Tesi: "Eosinophil"

1

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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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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2

Seton, Kristina. "Eosinophil Apoptosis". Doctoral thesis, Uppsala University, Department of Medical Sciences, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3427.

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Apoptosis or programmed cell death is crucial for the resolution of inflammation, and phagocytosis of apoptotic cells initiates the release of actively anti-inflammatory responses from the phagocytes. Eosinophils are one of the most potent inflammatory cells in the body and is involved in a number of diseases, most commonly associated with parasitic infections and allergic diseases. Apoptosis in eosinophils is therefore one of the most important systems to avoid inflammation. This aim of the present investigation was to examine the mechanisms behind, and the consequences of this process in eosinophils. Apoptotic eosinophils have a unique surface receptor expression that indicates abilities to communicate with T-, B- and antigen presenting cells. They have a novel expression of CD49f, indicating an importance for binding to laminin or unknown functions of the VLA-6 receptor, possibly in the concept of phagocytosis of the apoptotic cell.

In apoptotic eosinophils the granules are translocated to the periphery of the cell, probably through a disruption of the cytoskeleton. This translocation makes the granules easily accessible and the apoptotic eosinophil can release considerable amounts of granule proteins in response to specific stimuli. The spontaneous release however, is decreased as compared with living cells.

Furthermore, the survival of eosinophils in response to an allergen challenge is increased in healthy subjects, but not in allergic patients. Mechanistically, this needs further investigation, but one theory is that it is due to the presence of specific IgE in patients in combination with differences in the response from the epithelial cells.

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3

Dewson, Grant. "Regulation of human eosinophil apoptosis". Thesis, University of Leicester, 2001. http://hdl.handle.net/2381/29380.

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Eosinophils play a pivotal role in the pathogenesis of asthma and allergic disease. The accumulation and persistence of eosinophils at sites of inflammation are mediated at least in part by the extended survival of eosinophils in response to circulating hematopoietins IL-3, IL-5 and GM-CSF. The apoptosis and subsequent clearance of eosinophils without histotoxic mediator release is thought to be crucial in the resolution of airway inflammation in asthma. This study characterised the morphological and biochemical events of human eosinophil apoptosis in vitro and investigated the mechanism by which IL-5 induces eosinophil survival. Peripheral blood eosinophils have a distinct expression profile of Bcl-2 homologues, critical regulators of apoptosis, with detectable expression of pro-apoptotic family homologues Bax, Bcl-xs, Bim, Bak, Bid, and Bad, and anti-apoptotic homologue Bcl-xL, with little or no detectable Bcl-2 expression. Stimulation with IL-5 induced modest upregulation of Bcl-2 mRNA and protein, with no significant modulation of the other Bcl-2 homologues examined. Caspases are the conserved executioners of the apoptosis. Eosinophils endogenously expressed 'initiator' caspase-8 and -9, and 'effector' caspase-3, -6, and -7. Spontaneous eosinophil apoptosis involved caspase-independent translocation of Bax to the mitochondria, resulting in perturbation of the mitochondrial membrane, cytochrome c release, and subsequent activation of caspase-3, -6, -7, -8, and -9. IL-5 inhibited constitutive eosinophil apoptosis at a site upstream of Bax translocation to the mitochondria, thereby preventing cytochrome c release and caspase activation. Eosinophils constitutively expressed the conformationally active form of Bax diffusely in the cytosol, but predominantly in the nucleus. Apoptosis induced by Fas receptor ligation involved detectable activation of caspase-3 and -8, and caspase-dependent Bax translocation to the mitochondria, supporting classification of eosinophils as a Type II cell in terms of apoptotic control. The data implicate Bax and mitochondria as pivotal regulators of eosinophil apoptosis in response to diverse stimuli.

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4

Al-Khabuli, JumaÊ¾. "Role of eosinophil in oral squamous cell carcinoma and traumatic ulcerative granuloma with stromal eosinophilia". Thesis, University of Leeds, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418167.

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5

Humbles, Alison Anita. "The relationship between the generation of an eosinophil-selective chemoattractant, ecotoxin and eosinophil accumulation in vivo". Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267879.

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6

Byström, Jonas. "Eosinophil Cationic Protein : Expression Levels and Polymorphisms". Doctoral thesis, Uppsala University, Department of Medical Sciences, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2059.

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The eosinophil cationic protein (ECP) is usually associated with the eosinophil granulocyte. In this thesis the presence and production of this protein has been studied in two other cells. The circulating monocyte was found to contain ECP mRNA and small amounts of ECP, one thousand times less than that found in the eosinophil. The production decreased by differentiation of the myelomonoblastic cell line U937 into a macrophage phenotype. Submucosal lung macrophages did not stain for ECP and alveolar macrophages did not contain ECP mRNA. The circulating neutrophil contains ECP at a level hundred fold less than the eosinophil. We found that the protein is located to the primary granules of the neutrophil but could detect no ECP mRNA in the cell. It was shown in vitro that the protein was taken up by the cell and partly transported to the primary granules. The uptake did not seem to be receptor mediated. Upon stimulation of the neutrophils, ECP previously taken up, was re-secreted.

The ECP protein is heterogeneous both to molecular characteristics and to function. To evaluate if a genetic component is involved, the ECP gene was analysed in 70 individuals. Three single nucleotide polymorphisms (SNP´s) were found, denoted 277(C>T), 434(G>C) and 562(G>C). The two first were located to the mature peptide-coding region and would change the amino acids, arg45cys and arg97thr. The prevalence of the most common SNP, 434, was evaluated in two eosinophil-related diseases, allergy/asthma and Hodgkin Lymphoma (HL). Forty-three HL patients were evaluated and it was found that the 434GG was significantly more prevalent in patients having nodular sclerosis (NS) as compared to other histologies (p=0.03). Erythrocyte sedimentation rate was also related to the 434GG genotype (p=0.009). In 209 medical students 434GG was more common (p=0.002) in those who indicated allergy. The genotype was unrelated to the production of IgE antibodies to allergens. In analysis of 76 subjects with asthma it was found that the 434GG genotype was significantly more common among allergic asthmatics (p=0.04). Asthma and HL-NS are characterized by fibrosis and eosinophils and ECP has been suggested in fibrosis development.

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7

Admiraal, Claudia Johanna. "Eosinophil degranulation as an allergy activation marker". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2001. http://dare.uva.nl/document/59048.

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8

Sandig, Hilary. "CRTH2 and its ligands in eosinophil biology". Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430475.

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9

Hallsworth, Matthew Pearce. "GM-CSF and eosinophil survival in asthma". Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341883.

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10

Flemmig, Jörg, Johannes Remmler, Josefin Zschaler e Jürgen Arnhold. "Detection of the halogenating activity of heme peroxidases in leukocytes by aminophenyl fluorescein". Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-201836.

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The formation of hypochlorous and hypobromous acids by heme peroxidases is a key property of certain immune cells. These products are not only involved in defense against pathogenic microorganisms and in regulation of inflammatory processes, but contribute also to tissue damage in certain pathologies. After a short introduction about experimental approaches for the assessment of the halogenating activity in vitro and in cell suspensions, we are focusing on novel applications of fluorescent dye systems to detect the formation of hypochlorous acid (HOCl) in leukocytes. Special attention is directed to properties and applications of the non-fluorescent dye aminophenyl fluorescein that is converted by HOCl, HOBr, and other strong oxidants to fluorescein. This dye allows the detection of the halogenating activity in samples containing free myeloperoxidase and eosinophil peroxidase as well as in intact granulocytes using fluorescence spectroscopy and flow cytometry, respectively.

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11

Egesten, Arne. "On storage and release of eosinophil granule proteins". Lund : Division of Hematology, Dept. of Medicine, University of Lund, 1995. http://catalog.hathitrust.org/api/volumes/oclc/39104245.html.

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12

Kottyan, Leah Claire. "Airway Acidification in Asthma". University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1280778640.

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13

Felton, Jennifer Marie. "Investigation of the role of Mcl-1 and Mer in the regulation of eosinophil apoptosis and efferocytosis". Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28833.

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Regulation of the inflammatory response is essential for the successful resolution of inflammation, and restoration of normal tissue homeostasis. Eosinophils are granulocytic cells of the innate immune system historically considered to be primarily involved in the defence against parasitic infection. Eosinophils are also key effector cells in the allergic inflammatory response, initiation of which is associated with the recruitment and activation of eosinophils culminating in the release of their intracellular granule contents. Eosinophil granules contain a range of cytotoxic proteins (major basic protein, eosinophil cationic protein and eosinophil peroxidase) that act to destroy infectious and parasitic organisms. However, these cytotoxic proteins can also cause damage to surrounding host tissue cells. The resolution of the inflammatory response acts to limit the extent of eosinophil-mediated tissue damage. Programmed cell death (apoptosis) of eosinophils represents an important component of this resolution process, limiting release of granule contents and triggering efferocytosis (the removal of apoptotic cells by phagocytes). Apoptosis is initiated by the activation of intracellular caspases, a family of cysteine proteases. Caspase activation primarily occurs as a result of changes in the balance of intracellular pro- and anti-apoptotic Bcl-2 family proteins. Mcl-1, an anti-apoptotic Bcl-2 protein has been shown to play a pivotal role in the regulation of neutrophil apoptosis. Pharmacological down-regulation of Mcl-1 initiates apoptosis and promotes the resolution of neutrophil-dominant inflammation. The importance of Mcl-1 in the regulation of apoptosis was shown using cyclin-dependent kinase inhibitors (CDKis), where induction of neutrophil apoptosis by CDKis was due to down-regulation of intracellular Mcl-1. Apoptotic cells display distinct surface molecules known as ‘eat-me’ signals that identify them for phagocytosis by macrophages and other phagocytes. One key receptor involved in the removal of apoptotic cells from tissue is the receptor tyrosine kinase Mer, a member of the Tyro3/Axl/Mer (TAM) family, which recognises the ‘eat me’ signal phosphatidylserine expressed on apoptotic cells. In the absence of Mer expression, clearance of apoptotic cells is compromised delaying the resolution of neutrophil-dominant inflammation. However, the roles of Mcl-1 and Mer in eosinophil apoptosis and clearance, respectively, and the resolution of allergic inflammation are not known. Asthma is a chronic inflammatory lung disease characterised by shortness of breath, airway obstruction, wheeze, non-specific bronchial hyper-responsiveness, excessive airway mucus production and an eosinophil dominant inflammatory infiltrate. The persistent presence of eosinophils in the lung, in chronic asthma, is likely due to a combination of excessive eosinophil recruitment and activation together with impaired eosinophil apoptosis. Investigation into the underlying mechanisms of these processes in allergic airway disease is of critical importance, as blocking eosinophil recruitment and/or promoting eosinophil apoptosis could provide a therapeutic approach to reduce associated eosinophil-mediated tissue damage. Understanding the regulation of eosinophil apoptosis and phagocytic clearance may identify novel pharmacological targets to enhance the resolution of allergic inflammation. We hypothesise that Mcl-1 and Mer play vital roles in the successful resolution of allergic airway inflammation. To investigate this hypothesis, we have used pharmacological and genetic manipulation of intracellular eosinophil Mcl-1 levels, and phagocyte Mer expression, to determine the role they play in the regulation of eosinophil apoptosis and phagocytic clearance of apoptotic eosinophils, respectively. Human and mouse eosinophils were cultured, and rates of constitutive and CDKi-induced apoptosis were determined, to investigate eosinophil apoptosis in vitro. Mice expressing human Mcl-1 (hMcl-1) were used to determine the effect of over-expression of Mcl-1 on eosinophil viability in vitro. The effect of hMcl-1 on eosinophil viability and disease severity in vivo was determined using an ovalbumin-induced model of allergic airway inflammation, which mimicked the symptoms of human asthma. Apoptotic eosinophils were co-incubated with macrophages in vitro to investigate the capacity for phagocytosis by different macrophage populations. Apoptotic cell clearance was further investigated using a Mer-kinase-dead mouse, which lacked Mer expression, to determine the role of Mer-dependent phagocytosis on the process of resolution of inflammation in vivo. Over-expression of Mcl-1 in eosinophils significantly delayed both constitutive and CDKi-induced apoptosis in vitro. In vivo in the ovalbumin-induced model of allergic airway inflammation, over-expression of Mcl-1 resulted in a significantly increased number of eosinophils in the lung and delayed rate of resolution of allergic airway inflammation. Alveolar and bone marrow-derived macrophages exhibited Mer-dependent phagocytosis of eosinophils, which was significantly reduced by an inhibitor of Mer kinase activity (BMS777607) or lack of macrophage Mer expression. The absence of Mer expression resulted in a significant increase in the number of apoptotic eosinophils in the lung together with a delayed rate of resolution of allergic airway inflammation in vivo. Together this work has shown that delayed rates of eosinophil apoptosis and impaired phagocytic clearance both delayed the resolution of allergic airway inflammation. These data suggest that both Mcl-1 and Mer are pivotal for the successful regulation of eosinophil apoptosis and phagocytic clearance of apoptotic eosinophils in asthma and may provide attractive novel therapeutic targets.

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14

Costain, Darren James. "Hypodense eosinophil tumouricidal activity, an in vitro analysis". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0022/MQ36419.pdf.

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15

Jenkins, Gareth Raymond. "Neutrophil and eosinophil mediated inflammation in childhood asthma". Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407789.

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16

Ali, Shahina. "Molecular mechanisms of eosinophil recruitment to breast carcinoma sites". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ64939.pdf.

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17

De, Souza Patricia Manuela. "Signal transduction mechanisms regulating human eosinophil and neutrophil apoptosis". Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397695.

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18

Palframan, Roger Thomas. "Regulation of acute eosinophil mobilisation from the bone marrow". Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314279.

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19

Teran, Luis Manuel. "Identification of neutrophil and eosinophil chemotactic factors in asthma". Thesis, University of Southampton, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295930.

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20

Bourne, Andrew D. "Investigation of transduction mechanisms for agonist-induced eosinophil responses". Thesis, University of Bath, 1995. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296317.

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21

Davis, Benjamin. "Genetic and Functional Analysis of Calpain-14 in Eosinophilic Esophagitis". University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1447688593.

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22

Kämpe, Mary. "Eosinophil Inflammation in Allergic Disease : Clinical and experimental studies in allergic asthma and allergic rhinitis". Doctoral thesis, Uppsala universitet, Lungmedicin och allergologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-130949.

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Allergic diseases are chronic inflammatory conditions, characterised by eosinophil inflammation systemically and in target organs, where cytotoxic granule proteins are responsible for tissue injury. Allergic rhinitis is known to be a risk factor for the development of asthma, yet not all with rhinitis develop asthma. The overall aim was to investigate the involvement of eosinophils in allergic rhinitis and allergic asthma in vivo and in experimental settings, with a focus on differences between rhinitis and asthma. Birch pollen allergy was used as a model and patients were studied during pollen season and after nasal and bronchial allergen challenge. During pollen season and at baseline, allergic rhinitis and allergic asthma had the same degree of systemic eosinophil inflammation. Despite this, impairment in lung function during season and increased bronchial responsiveness at baseline were more common in the asthmatics. Systemic inflammation was more pronounced after seasonal exposure than after experimental challenge. Allergic rhinitis and allergic asthma had the same degree of eosinophil airway inflammation after bronchial challenge, but only the asthmatics had increased bronchial responsiveness measured as PD20 for birch allergen. Allergen primed eosinophils were investigated in vitro for C3b-induced degranulation after seasonal and experimental challenge. The released amount of eosinophil granule proteins was within the same range for all three allergen challenge models with just minor differences in propensity for degranulation between rhinitics and asthmatics. Signalling through PI3K for degranulation was studied with the specific inhibitor Wortmannin. PI3K signalling for eosinophil degranulation was clearly involved in allergic rhinitis and allergic asthma irrespective of the model for allergen exposure. Asthmatics demonstrated less inhibition of degranulation through PI3K during pollen season, indicating that other pathways contribute to eosinophil degranulation in allergic asthmatics. Conclusion: Allergic rhinitis and allergic asthma present with the same degree of systemic and local eosinophil inflammation. The eosinophils are primed for degranulation equally and follow the same pathway through PI3K for degranulation. Our data indicates that eosinophil inflammation per se is not sufficient for the development of asthma.

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23

Sanmugalingam, Devika. "Human lung mast cell and eosinophil adhesion to bronchial epithelium". Thesis, University of Leicester, 2001. http://hdl.handle.net/2381/29394.

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Asthma is initiated at the mucosal surface upon aeroallergen exposure and mast cell activation. Release of eosinophil cationic proteins is thought to be responsible for epithelial damage. In this study, human peripheral blood eosinophil and human lung mast cell (HLMC) adhesion to bronchial epithelium were investigated. A high proportion of HLMC adhered to epithelial cell monolayers compared to eosinophils. In both cases, adhesion was cation-independent, and was not inhibited by function-blocking ICAM-1 mAb, despite increased basal epithelial ICAM-1 expression upon cytokine activation. HLMC adhesion was not modulated by function blocking mAb to cell adhesion molecule families, preincubation with carbohydrates, HLMC activation (SCF or TGF-P), or epithelial activation (cytokines). A significant reduction in adhesion was observed upon pretreatment with anti-IgE, pronase, -galactosidase or endo--N-acetylgalactosaminidase (HLMC) or 4% paraformaldehyde (epithelium). No evidence for galectin involvement in adhesion was observed. Eosinophil adhesion to alveolar epithelium was not modulated by eosinophil activation with PAF. Adhesion to bronchial epithelium was enhanced upon activation of both eosinophils (Mn2+) and epithelium (cytomix). A proportion of the enhanced adhesion was 2 (CD 18) integrin-mediated. In conclusion, the adhesion mechanisms of mast cells and eosinophils to bronchial epithelium were different, possibly relating to their divergent in vivo functions. The differences in proportions of adherent mast cells and eosinophils to bronchial epithelium during asthma may result in the widely documented lack of mast cells compared to eosinophils in sputum and BAL in vivo.

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24

McNulty, Clare A. "Studies on the molecular basis of eosinophil adhesion to endothelium". Thesis, University of Leicester, 2001. http://hdl.handle.net/2381/29391.

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Selective adhesion may be important for the preferential accumulation of eosinophils in asthma and allergic diseases. The Stamper-Woodruff frozen section assay (FSA) was used to define the adhesion of human peripheral blood eosinophils and neutrophils to endothelium in a model of chronic airway inflammation, the nasal polyp. Eosinophil and neutrophil adhesion to nasal polyp endothelium (NPE) was (32 integrin-dependent. Eosinophil adhesion was inhibited to a lesser extent by mAbs against pi integrins and VCAM-1. Adhesion of both eosinophils and neutrophils to NPE was activation-dependent. as shown by inhibition with azide. Neutrophil adhesion was mediated by PAF and IL-8 signalling through pertussis toxin (PTX)-scnsitive G-protein coupled receptors (GPCR). In contrast, eosinophil adhesion was PTX-insensitive. and the chemokine receptor CCR3 was not involved. The eosinophil activation step was further explored under shear flow conditions. Neutrophils firmly arrested on TNF-a-stimulated human umbilical vein endothelial cells (HUVEC) under flow. In contrast, eosinophils rolled unless exogenous chemoattractants such as PAF, eotaxin, and RANTES were added. Priming eosinophils with IL-5 before addition to HUVEC caused arrest of the entire population. The flow assay was also used to investigate the receptors involved in leukocyte adhesion to IL-13- stimulated HUVEC. Eosinophils but not neutrophils showed enhanced binding to IL-13- stimulated HUVEC compared to medium-cultured cells. This adhesion was mediated by P-selectin/ PSGL-1. and to a lesser extent VLA-4/ VCAM-1. These findings were consistent with the pattern of adhesion receptor expression in nasal mucosa, with weak expression of VCAM-1 compared with P-selectin. In summary, I have demonstrated a difference in integrin usage and the mechanism of integrin activation between eosinophils and neutrophils. An additional priming step in the adhesion cascade appears to be required for eosinophils, but not neutrophils, to respond to an activating stimulus and arrest on endothelium. P-selectin/ PSGL-1 interactions were pivotal to eosinophil arrest on Th2- cytokine-stimulated endothelium and are potential targets for inhibition of eosinophil migration.

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25

Turner, Darryl Griffith. "The characterisation of haeomonchus contortus products which affect eosinophil activity". Thesis, Edinburgh Napier University, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.506341.

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26

Foweraker, J. E. "A study of eosinophil granule proteins and in vitro degranulation". Thesis, University of Cambridge, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377204.

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27

Flemmig, Jörg, Johannes Remmler, Josefin Zschaler e Jürgen Arnhold. "Detection of the halogenating activity of heme peroxidases in leukocytes by aminophenyl fluorescein". Free radical research (2015) 49, S. 768-776, 2015. https://ul.qucosa.de/id/qucosa%3A14678.

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Abstract (sommario):

The formation of hypochlorous and hypobromous acids by heme peroxidases is a key property of certain immune cells. These products are not only involved in defense against pathogenic microorganisms and in regulation of inflammatory processes, but contribute also to tissue damage in certain pathologies. After a short introduction about experimental approaches for the assessment of the halogenating activity in vitro and in cell suspensions, we are focusing on novel applications of fluorescent dye systems to detect the formation of hypochlorous acid (HOCl) in leukocytes. Special attention is directed to properties and applications of the non-fluorescent dye aminophenyl fluorescein that is converted by HOCl, HOBr, and other strong oxidants to fluorescein. This dye allows the detection of the halogenating activity in samples containing free myeloperoxidase and eosinophil peroxidase as well as in intact granulocytes using fluorescence spectroscopy and flow cytometry, respectively.

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28

Maziero, Aline Mendes 1981. "Inibição da agregação de plaquetas humanas por eosinófilos". [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312670.

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Orientador: Gilberto De Nucci
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-24T16:13:57Z (GMT). No. of bitstreams: 1 Maziero_AlineMendes_D.pdf: 2175096 bytes, checksum: b3e712ed8baf6a7f7d4ef12131b9e85a (MD5) Previous issue date: 2014
Resumo: Os eosinófilos participam de processos inflamatórios e alérgicos. Estando relacionados com o sistema de imunidade inata do organismo, eles representam uma linha fundamental de defesa contra invasão microbiana e, quando ativados, produzem uma série de mediadores solúveis que atuam nas respostas inflamatórias e alérgicas. A relação entre a atividade dos eosinófilos e plaquetas foi observada nas últimas décadas por muitos cientistas. Estas observações incluem o aumento do número de eosinófilos associados a desordens plaquetárias, incluindo alterações na cascata de coagulação e agregação plaquetária. Com base nessas observações, a interação entre os eosinófilos e plaquetas foram analisadas na agregação plaquetária. Plaquetas humanas foram incubadas com a fração citosólica de eosinófilos, linhagem celular promielocítica humana HL-60 clone 15 e proteína catiônica do eosinófilo (ECP). A agregação em plasma rico em plaquetas (PRP) foi induzida por difosfato de adenosina, fator de ativação plaquetária, ácido araquidônico e colágeno, e as plaquetas lavadas (PL) foram ativadas por trombina. A agregação induzida por todos os agonistas foi inibida de maneira concentração de células dependente pela fração citosólica de eosinófilos. Esta inibição foi apenas parcialmente revertida pela prévia incubação dos eosinófilos com L-Nitro-Arginina-metil-éster (L-NAME). A prévia incubação com indometacina não impediu a inibição induzida pela fração citosólica. A separação da fração citosólica de eosinófilos por gel filtração em Sephadex G-75 mostrou que a atividade inibitória foi concentrada na fração de peso molecular mais baixo. As células HL -60 clone 15 diferenciadas em eosinófilos por 5 e 7 dias foram capazes de inibir a agregação plaquetária. A proteína de ECP inibiu a agregação plaquetária em PRP e PL. Esta inibição foi mais evidente em PL, e o ensaio de citotoxicidade com MTT demonstrou a viabilidade de plaquetas testadas, indicando que a inibição observada pela proteína ECP não ocorre simplesmente pela morte celular. A proteína EDN, clonada e expressa em sistema eucarioto, também apresentou efeito de inibição sobre a agregação plaquetária em PRP, enquanto que a proteína MBP não apresentou efeito de inibição da agregação plaquetária significativo. Os nossos resultados indicam que os eosinófilos desempenham um papel fundamental na inibição da agregação plaquetária
Abstract: Eosinophils participate in allergic and inflammatory processes, being related to innate immunity system of the body, they represent a fundamental line of defense against microbial invasion and when activated produce a number of soluble mediators that act in inflammatory and allergic responses. The relationship between the activity of eosinophils and platelets has been observed in recent decades by many scientists. These observations include increased numbers of eosinophils associated with platelet disorders, including changes in the coagulation cascade and platelet aggregation. Based on these observations, the interaction between eosinophils and platelets in platelet aggregation was analyze. Human platelets were incubated with eosinophil cytosolic fraction, promyelocytic human HL-60 clone 15 cell lineage, and eosinophil cationic protein (ECP). Platelet rich plasma (PRP) aggregation was induced by adenosine diphosphate, platelet activating factor, arachidonic acid, and collagen, and washed platelets (WP) were activated by thrombin. Aggregation induced by all agonists was dose dependently inhibited by eosinophil cytosolic fraction. This inhibition was only partially reversed by previous incubation of the eosinophils with L-Nitro-Arginine-Methyl-Ester (L-NAME). Previous incubation with indomethacin did not prevent the cytosolic fraction induced inhibition. The separation of eosinophil cytosolic fraction by gel filtration on Sephadex G-75 showed that the inhibitory activity was concentrated in the lower molecular weight fraction. HL-60 clone 15 cells differentiated into eosinophils for 5 and 7 day were able to inhibit platelet aggregation. The ECP protein inhibited the platelet aggregation on PRP and WP. This inhibition was more evident in WP, and the citotoxicity MTT assay proved the viability of tested platelets, showing that the observed inhibition by the ECP protein does not occur simply by cell death. The EDN protein, cloned and expressed in eukaryotic system, also showed inhibitory effect on platelet aggregation in PRP, whereas the protein MBP had no effect significative inhibiting platelet aggregation. Our results indicate that eosinophils play a fundamental role in platelet aggregation inhibition
Doutorado
Farmacologia
Doutora em Farmacologia

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29

Lampinen, Maria. "Cytokine-regulated eosinophil migration in inflammatory disorders : Clinical and experimental studies". Doctoral thesis, Uppsala University, Department of Medical Sciences, 2000. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-528.

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Abstract (sommario):

The accumulation of eosinophil granulocytes (EOS) at sites of inflammation is a common feature of astma, allergic rhinitis and inflammatory bowel disease. The aim of the present investigation was to study the mechanisms involved in this accumulation.

Bronchoalveolar lavage (BAL) fluid obtained from patients with birch-pollen allergy lavaged during season exhibited increased eosinophil chemotactic activity compared with pre-season BAL fluid from the same patients. We identified IL-5, IL-8 and RANTES as the main eosinophil chemotactic agents in the BAL fluid. Only EOS from allergic donors responded to IL-8. IL-2 inhibited albumin-stimulated eosinophil migration towards buffer or chemoattractants. EOS from allergic subjects were less sensitive to this inhibition than EOS from normal subjects, and in vitro priming of the EOS with IL-5 prevented the inhibitory effect of IL-2. We therefore hypothesise that IL-2 acts as an autocrine regulator of EOS migration, and that this inhibitory effect may be down-regulated in allergy, resulting in increased migration of EOS towards chemotactic factors. The stimulation of eosinophil migration by albumin is mediated by PI3 kinase. Decreased expression of CD49d and CD49f caused by albumin may decrease the adhesiveness of the EOS, which in turn may facilitate migration. We found a higher chemotactic activity in perfusion fluids from patients with ulcerative colitis than from control patients. The chemotactic activity correlated with the concentrations of eosinophil granule proteins in the perfusion fluids. IL-5 and TNF-α were identified as two of the chemotactic agents in the perfusion fluid that were inhibited by steroid treatment. Agents with steroid-insensitive chemotactic activity remain to be identified.

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30

Nopp, Anna. "Characterisation of eosinophil activity markers : relation to allergic inflammation and apoptosis /". Stockholm : Karolinska Univ. Press, 2002. http://diss.kib.ki.se/2002/91-7349-129-2.

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31

Farahi, Neda. "Characterisation of a pulmonary artery endothelium cell-derived eosinophil survival activity". Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615872.

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32

Lee, Elaine. "The effect of leukotriene inhibition in neutrophil, eosinophil and monocyte apoptosis". Thesis, University of Sunderland, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399656.

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33

Grix, Suzanna Peta. "Pharmacological characterisation of the role of Ca²⁺ in human eosinophil activation". Thesis, University of Bath, 1995. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295455.

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34

Ferreira, Lauren. "Cytokine properties of CD23 on human Eosinophilic cells". Thesis, Nelson Mandela Metropolitan University, 2007. http://hdl.handle.net/10948/503.

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CD23, the low affinity IgE receptor, is expressed by various cell types and has numerous functions depending on the form of the protein, its interaction with various ligands and the type of cell involved. CD23 is pivotal in the regulation of IgE, with the soluble form involved in up-regulation, while the membrane bound form is involved in the down-regulation. It is clear why it is believed to be a central molecule in allergic responses, and a therapeutic target for the treatment of allergic disease. In this study a recombinant form of the entire extracellular domain of the protein, exCD23, was produced by PCR cloning and expressed in E. coli. His•Tag™s were introduced onto the C-terminus and N-terminus, respectively, in order to simplify the purification procedure. After renaturation and purification, the recombinant exCD23 bound IgE, indicating its activity. From the IgE binding studies it was established that the position of the tag did not influence the binding. GST•Tagged™ exCD23 was also produced in an attempt to increase the solubility of the recombinant protein, but this proved unsuccessful. Butyrate differentiated EoL-1 cells were treated with the Nterminal His•Tagged™ exCD23, and the protein appeared to suppress the secretion of the constitutively expressed cytokines, especially IL-8 and IFN- , when compared to untreated cells. In addition, treatment of the EoL-1 cells with exCD23 had a significant proliferative effect, but could not induce differentiation of this cell line into mature eosinophilic-like cells.

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35

Lilliehöök, Inger. "Studies of blood eosinophil and neutrophil granulocytes in healthy and diseased dogs /". Uppsala : Swedish Univ. of Agricultural Sciences (Sveriges lantbruksuniv.), 1999. http://epsilon.slu.se/avh/1999/91-576-5409-3.pdf.

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36

Warren, David John. "Studies on an eosinophil differentiation factor produced by a T-hybrid line". Thesis, Brunel University, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.290954.

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37

Li, Ming-Shi. "Structure and expression of the gene encoding human eosinophil major basic protein". Thesis, St George's, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307257.

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38

Stevenson, Lesley Margaret. "Studies on the role of the eosinophil leukocyte in ovine nematode infections". Thesis, Edinburgh Napier University, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386225.

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39

Maxwell, M. H. "Studies on the avian eosinophil leucocyte with special reference to its stimulation". Thesis, University of Strathclyde, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.371960.

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40

Toor, Iqbal Singh. "Investigating the role of eosinophils in cardiac remodelling following myocardial infarction". Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31187.

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Abstract (sommario):

Myocardial infarction (MI) occurs following acute thrombotic occlusion of a coronary artery, and triggers a robust inflammatory response. Within hours, neutrophils are recruited to the infarcted myocardium followed by the infiltration of pro-inflammatory Ly6Chi monocytes. Transition from the pro-inflammatory macrophage phenotype (M1) to an anti-inflammatory, pro-resolution phenotype (M2-like) is critical to successful infarct healing. Interventions that polarize macrophages towards an anti-inflammatory 'M2-like' phenotype improve infarct healing in the experimental MI mouse model and reduce subsequent adverse remodelling of the myocardium, but the endogenous mechanisms that regulate repair are not well understood. Furthermore, differences in the resolution of inflammation in C57BL/6 and BALB/c mice, which are two of the commonly used wild-type mouse strains in experimental MI have not been characterised. We previously found that low peripheral blood eosinophil count is associated with increased short-term risk of mortality in low-intermediate risk patients with ischaemic heart disease. This suggests that eosinophils may have a role in the successful remodelling and repair of the heart following myocardial infarction. Eosinophils express a number of immuno-modulating cytokines and lipid mediators implicated in the resolution of inflammation. Increasingly prominent is interleukin-4 (IL-4), a cytokine that has been found to maintain the anti-inflammatory M2-like phenotype in macrophages. We therefore hypothesised that IL-4Rα signalling and recruitment of eosinophils to the myocardium following infarction are key in regulating the subsequent inflammatory response and scar tissue formation during infarct repair and cardiac remodelling. Experimental MI was induced by permanent left anterior descending artery ligation in isofluorane anaesthetized 12-15 week-old male wild-type (WT) BALB/c, WT C57BL/6, IL4Rα-/-, IL-4Rαflox/-, IL-4Rαflox/-LysMCre mice and eosinophil-deficient ΔdblGATA mice. Cardiac function was characterised by high-resolution ultrasound and immune cell infiltration by flow cytometry of single cell infarct and remote zone tissue digests. Blood eosinophil count and 6-month all-cause mortality were assessed in 732 consecutive patients undergoing primary percutaneous coronary intervention for ST-segment elevation myocardial infarction (STEMI). The rate of mortality due to cardiac rupture was significantly higher in C57BL/6 mice in comparison with BALB/c mice at Day 7 post-MI. This was associated with a higher proportion of pro-inflammatory Ly-6Chi macrophages infiltrating the infarct zone tissue of C57BL/6 mice following MI. An accompanying reduction in the number of splenic Ly-6Chi monocytes post-MI, suggestive of splenic monocyte mobilisation, was seen in C57BL/6 mice but not found in BALB/c mice. Furthermore, C57BL/6 mice had a delayed transition in macrophage polarisation towards an anti-inflammatory phenotype. Disruption of IL4Rα signalling, in mice null for the IL4Rα gene, resulted in increased F4/80+ macrophage and pro-inflammatory Ly6Chi macrophage infiltration of the infarct zone and reduced expression of the anti-inflammatory macrophage marker CD206, compared to wild-type controls. Furthermore, expression of GATA3 and ST2, both associated with the immunosuppressive function of (CD4+ Foxp3+) regulatory T cells, was reduced in infarct zone regulatory T cells from IL4Rα-/- mice. These findings were associated with defective wound healing with impaired angiogenesis, increased scar size, disarrayed infarct zone collagen deposition, accompanied by modified expression of plod2 that encodes the collagen cross-linking enzyme lysyl hydroxylase 2. Resulting in greater left ventricular dilatation and loss of cardiac function, as well as a higher 7- day mortality due to cardiac rupture in IL4Rα-/- mice. This indicates that successful infarct repair requires the engagement of IL-4Rα signalling to facilitate the accumulation of anti-inflammatory macrophages and highly immunosuppressive ST2+ regulatory T cells in the heart following MI. Resident cardiac macrophages from naïve hearts of IL-4Rαflox/-LysMCre mice failed to undergo LysMCre-mediated deletion of the IL-4Rα gene, potentially because low or absent expression of Lyz2 (encoding lysozyme M). In both ST-elevation MI (STEMI) patients and mice after acute MI, there was a decline in peripheral blood eosinophil count, with activated eosinophils being recruited to the infarct zone and paracardial adipose tissue of mice. The transcription factors GATA-1 plays a role in the differentiation of eosinophils from eosinophil progenitor cells. Deletion of GATA-1 results in loss of the eosinophil lineage and has been exploited to develop the eosinophil-deficient ΔdblGATA mouse. ΔdblGATA mice were used to address the role of eosinophils in cardiac remodelling following MI. ΔdblGATA mice had increased left ventricular dilatation and reduced ejection fraction after induction of MI, relative to wild-type mice. ΔdblGATA mice had increased scar size with disarrayed infarct zone collagen deposition, accompanied by modified expression of the genes plod2 and lox, which are associated with collagen cross-linking. The proportion of CD206+ anti-inflammatory macrophages was less in the infarct zone of ΔdblGATA mice, but was restored by adoptive transfer of eosinophils from WT mice. Furthermore, adverse cardiac remodelling in eosinophil-deficient ΔdblGATA mice was rescued by provision of IL-4 complex following MI. In conclusion, an enhanced inflammatory response following MI underlies the increased risk of cardiac rupture seen with WT C57BL/6 mice in comparison to WT BALB/c mice. WT BALB/c mice are protected from cardiac rupture, which was associated with an absence of splenic monocyte mobilisation following ischaemic injury. The resolution of inflammation was found to be dependent on IL4Rα signalling which is crucial for cardiac repair and remodelling, through modulating inflammatory cell recruitment and phenotype, as well as scar formation. Eosinophils are recruited to the heart post-MI and are essential for regulating cardiac repair and remodelling, likely through provision of IL-4. Therefore, we were able to show that IL-4Rα signalling and recruitment of eosinophils to the myocardium following infarction are both key in regulating the subsequent inflammatory response and scar tissue formation during infarct healing and cardiac remodelling.

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41

Guay, Caroline. "Expression et rôle d'une nouvelle protéase à sérine: l'«eosinophil serine protease»-1". Thesis, Université Laval, 2007. http://www.theses.ulaval.ca/2007/24677/24677.pdf.

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42

Song, Wei. "MASS SPECTROMETRY-BASED HIGH THROUGHPUT APPROACH FOR IDENTIFICATION OF MOLECULAR MODIFICATION OF OXIDATIVE PROCESS IN RESPIRATORY". Cleveland State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=csu1226685494.

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43

NOEL, RICHARD JOSEPH. "DEMOGRAPHIC ANALYSIS OF ESOPHAGITIS: A POPULATION-BASED STUDY". University of Cincinnati / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1085675249.

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44

Davies, Dawn. "The role of calcitonin gene related peptide in the activation of the eosinophil leukocyte". Thesis, University of Bristol, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240801.

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45

Greenaway, Elona Clare. "Protein kinase C in eosinophils from normal and allergic ponies". Thesis, Royal Veterinary College (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367564.

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46

Stamatiou, Panagiota. "5-oxo-ETE and its effect on eosinophil recruitment in the Brown Norway rat lung". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ50886.pdf.

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47

Stamatiou, Panagiota. "5-oxo-ETE and its effect on eosinophil recruitment in the Brown Norway rat lung". Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21646.

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Abstract (sommario):

The 5-lipoxygenase product 5-oxo-6,8,11,14-eicosatetraenoic acid (5-oxo-ETE) is a potent eosinophil chemoattractant in vitro. To determine whether it is active in vivo, 5-oxo-ETE was administered intratracheally to BN rats and pulmonary eosinophils were immunostained with an antibody to major basic protein. 5-Oxo-ETE induced a dramatic increase in eosinophils, which reached maximal levels (5 times control) between 15 and 24 h following administration, and thereafter declined. LTB4 had a similar effect to 5-oxo-ETE but appeared to be somewhat less effective. In contrast, LTD4 and LTE4 were inactive. 5-Oxo-ETE-induced eosinophilia was inhibited by 75% following pretreatment of the animals with antibodies to integrins VLA-4 or LFA-1, but was not significantly inhibited by an antibody to Mac-1, nor after pretreatment with receptor antagonists to LTB4 (LY255283) or PAF (WEB 2170). These observations raise the possibility that 5-oxo-ETE may be an important physiological mediator in inflammatory diseases characterized with eosinophil recruitment, such as asthma.

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48

Lavinskienė, Simona. "Peripheral blood neutrophil and eosinophil activity during allergen-induced late-phase airway inflammation in asthma". Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2015. http://vddb.library.lt/obj/LT-eLABa-0001:E.02~2014~D_20150106_083713-90371.

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There is no doubt that eosinophils and neutrophils are important cells participating in asthma pathogenesis. The most prominent feature reflecting asthma pathogenesis is late-phase airway inflammation, which occurs a few hours after allergen inhalation. The worldwide published studies on asthma show that most attention is paid to individual, not complex, functions of neutrophils and eosinophils in the airways. Moreover, associations between peripheral blood neutrophil and eosinophil activity and infiltration of these cells in the airways during asthma have not been com¬pletely elucidated yet. There are no data about peripheral blood neutrophil and eosinophil activity during allergen-induced late-phase airway inflam¬mation in asthma patients. Therefore, the aim of this study was to evaluate peripheral blood neutrophil and eosinophil functional activity during allergen-induced late-phase airway inflammation in asthma. We found that an inhaled allergen activates peripheral blood neutrophil and eosinophil chemotaxis, phagocytosis, generation of reactive oxygen species and also reduces apoptosis during late-phase airway inflammation in asthma. Furthermore, altered peripheral blood neutrophil and eosinophil functional activity is related with airway neutrophilia and eosinophilia. Our findings provide new evidence about neutrophil and eosinophil functional activity during allergen-induced late-phase airway inflammation in asthma patients.
Mokslininkai neabejoja, jog eozinofilai ir neutrofilai yra vienos svarbiausių ląstelių, dalyvaujančių astmos patogenezėje, kurią labiausiai atspindi vėlyva kvėpavimo takų uždegimo fazė, išsivystanti praėjus kelioms valandoms po alergeno įkvėpimo. Pasaulinėje literatūroje publikuojami darbai, nagrinėja atskirus kvė¬pavimo takų neutrofilų ir eozinofilų aktyvumo pokyčius. Ypač mažai darbų apie periferinio kraujo neutrofilų ir eozinofilų funkcijas bei jų ryšį su šių ląstelių pagausėjimu kvėpavimo takuose, sergant astma. Taip pat nėra tyrimų, vertinančių periferinio kraujo uždegimo ląstelių (neutrofilų ir eozi¬nofilų) funkcijų alergeno sukeltos vėlyvos fazės kvėpavimo takų uždegimo metu. Todėl šio tyrimo tikslas buvo įvertinti periferinio kraujo neutrofilų ir eozinofilų funkcinį aktyvumą alergeno sukeltos vėlyvos fazės kvėpavimo takų uždegimo metu sergant astma. Tyrimo metu nustatėme, kad įkvėptas alergenas aktyvina periferinio kraujo neutrofilų ir eozinofilų funkcijas - chemotaksį, fagocitozę, reaktyvių deguonies formų susidarymą, degranuliaciją bei silpnina apoptozę vėlyvos fazės kvėpavimo takų uždegimo metu. O šių ląstelių aktyvumo pokyčiai yra susiję su kvėpavimo takų neutrofilija ir eozinofilija. Moksliniame darbe pateikiami rezultatai suteikia naujų duomenų apie sergančiųjų alergine astma periferinio kraujo neutrofilų ir eozinofilų funkcinių savybių ypatumus ir parodo jų pokyčius alergeno sukeltos vėlyvos fazes kvėpavimo takų uždegimo metu.

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49

Milne, Elodie Marie. "Characterisation of the receptor subtype and mechanism by which PGE2 inhibits neutrophil and eosinophil activation". Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/21424.

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The aim of this thesis was to identify the EP-receptor subtype(s) mediating: - inhibition of the superoxide anion generation in human neutrophils stimulated by formyl methionyl leucine phenylalanine (FMLP), - inhibition of eosinophil cationic protein (ECP) release in a mixed population of PMN stimulated by FMLP, - inhibition of ECP release of superoxide anion generation in a pure population of human eosinophils stimulated by FMLP and C5a respectively, Another part of this study was to test the hypothesis that cAMP is the second messenger mediating inhibition of neutrophil and eosinophil activation, by PGE₂. In the neutrophils, PGE₂ and the selective EP₂-receptor agonists produced a concentration-related inhibition of superoxide anion generation. These results taken together with agents which interfere with the cAMP pathway suggested that inhibition of neutrophil superoxide anion generation by PGE₂ is mediated by stimulation of EP₂ receptors and subsequent activation of adenylate cyclase. From the work carried out using a mixed population of PMN it was not possible to identify the subtype of EP-receptor involved in eosinophil activation. However, since the presence of neutrophils in the preparation could influence the effects of agonists on eosinophil activation, experiments were repeated using a pure population of eosinophils. The results obtained would support the involvement of an EP₂ receptor mediating the inhibition of ECP release produced by PGE₂. The study of the possible role for cAMP as a second messenger was mainly performed in a mixed population of PMN not enabling us to draw any conclusion. However, the measurement of cAMP levels in a pure population of eosinophils support this hypothesis, but further study is required in order to definitively conclude on this matter.

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50

De, Salvo Carlo <1975&gt. "Pathogenic role of IL-33-mediated eosinophil infiltration and function in experimental inflammatory bowel disease". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5286/1/De_Salvo_Carlo_tesi.pdf.

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IL-33/ST2 axis is known to promote Th2 immune responses and has been linked to several autoimmune and inflammatory disorders, including inflammatory bowel disease (IBD), and recent evidences show that it can regulate eosinophils (EOS) infiltration and function. Based also on the well documented relationship between EOS and IBD, we assessed the role of IL-33-mediated eosinophilia and ileal inflammation in SAMP1/YitFc (SAMP) murine model of Th1/Th2 chronic enteritis, and we found that IL-33 is related to inflammation progression and EOS infiltration as well as IL-5 and eotaxins increase. Administering IL-33 to SAMP and AKR mice augmented eosinophilia, eotaxins mRNA expression and Th2 molecules production, whereas blockade of ST2 and/or typical EOS molecules, such as IL-5 and CCR3, resulted in a marked decrease of inflammation, EOS infiltration, IL-5 and eotaxins mRNA expression and Th2 cytokines production. Human data supported mice’s showing an increased colocalization of IL-33 and EOS in the colon mucosa of UC patients, as well as an augmented IL-5 and eotaxins mRNA expression, when compared to non-UC. Lastly we analyzed SAMP raised in germ free (GF) condition to see the microbiota effect on IL-33 expression and Th2 responses leading to chronic intestinal inflammation. We found a remarkable decrease in ileal IL-33 and Th2 cytokines mRNA expression as well as EOS infiltration in GF versus normal SAMP with comparable inflammatory scores. Moreover, EOS depletion in normal SAMP didn’t affect IL-33 mRNA expression. These data demonstrate a pathogenic role of IL-33-mediated eosinophilia in chronic intestinal inflammation, and that blockade of IL-33 and/or downstream EOS activation may represent a novel therapeutic modality to treat patients with IBD. Also they highlight the gut microbiota role in IL-33 production, and the following EOS infiltration in the intestinal mucosa, confirming that the microbiota is essential in mounting potent Th2 response leading to chronic ileitis in SAMP.

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