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dc.contributor.authorGekara, Nelson O
dc.contributor.authorWeiss, Siegfried
dc.date.accessioned2009-02-03T09:38:58Z
dc.date.available2009-02-03T09:38:58Z
dc.date.issued2008-01
dc.identifier.citationMast cells initiate early anti-Listeria host defences. 2008, 10 (1):225-36 Cell. Microbiol.en
dc.identifier.issn1462-5822
dc.identifier.pmid17714516
dc.identifier.doi10.1111/j.1462-5822.2007.01033.x
dc.identifier.urihttp://hdl.handle.net/10033/48373
dc.description.abstractThe Gram-positive bacterium Listeria monocytogenes (L. m.) is the aetiological agent of listeriosis. The early phase listeriosis is characterized by strong innate host responses that play a major role in bacterial clearance. This is emphasized by the fact that mice deficient in T and B cells have a remarkable ability to control infection. Mast cells, among the principal effectors of innate immunity, have largely been studied in the context of hyper-reactive conditions such as allergy and autoimmune diseases. In the present study, we evaluated the significance of mast cells during the early phase of listeriosis. Compared with controls, mice depleted of mast cells showed hundred-fold higher bacterial burden in spleen and liver and were significantly impaired in neutrophil mobilization. Although L. m. interacts with and triggers mast cell degranulation, bacteria were hardly found within such cells. Mainly neutrophils and macrophages phagozytosed L. m. Thus, mast cells control infection not via direct bacterial uptake, but by initiating neutrophils influx to the site of infection. We show that this is initiated by pre-synthesized TNF-alpha, rapidly secreted by mast cell upon activation by L. m. We also show that upon recruitment, neutrophils also become activated and additionally secrete TNF-alpha thus amplifying the anti-L. m. inflammatory response.
dc.language.isoenen
dc.subject.meshAnimalsen
dc.subject.meshColony Count, Microbialen
dc.subject.meshLeukocyte Reduction Proceduresen
dc.subject.meshListeria Infectionsen
dc.subject.meshListeria monocytogenesen
dc.subject.meshLiveren
dc.subject.meshMacrophagesen
dc.subject.meshMast Cellsen
dc.subject.meshMiceen
dc.subject.meshMice, Inbred BALB Cen
dc.subject.meshNeutrophilsen
dc.subject.meshPhagocytosisen
dc.subject.meshSpleenen
dc.titleMast cells initiate early anti-Listeria host defences.en
dc.typeArticleen
dc.contributor.departmentHelmholtz Centre for Infection Research, Department of Molecular Immunology, Inhoffenstrasse 7, 38124 Braunschweig, Germany. Nelson.Gekara@helmholtz-hzi.deen
dc.identifier.journalCellular microbiologyen
refterms.dateFOA2018-06-12T22:49:54Z
html.description.abstractThe Gram-positive bacterium Listeria monocytogenes (L. m.) is the aetiological agent of listeriosis. The early phase listeriosis is characterized by strong innate host responses that play a major role in bacterial clearance. This is emphasized by the fact that mice deficient in T and B cells have a remarkable ability to control infection. Mast cells, among the principal effectors of innate immunity, have largely been studied in the context of hyper-reactive conditions such as allergy and autoimmune diseases. In the present study, we evaluated the significance of mast cells during the early phase of listeriosis. Compared with controls, mice depleted of mast cells showed hundred-fold higher bacterial burden in spleen and liver and were significantly impaired in neutrophil mobilization. Although L. m. interacts with and triggers mast cell degranulation, bacteria were hardly found within such cells. Mainly neutrophils and macrophages phagozytosed L. m. Thus, mast cells control infection not via direct bacterial uptake, but by initiating neutrophils influx to the site of infection. We show that this is initiated by pre-synthesized TNF-alpha, rapidly secreted by mast cell upon activation by L. m. We also show that upon recruitment, neutrophils also become activated and additionally secrete TNF-alpha thus amplifying the anti-L. m. inflammatory response.


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