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The primed neutrophil: a friend or a foe in inflammation
Linköpings universitet, Institutionen för molekylär och klinisk medicin, Infektionsmedicin. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Medicinsk mikrobiologi. Linköpings universitet, Hälsouniversitetet.
1991 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

Human neutrophils are the most abundant of the white blood cells in circulation and represent the first line of defense against invading microorganisms. With a membrane-bound enzyme system (the NADPH oxidase), these cells can generate reactive oxygen metabolites that serve efficiently in antimicrobial defense. Neutrophils are normally dormant in the circulation but may become primed; in that state they can produce an enhanced respiratory burst response upon activation and thereby strengthen the immune response.

During bacterial infections, endogenous inflammatory mediators orbacterial products induce metabolic priming of neutrophils, which thenexpose an increased number of receptors to the peptide f-Meth-Leu-Phe(fMLP). There is, however, no correlation between the increased level ofrespiratory burst response and the level of receptor upregulation, indicating that post-receptor events in the activation sequence are also involved. Neutrophils isolated from an inflammatory focus were found tobe metabolically deactivated as far as the agonists NAP-1/IL 8 and C5awere concerned but primed in relation to tMLP. Further characterizationof exudated cells revealed that the mechanism of priming involves protein kinase C but not a rise in intracellular Ca2+ or a decreased inactivation rate of the oxidase. In primed cells most of the increased production of reactive oxygen species induced by fMLP is located intracellularly, whereas, an increased extracellular release of reactive oxygen species occurs during phagocytosis. The fact that primed cells can both produce and, under certain conditions, release increased amounts of hydrogen peroxide raises the question of whether the primed cell is a friend or a foe in the inflammatory reaction.

sted, utgiver, år, opplag, sider
Linköping: Linköpings universitet , 1991. , s. 48
Serie
Linköping University Medical Dissertations, ISSN 0345-0082 ; 335
HSV kategori
Identifikatorer
URN: urn:nbn:se:liu:diva-28563Lokal ID: 13716ISBN: 91-7870-626-2 (tryckt)OAI: oai:DiVA.org:liu-28563DiVA, id: diva2:249374
Disputas
1991-05-24, Patologiska Institutionens föreläsningssal, Regionsjukhuset, Linköping, 09:00 (svensk)
Opponent
Merknad
Papers, included in the Ph.D. thesis, are not registered and included in the posts from 1999 and backwards.Tilgjengelig fra: 2009-10-09 Laget: 2009-10-09 Sist oppdatert: 2012-07-18bibliografisk kontrollert

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Totalt: 196 treff
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