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  • 1
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    The development of allergic inflammation (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-07-25
    Description: Allergic disorders, such as anaphylaxis, hay fever, eczema and asthma, now afflict roughly 25% of people in the developed world. In allergic subjects, persistent or repetitive exposure to allergens, which typically are intrinsically innocuous substances common in the environment, results in chronic allergic inflammation. This in turn produces long-term changes in the structure of the affected organs and substantial abnormalities in their function. It is therefore important to understand the characteristics and consequences of acute and chronic allergic inflammation, and in particular to explore how mast cells can contribute to several features of this maladaptive pattern of immunological reactivity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3573758/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3573758/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galli, Stephen J -- Tsai, Mindy -- Piliponsky, Adrian M -- R01 AI023990/AI/NIAID NIH HHS/ -- R01 AI023990-20/AI/NIAID NIH HHS/ -- R01 AI070813/AI/NIAID NIH HHS/ -- R01 AI070813-01/AI/NIAID NIH HHS/ -- R01 CA072074/CA/NCI NIH HHS/ -- R01 CA072074-15/CA/NCI NIH HHS/ -- England -- Nature. 2008 Jul 24;454(7203):445-54. doi: 10.1038/nature07204.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, California 94305, USA. sgalli@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18650915" target="_blank"〉PubMed〈/a〉
    Keywords: Allergens/immunology ; Animals ; Chronic Disease ; Epithelium/immunology ; Humans ; Hypersensitivity/genetics/*immunology/*pathology ; Immunoglobulin E/immunology ; Inflammation/genetics/*immunology/*pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Mast cells can enhance resistance to snake and honeybee venoms (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-29
    Description: Snake or honeybee envenomation can cause substantial morbidity and mortality, and it has been proposed that the activation of mast cells by snake or insect venoms can contribute to these effects. We show, in contrast, that mast cells can significantly reduce snake-venom-induced pathology in mice, at least in part by releasing carboxypeptidase A and possibly other proteases, which can degrade venom components. Mast cells also significantly reduced the morbidity and mortality induced by honeybee venom. These findings identify a new biological function for mast cells in enhancing resistance to the morbidity and mortality induced by animal venoms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Metz, Martin -- Piliponsky, Adrian M -- Chen, Ching-Cheng -- Lammel, Verena -- Abrink, Magnus -- Pejler, Gunnar -- Tsai, Mindy -- Galli, Stephen J -- P50 HL067674/HL/NHLBI NIH HHS/ -- P50 HL67674/HL/NHLBI NIH HHS/ -- R01 AI023990/AI/NIAID NIH HHS/ -- R01 CA072074/CA/NCI NIH HHS/ -- R01 CA72074/CA/NCI NIH HHS/ -- R37 AI23990/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 28;313(5786):526-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305-5324, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16873664" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bee Venoms/*antagonists & inhibitors/toxicity ; Carboxypeptidases A/antagonists & inhibitors/*metabolism ; Cell Degranulation ; Chymases ; Crotalid Venoms/*antagonists & inhibitors/metabolism/toxicity ; Hypothermia/etiology ; Immunity, Innate ; Mast Cells/enzymology/immunology/*physiology ; Mice ; Mice, Inbred C57BL ; Peptide Hydrolases/metabolism ; Peritoneal Cavity/cytology ; Plant Proteins/pharmacology ; Protease Inhibitors ; Serine Endopeptidases/metabolism ; Viper Venoms/*antagonists & inhibitors/metabolism/toxicity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
    Electronic Resource
    Electronic Resource
    Regulation of apoptosis in mast cells (2000)
    Springer
    Apoptosis 5 (2000), S. 435-441 
    Details
    ISSN: 1573-675X
    Keywords: activation ; apoptosis ; death receptors ; glucocorticosteroids ; mast cells ; survival factors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Apoptosis is a physiological process of cell death that occurs in all multicellular organisms. Its dysregulation has been postulated as one of the main causes in the development of diseases such as cancer, AIDS, autoimmune diseases and allergy. Apoptosis has been mainly studied in the inflammatory cells that participate in the late and chronic stages of allergy (eosinophils, neutrophils, lymphocytes and macrophages) as a new way to elucidate the pathogenesis of this disease. Nevertheless, much less it is known about the regulation of apoptosis in the “initiators” of the allergic process: The Mast Cells. In normal conditions, mast cells are described as long-living cells that keep a constant number of cells in tissues. However, increased numbers of mast cells are observed in the late phase of asthma and in both the inflammatory and in the repair/remodeling stage of various inflammatory/fibrotic disorders. In this report, we discuss the possible mechanisms that regulate the apoptotic process in normal conditions and disease, such as survival factors and death receptors. A link between mast cell activation, during the early stages of the allergic process, and triggering of anti-apoptotic signaling pathways is also suggested as an important contributor to the extended life of mast cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1009680500988
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  • 4
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    Mast cell degranulation by a hemolytic lipid toxin decreases GBS colonization and infection (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-07-19
    Description: Ascending infection of microbes from the lower genital tract into the amniotic cavity increases the risk of preterm birth, stillbirth, and newborn infections. Host defenses that are critical for preventing ascending microbial infection are not completely understood. Group B Streptococcus (GBS) are Gram-positive bacteria that frequently colonize the lower genital tract of healthy women but cause severe infections during pregnancy, leading to preterm birth, stillbirth, or early-onset newborn infections. We recently described that the GBS pigment is hemolytic, and increased pigment expression promotes GBS penetration of human placenta. Here, we show that the GBS hemolytic pigment/lipid toxin and hyperpigmented GBS strains induce mast cell degranulation, leading to the release of preformed and proinflammatory mediators. Mast cell–deficient mice exhibit enhanced bacterial burden, decreased neutrophil mobilization, and decreased immune responses during systemic GBS infection. In a vaginal colonization model, hyperpigmented GBS strains showed increased persistence in mast cell–deficient mice compared to mast cell–proficient mice. Consistent with these observations, fewer rectovaginal GBS isolates from women in their third trimester of pregnancy were hyperpigmented/hyperhemolytic. Our work represents the first example of a bacterial hemolytic lipid that induces mast cell degranulation and emphasizes the role of mast cells in limiting genital colonization by hyperpigmented GBS.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
    Published by American Association for the Advancement of Science (AAAS)
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