Last edited by Zuhn
Wednesday, July 22, 2020 | History

3 edition of Regulation of Human Eosinophil Transmigration Across Lung Epithelium found in the catalog.

Regulation of Human Eosinophil Transmigration Across Lung Epithelium

Liu, Lixin.

Regulation of Human Eosinophil Transmigration Across Lung Epithelium

by Liu, Lixin.

  • 372 Want to read
  • 14 Currently reading

Published by Uppsala Universitet .
Written in English

    Subjects:
  • Life Sciences - Anatomy & Physiology,
  • Life Sciences - Cytology,
  • Cytology,
  • Respiratory System Physiology,
  • Science,
  • Medical

  • Edition Notes

    SeriesComprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, 1044
    The Physical Object
    FormatPaperback
    Number of Pages48
    ID Numbers
    Open LibraryOL12854322M
    ISBN 109155450423
    ISBN 109789155450427

      Acute inflammation of the intestine is characterized by polymorphonuclear leucocytes (PMN) migration first into the mucosa, then across the epithelium and . Asthma is a pulmonary inflammatory disease dependent on eosinophil and mast cell infiltration into the lung. CD34 is a sialomucin expressed by both of these cell types, and we have used CD34 −/− mice and a standard mouse model of asthma to evaluate the importance of CD34 expression on disease development. In comparison with wild-type (wt) mice, CD34 −/− mice exhibited a dramatic.

    Eosinophils have long been known to infiltrate tumors, and in most cases, this is associated with an improved prognosis. However, the reasons behind this infiltration and the mechanism of action of the eosinophil have remained elusive. In this article, we explore the biology of eosinophils and examine their function in homeostasis and disease states, specifically focusing on what is currently. In contrast to studies demonstrating impaired eosinophil migration across the airway epithelium following acute OVA challenge, the transmigration of eosinophils from the lung into the airway lumen in MMPdeficient mice repetitively challenged with allergen was not impaired, as MMPdeficient mice had a similar reduction in peribronchial.

    We hypothesized that transmigration across the endothelium-epithelium bilayer suppresses PMN apoptosis and sought to elucidate the underlying mechanisms. PMNs freshly isolated from normal volunteers were allowed to migrate across polycarbonate membranes alone or membranes coated with a bilayer of human lung endothelial and epithelial cells. Here, we investigated the role of PGE(2) and its receptor, E-type prostanoid receptor (EP)-4, in the regulation of eosinophil interaction with human pulmonary microvascular endothelial cells.


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Regulation of Human Eosinophil Transmigration Across Lung Epithelium by Liu, Lixin. Download PDF EPUB FB2

Taken together, these results show the importance of Ca2+ in eosinophil migration across lung epithelium and support a distinctive regulatory role of intracellular and extracellular Ca2+ for the two cell types involved in this process; i.e., the transmigration of human eosinophils across a monolayer of lung epithelial cells is regulated by the Cited by: Eosinophil infiltration into the lung tissues and airways is a hallmark of allergic asthma.

To reach the lung lumen, eosinophils migrate across the vascular endothelium, through the interstitial matrix and across lung epithelium.

The present investigation deals with the regulatory mechanisms of human eosinophil transmigration across lung. Effect of extracellular Ca 2 on eosinophil transmigration across H epithelial cell monolayers (A) and eosinophil migration in the Boyden chamber chemotaxis assay in the absence of epithelial.

In patients with asthma, eosinophils are primed and massively infiltrate lung tissues and migrate across epithelia into airways. Using blocking monoclonal antibodies, we found that eosinophil transmigration across a lung epithelial cell monolayer depended on the functions of Cited by:   We have recently established an in vitro model to study the regulation of human eosinophil transmigration across a monolayer of lung epithelial cells (15, 16).

We found that priming eosinophils with cytokines such as interleukin (IL)-5 or with platelet-activating factor (PAF) enhances their transmigration across lung epithelium toward Cited by: transmigration across lung epithelium.

Both responses are the regulation of human eosinophil transmigration across therefore elicited by extracellular Ca2. We suggest that, as a monolayer of lung epithelial cells (15, 16).

We found an important priming signal for human eosinophil functional that priming eosinophils with cytokines such as. Abstract. In this chapter we describe an optimized eosinophil transmigration assay.

Transmigration of purified human peripheral blood eosinophils can be studied using special insert with membrane coated with extracellular matrix components or membrane covered with cells growing as a confluent monolayer, such as vascular endothelial cells of any origin or airway epithelial cells.

GASTROENTEROLOGY ; Human Eosinophils Migrate Across an Intestinal Epithelium in Response to Platelet-Activating Factor MURRAY B. RESNICK, SEAN P. COLGAN, CHARLES A. PARKOS, CHARLENE DELP-ARCHER, DEIDRE MCGUIRK, PETER F. WELLER, and JAMES L. MADARA Division of Gastrointestinal Pathology, Department of Pathology.

To reach the lung lumen, eosinophils must migrate across the vascular endothelium, through the interstitial matrix, and across the lung epithelium. The regulation of this process is obscure. Chronic obstructive pulmonary disease (COPD) is a common and important disease.

Neutrophils have been shown to play a fundamental role in its development and progression. Understanding the mechanisms underlying the trafficking of neutrophils across the vascular endothelium into the lung could potentially allow the development of targeted biological treatments.

The early stages of neutrophil. Effects of inflammatory cytokines on the permeability of human lung microvascular endothelial cell monolayers and differential eosinophil transmigration JB Sedgwick, WW. BusseDifferential regulation of eosinophil adhesion and transmigration by pulmonary microvascular endothelilal cells.

J Immunol, (), pp. Due to the key role of the lung in efficient transfer of oxygen in exchange for carbon dioxide, a controlled inflammatory response is essential for restoration of tissue homeostasis following airway exposure to bacterial pathogens or environmental toxins. Unregulated or prolonged inflammatory responses in the lungs can lead to tissue damage, disrupting normal tissue architecture, and.

In patients with asthma, eosinophils are primed and massively infiltrate lung tissues and migrate across epithelia into airways. Using blocking monoclonal antibodies, we found that eosinophil transmigration across a lung epithelial cell monolayer depended on the functions of αMβ2 integrin CD11b/CD To study the role of Ca2+ in eosinophil priming and transepithelial migration, we treated.

Methods. Purified blood eosinophils were treated with or without montelukast; MK, a 5-lipoxygenase–activating protein inhibitor; or leukotriene (LT) D ion assays through Matrigel were performed in the presence of 5-oxo-6,8,11,eicosatetraenoic acid (5-oxo-ETE), a potent eosinophil chemotactic factor, or LTD sion of molecules implicated in plasmin generation.

Interestingly, both the eosinophil chemoattractant eotaxin-3 and periostin have been shown to be overexpressed following vascular injury. 36, 37 It has been demonstrated that eotaxin-3 is the single eosinophil chemoattractant induced in EE; its expression is localized in the epithelial layer.

14 Based on these collective results, we propose a. Epithelial cells are targets for regulation by SPMs that act to attenuate pro-inflammatory responses and promote epithelial restitution.

Accelerates resolution of lung eosinophils, reduces airway hyperresponsiveness Serhan CN, Parkos CA, Delp-Archer C, Madara JL. Lipoxin A4 modulates transmigration of human neutrophils across intestinal.

To reach the lung lumen, eosinophils must migrate across the vascular endothelium, through the interstitial matrix, and across the lung epithelium. The regulation of this process is obscure. In this study, we investigated the migration of human eosinophils across confluent monolayers of either human lung H epithelial cells or primary human.

A subset of human eosinophils, especially after cytokine treatment, has been reported to express the Mig receptor CXCR3. To determine whether allergen-induced expression of Mig could be responsible, at least in part, for eosinophil lung recruitment, we examined CXCR3 expression on murine eosinophils.

A recent study provided insight into mechanisms by which transmigration of eosinophils across endothelial cells may occur in the lung.

BAL fluid obtained from patients with AEP-induced eosinophil transmigration across endothelial cells in vitro, which was blocked when anti-β2 integrin antibodies were added to the system (33). Pathogen induced migration of neutrophils across mucosal epithelial barriers requires epithelial production of the chemotactic lipid mediator, hepoxilin A 3 (HXA 3).HXA 3 is an eicosanoid derived from arachidonic acid.

Although eosinophils are also capable of penetrating mucosal surfaces, eosinophilic infiltration occurs mainly during allergic processes whereas neutrophils dominate mucosal. Paige Lacy, in Cytokine Effector Functions in Tissues, CCL11/Eotaxin.

CCL11/ Eotaxin is an important eosinophil-specific chemokine that is associated with the recruitment of eosinophils into sites of inflammation.

It is generated in the lungs of asthmatic patients and has a role in targeting eosinophils at inflammatory foci. 97, Mouse models of allergic airway inflammation.Sean Jedrzkiewicz's 6 research works with citations and reads, including: Resident CD8(+) T cells suppress CD4(+) T cell-dependent late allergic airway responses.Eosinophils are most numerous in tissues with a mucosal epithelial interface with the environment, such as the respiratory, gastrointestinal, and lower genitourinary tracts.

Eosinophils are not present in the lungs of healthy people, so their presence in tissue or bronchoalveolar lavage fluid (> 5% of differential count) identifies a.