA de ratos pré-expostos à SEA e desafiados com OVA, notamos uma elevação significativa nos níveis de TNF-? e eotaxina, mas não de IL-10. Os níveis de eotaxina presentes em sobrenadante de cultura de macrófagos alveolares tratados com SEA in vitro aumentaram cerca de 3 vezes em relação a macrófagos não estimulados com SEA. Concluímos que a pré-exposição (mas não a pós-exposição) das vias aéreas de ratos à SEA aumenta seletivamente o número de eosinófilos presente no LBA, tecido pulmonar e medula óssea de ratos desafiados com OVA por mecanismos que envolvem o aumento na síntese de TNF-? e eotaxina
Abstract: Gram-positive Staphylococcus aureus releases classical enterotoxins which aggravates allergic airway diseases. However, little is known about the mechanisms underlying the cell influx exacerbation in asthmatic individuals under exposure to Staphylococcal enterotoxins. We therefore aimed to investigate the effects of airways exposure to Staphylococcal enterotoxin A (SEA) to pulmonary leukocyte recruitment in rats sensitized and challenged with ovalbumin (OVA). Rats were exposed to SEA at 4 h prior to OVA challenge or at 4 h post-OVA challenge. Bronchoalveolar lavage (BAL) fluid, bone marrow and lung tissue were obtained at 24 h after OVA challenge. Preexposure to SEA markedly enhanced the eosinophil counts in both BAL fluid and pulmonary tissue in OVA-challenged rats, whereas neutrophil and mononuclear cell counts remained unchanged. In bone marrow, pre-exposure to SEA alone significantly increased the number of eosinophils, and that was further increased in OVA-challenged rats. Exposure to SEA post-OVA challenge did not affect the number of eosinophils, neutrophils and mononuclear cells in BAL fluid. Pre-exposure to the endotoxin lipopolyssacharide (LPS) in OVA-challenged animals rather enhanced the neutrophil number in BAL fluid. In rats pre-exposed to SEA and OVA-challenged, a marked elevation in the levels of TNF-? and eotaxin (but not of IL-10) in BAL fluid was observed. The eotaxin levels increased by about of 3-fold in alveolar macrophages treated with SEA in vitro. In conclusion, airways pre-exposure to SEA (but not the postexposition) causes a selective increase in eosinophil number in BAL fluid, lung tissue and bone marrow of OVA-challenged rats by mechanisms involving enhancement of TNF-? and eotaxin synthesis
Mestrado
Farmacologia
Mestre em Farmacologia
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Bodman, Lee Graham. "The effect of glycosylation on the biological activity of eotaxin and related chemokines". Thesis, Imperial College London, 2004. http://hdl.handle.net/10044/1/11889.

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Ghaffar, Omar. "Constitutive and cytokine-stimulated expression of eotaxin by human airway smooth muscle cells". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0024/MQ50776.pdf.

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Menzies-Gow, Andrew Neil. "The roles of interleukin-5 and eotaxin in oesinophil recruitment, maturation and activation". Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429161.

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Kirchem, Antje. "Investigation of the signalling pathways coupled to the eotaxin receptor CCR3 in human eosinophils". Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406094.

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Konikoff, Michael R. "Non-Invasive Biomarkers of Eosinophilic Esophagitis: Blood Eosinophil Level, Eosinophil-Derived Neurotoxin, and Eotaxin-3". Cincinnati, Ohio : University of Cincinnati, 2006. http://www.ohiolink.edu/etd/view.cgi?acc_num=ucin1148043525.

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Abstract (sommario):
Thesis (M.S.)--University of Cincinnati, 2006.
Advisor: Dr. James E. Heubi. Title from electronic thesis title page (viewed June 3, 2009). Includes abstract. Keywords: Eosinophilic esophagitis; biomarker; eosinophil; eosinophil-derived neurotoxin; eotaxin-3. Includes bibliographical references.
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Lieschke, Simone [Verfasser]. "Untersuchung der Rolle von Eotaxin-1 nach ischämischem Schlaganfall im Mausmodell: Neuroprotektion, Neuroregeneration oder destruktiv-proinflammatorische Rolle? / Simone Lieschke". Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2021. http://d-nb.info/1232492825/34.

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Capitoli di libri sul tema "Eotaxin"

1

Conroy, Dolores M., e Timothy J. Williams. "Eotaxin in Disease". In Chemokines in Disease, 123–38. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-706-2_8.

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Williams, T. J., e P. J. Jose. "Role of Eotaxin and Related CC Chemokines in Allergy and Asthma". In Immunological Mechanisms in Asthma and Allergic Diseases, 166–77. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000058825.

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Mitchell, Tracey J., e Timothy J. Williams. "The role of eotaxin and related CC-chemokines in asthma and allergy". In Inflammatory Processes: Molecular Mechanisms and Therapeutic Opportunities, 1–12. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8468-6_1.

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Williams, Timothy John, e James Edward Pease. "Eotaxins (CCL11, CCL24, CCL26)". In Encyclopedia of Signaling Molecules, 1554–58. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101627.

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5

Williams, Timothy John, e James Edward Pease. "Eotaxins (CCL11, CCL24, CCL26)". In Encyclopedia of Signaling Molecules, 1–5. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101627-1.

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6

"Eotaxin". In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 617. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_5409.

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7

"Eotaxin". In Encyclopedia of Immunotoxicology, 298. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_200451.

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8

Enna, S. J., e David B. Bylund. "Eotaxin". In xPharm: The Comprehensive Pharmacology Reference, 1. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.61690-3.

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9

Vaddi, Krishna, Margaret Keller e Robert C. Newton. "Eotaxin". In The Chemokine FactsBook, 135–37. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012709905-7/50024-5.

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10

"Eotaxin-1". In Encyclopedia of Signaling Molecules, 1553. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101126.

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Atti di convegni sul tema "Eotaxin"

1

Murphy, GE, NI Pitman, M. Kurowska-Stolarska, P. Kewin, D. Xu, C. McSharry, NC Thomson e MC Shepherd. "Murine Airway Eosinophilia Following IL-33 Administration Is Eotaxin Dependent." 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.a4253.

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2

Farghly, Saher, Atef Farouk El-Karn, Mahmoud Farouk Sherif, Mohamed Ismail Seddik, Safaa Abdelgayed e Mohammed Abdelghany. "Serum periostin and eotaxin-2 as promising biomarkers in asthmatic smokers". In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa1135.

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3

Lababidi, RR, JL Cane e M. Bafadhel. "P54 Eosinophil migration is enhanced towards il-5 and eotaxin in copd". In British Thoracic Society Winter Meeting 2017, QEII Centre Broad Sanctuary Westminster London SW1P 3EE, 6 to 8 December 2017, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2017. http://dx.doi.org/10.1136/thoraxjnl-2017-210983.196.

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4

Gela, Anele, Gopinath Kasetty, Sandra Jovic, Maria Ekoff, Gunnar Nilsson, Sven Kjellstrom, James Pease e Arne Egesten. "Eotaxin-3 exerts innate host defense activities that are modulated by mast cell proteases". In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4032.

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5

Yocum, G. T., J. J. Hwang e C. W. Emala. "6-shogaol, A Component of Ginger, Inhibits Human Airway Smooth Muscle Eotaxin Expression In Vitro". In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4399.

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Lee, AH, SE Wenzel, JB Trudeau e AT Mustovich. "Increased Eotaxin-2 mRNA in Asthmatic Bronchial Epithelial Cells Ex Vivo: Correlations with Clinical/Inflammatory Parameters." 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.a5412.

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Smith, Steven G., Haruki Imoaka, Karen J. Howie, Rick Watson, Roma Sehmi e Gail M. Gauvreau. "The Effects Of Low Dose Peroxisome Proliferator-Activated Receptor (PPAR) Agonists On Eotaxin-Induced Eosinophil Chemotaxis". 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.a4356.

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Couillard, Simon, James Melhorn, Akul Singhania, Daniel Horowitz, Ratko Djukanović, Christpher H. Woelk e Timothy S. C. Hinks. "Correlation of eotaxin-3 gene expression and other IL-13-induced genes in patients with asthma". In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa825.

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9

Naik, Chetan, John Trudeau, Sally E. Wenzel e Amy Lee. "Increased Expression Of Eotaxin-2 In The Airway Epithelium Correlates With Airway Eosinophilia And Severity Of Asthma". 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.a4443.

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Huang, M., J. Zhang e Z. Chen. "Exposure to Ambient Particles Amplifies the Eotaxin-1 Release from Alternatively Activated Macrophages in Allergen-Sensitized Mice". 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.a3797.

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